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0 | The effect of amiodarone pretreatment on survival of mice with cocaine toxicity. | Cocaine is a common drug of abuse and use has been associated with ventricular dysrhythmias. Published guidelines suggest that amiodarone is the first line antidysrhythmic for ventricular tachycardia and fibrillation. However, the effects amiodarone in the setting of cocaine toxicity are unknown and unstudied. The purpose of this study was to evaluate the safety and efficacy of amiodarone pretreatment in a murine model of acute cocaine toxicity.</AbstractText>This was a randomized, blinded, placebo controlled investigation using male CF-1 mice weighing 29-37 g. First, the safety of an intraperitoneal dose of amiodarone (40 mg/kg) was confirmed in 5 mice. Second, based on preliminary investigations, an approximate intraperitoneal LD50 dose of cocaine (110 mg/kg) was identified and used as the cocaine dose in this study. Animals were then randomized to 2 groups. The control group received 0.5 mL of intraperitoneal 0.9% saline 30 minutes before cocaine. The study group received 40 mg/kg of intraperitoneal amiodarone (40 mg/kg) 30 minutes before cocaine. A blinded observer monitored mice for 2 hours after cocaine administration.</AbstractText>No mice in the amiodarone-only group developed any signs of toxicity or died. In the saline + cocaine group 31/32 (96.9%; 95% CI 83.8 to 99.9) mice seized with a median time to seizure of 2.5 minutes, and 23/32 (71.9%; 95% CI 52.3 to 86.3) died with a median time to death of 5.5 minutes. In the amiodarone + cocaine group 31/33 (93.9%; 95% CI 79.0 to 99.3) mice seized with a median time to seizure of 2.0 minutes, and 24/33 (72.7%; 95% CI 54.5 to 86.7) died with a median time to death of 6.0 minutes. All animals that died did so within 9 minutes. The difference in the proportion of animals dying in the amiodarone + cocaine group compared to the saline + cocaine group was 0.008 (-21 to 22%).</AbstractText>In this study, pretreatment with amiodarone in cocaine poisoned mice resulted in no change in seizure incidenceor mortality. However, definite conclusions about the reason for these findings cannot be drawn from this model.</AbstractText> |
1 | Atenolol premedication in patients undergoing closed mitral commissurotomy. | Perioperative tachycardia is common in patients undergoing surgery. In patients with mitral valve stenosis, the tachycardia can precipitate congestive heart failure and pulmonary oedema. Efficacy of atenolol premedication (0.5 mg/kg) for haemodynamic stability was assessed in 37 patients undergoing closed mitral commissurotomy (Group I) and compared with 43 patients who did not receive it (Group II). Patients with mild aortic regurgitation, atrial fibrillation, mild to moderate pulmonary artery hypertension or severe pulmonary artery hypertension without right ventricular failure were all included in the study. All patients were premedicated with tablet diazepam 0.1 mg/Kg, on the previous night and on the day of surgery and intramuscular morphine 0.1 mg/kg and glycopyrrolate 0.2 mg 45 min before surgery. In addition, in group I, atenolol 0.5 mg / kg was administered at night and 2 hours prior to surgery. Anaesthesia was induced with thiopental, morphine, oxygen and isoflurane. Tracheal intubation was facilitated by pancuronium bromide 0.12 mg/kg. Maintenance was with morphine, isoflurane and nitrous oxide in oxygen. The study was confined to the periods of maximal anaesthetic and surgical haemodynamic stress like laryngoscopy, intubation, surgical incision and commissurotomy. For all periods of haemodynamic stress, heart rate was significantly lower in group I, (p<0.05) than Group II. Blood pressure variations were comparable in both the groups. A statistically significant (p<0.001) decrease in systolic, diastolic, and mean arterial pressures, were observed in patients of both groups before and during valvotomy. One patient in atenolol group experienced bradycardia of <45 beats per minute. This was not associated with hypotension and it was easily treated with atropine. This study documents that, selective ss - blockade with atenolol in patients undergoing closed mitral commissurotomy, ensure a predictable control of heart rate in the perioperative period. |
2 | Comparison of the immediate post-operative outcome of two different myocardial protection strategies: antegrade-retrograde cold St Thomas blood cardioplegia versus intermittent cross-clamp fibrillation. | The objective of this study was to compare the immediate post-operative outcome of two myocardial protection strategies. Data of consecutive elective first time coronary artery bypass grafting (CABG) were analysed: Group A (n=671, antegrade-retrograde cold St Thomas blood cardioplegia) and Group B (n=783, intermittent cross-clamp fibrillation). Age, angina class, myocardial infarction (MI), pre-operative rhythm, respiratory disease, smoking, diabetes mellitus (DM), hypertension (HT), renal function, cerebrovascular disease, body mass index (BMI) and Parsonnet score were comparable. Significant differences existed in gender (P=0.02), peripheral vascular disease (PVD) (P=0.04), heart failure class (P=0.0001), left ventricular (LV) function (P=0.01), disease severity (P=0.02), left main stem (LMS) (P=0.02) and preinduction intra-aortic balloon pump(IABP) (P=0.08). Group A had more grafts (P=0.008), longer bypass (P=0.0001) and cross-clamp time (P=0.0001). Post-operative inotrope, MI, arrhythmias, neurological, renal complications, multi-organ failure, sternal re-wiring, ventilation, length of stay and mortality were comparable. There was higher IABP usage and longer intensive therapy unit (ITU) stay (P=0.01) in Group B. Chronic obstructive airway disease (COAD), renal dysfunction, cross-clamp time, bypass time, post-operative inotrope or IABP and re-exploration predicted longer ITU stay. Intermittent cross-clamp fibrillation is a versatile and cost-effective method of myocardial protection, with the immediate post-operative outcome comparable to antegrade-retrograde cold St Thomas blood cardioplegia in elective first-time CABG. |
3 | Combined mitral valve repair, LVOT myectomy and left atrial cryoablation therapy. | Asymmetric septal hypertrophy (ASH) is a common cause of left ventricular (LV) outflow tract obstruction. Mitral valve (MV) regurgitation is present in 30% of those patients as well as biatrial enlargement. Furthermore, paroxysmal or chronic atrial fibrillation (AF) occurs in up to 22%. Two male patients were admitted for shortness of breath and decreased physical ability. Hypertrophic obstructive cardiomyopathy (HOCM) with ASH, severe MV regurgitation and chronic AF were diagnosed in both patients; present for 8 years in patient 1 and 1 year in patient 2. Both received MV annuloplasty, transaortic septal resection using the modified Morrow et al.'s technique and left atrial cryoablation therapy via median sternotomy. Intraoperative measurement revealed no residual gradients and competent MV, furthermore, both patients were discharged in sinus rhythm. |
4 | A huge pseudoaneurysm of the left ventricle after simple gluing of an oozing-type postinfarction rupture. | Left ventricular free wall rupture is a major complication after myocardial infarction. Simple gluing for a rupture site, without a cardiopulmonary bypass, has been reported useful.</AbstractText>We experienced a left ventricular pseudoaneurysm, of 8 cm in size, emerging at a previous rupture site 1 year after gluing with TachoComb for an oozing-type rupture due to an acute anteroseptal myocardial infarction.</AbstractText>The pseudoaneurysm was successfully extirpated, under a cardiopulmonary bypass, with induction of ventricular fibrillation.</AbstractText>Patients, after simple gluing for a left ventricular free wall rupture, should be carefully followed up regarding the occurrence of a pseudoaneurysm at the repair site.</AbstractText> |
5 | Microwave ablation of atrial fibrillation in conjunction with treatment of early postoperative massive left atrial thrombosis. | Left atrial thrombosis is a rare complication of both atrial fibrillation and mitral valve surgery. A patient with a massive atrial thrombosis associated with symptoms of severe heart failure is presented. Restoration of rhythmical ventricular contraction and, ultimately, atrial contractility is of great benefit for providing relief from symptoms and for preventing thrombus recurrence. We present an approach to surgically treat atrial fibrillation using a new microwave energy source in a patient with left atrial thrombosis who requires a mitral valve prosthesis replacement. |
6 | Factors affecting survival after prehospital asystolic cardiac arrest in a Basic Life Support-Defibrillation system. | Previous studies have shown a low but meaningful survival rate in cases of prehospital cardiac arrest with an initial rhythm of asystole. There may be, however, an identifiable subgroup in which resuscitation efforts are futile. This study identified potential field criteria for predicting 100% nonsurvival when the presenting rhythm is asystole in a Basic Life Support-Defibrillation (BLS-D) system.</AbstractText>This prospective cohort study, a component of Phases I and II of the Ontario Prehospital Advanced Life Support (OPALS) Study, was conducted in 21 Ontario communities with BLS-D level of care, and included all adult arrests of presumed cardiac etiology according to the Utstein Style Guidelines. Analyses included descriptive and appropriate univariate tests, as well as multivariate stepwise logistic regression to determine predictors of survival.</AbstractText>From 1991 to 1997, 9899 consecutive cardiac arrest cases with the following characteristics: male (67.2%), bystander-witnessed (44.7%), bystander CPR (14.2%), call response interval (CRI) </= 8 minutes (82%) and overall survival (4.3%) were enrolled. Of 9529 cases with available rhythm strip recordings, initial arrest rhythms were asystole in 40.8%, pulseless electrical activity in 21.2% and ventricular fibrillation or ventricular tachycardia in 38%. Of 3888 asystolic patients, 9 (0.2%) survived to discharge; 3 of these cases were unwitnessed arrests with no bystander CPR. There were no survivors if the CRI exceeded 8 minutes. Logistic regression analysis demonstrated that independent predictors of survival to admission were "CRI in minutes" (odds ratio [OR] = 0.87; 95% confidence interval [CI], 0.77-0.98) and "bystander-witnessed" (OR = 2.6; 95% CI, 1.5-4.4).</AbstractText>In a BLS-D system, there is a very low but measurable survival rate for prehospital asystolic cardiac arrest. CRIs of over 8 minutes were associated with 100% nonsurvival, whereas unwitnessed arrests with no bystander CPR were not. These data add to the growing literature that will help guide ethical decision-making for protocol development in emergency medical services systems.</AbstractText> |
7 | Hypothermic modulation of anoxic brain injury in adult survivors of cardiac arrest: a review of the literature and an algorithm for emergency physicians. | Anoxic brain injury is a common outcome after cardiac arrest. Despite substantial research into the pathophysiology and management of this injury, a beneficial treatment modality has not been previously identified. Recent studies show that induced hypothermia reduces mortality and improves neurological outcomes in patients resuscitated from ventricular fibrillation. This article reviews the literature on induced hypothermia for anoxic brain injury and summarizes a treatment algorithm proposed by the Canadian Association of Emergency Physicians Critical Care Committee for hypothermia induction in cardiac arrest survivors. |
8 | Development of optical mapping system with real-time feedback stimulation in the heart. | Recent studies showed that electrical stimuli in the excitable gaps during ventricular fibrillation (VF) are important for defibrillation requiring low electrical energy. We developed an optical mapping system that measures action potentials and controls the timings and sites of electrical stimulus to verify the effectiveness of electrical stimulation in the excitable gaps. In this paper, the time delay of feedback algorithms with our optical mapping system was evaluated and the feedback stimulation protocols were operated using isolated rabbit hearts. We optically mapped electrical activity from a surface of Langendorff-perfused rabbit hearts stained with a voltage sensitive dye using high-speed video cameras. Acquiring image data triggered a timing pulse after 5.5ms using LED. In the experiment using isolated rabbit hearts, the timing delay was 10.2 ms. The velocity and direction of wave propagation was calculated in real-time using two reference points on a field of view. The two electrical stimulating points was selected by the action potentials on electrical stimulation points. The electrical shock was delivered on the point that was triggered earlier than the other point. |
9 | Combined Bispectral and Bicoherency approach for Catastrophic Arrhythmia Classification. | Quantitative classification of cardiac arrhythmia is an important tool in ICU and CCU that enables on line monitoring of the cardiac activities. Among fatal arrhythmias are atrial fibraliation (AF), ventricular tachycardia (VT), and ventricular fibrillation that require special algorithms for detection and so for direct medical actions. In this paper, a combined bispectrum and bicoherency classification algorithm is introduced. It is based on extracting diagnostic features from the bispectrum contours and the bicoherency indices that better describe the arrhythmia. A simple classification scheme utilizing these features showed notable sensitivity and specificity. The obtained results are found comparable to the state of the art algorithms with the ability of being integrated for on line monitoring and classification. |
10 | Dose reponse behavior in a physiologically accurate defibrillation model. | Termination of an episode of ventricular fibrillation by electric countershock is a probabilistic phenomenon. In a clinical or experimental setting, defibrillation exhibits dose-response behavior. We demonstrate for the first time that a physiologically and anatomically accurate model of defibrillation is able to simulate this dose-response behavior. We also demonstrate the ability of this computational model to reproduce the full range of observed shock responses. Finally, we show that the brief cessation of electrical activity on the epicardial surface after a shock near the defibrillation threshold, the isoelectric window, can be explained by the slowed propagation velocity of transmural activation wavefronts around a filament of singularity in the myocardium. |
11 | Intravascular parasympathetic cardiac nerve stimulation prevents ventricular arrhythmias during acute myocardial ischemia. | Although previous animal studies clearly demonstrated antiarrhythmic effects of vagal stimulation during acute myocardial ischemia, highly invasive nature of vagal stimulation limited its clinical use. Recently, intravascular parasympathetic cardiac nerve stimulation (IPS) has emerged as a novel approach to the cardiac autonomic nervous system. We hypothesized that IPS might prevent ventricular arrhythmias during acute myocardial ischemia.</AbstractText>The IPS (36 V, 10 Hz) was performed in superior vena cava using an expandable electrode-basket catheter. In 18 open-chest dogs, left anterior descending coronary artery ligation was performed without IPS (control group, n= 6), with IPS (IPS group, n= 6) and with IPS and right atrial pacing at 180/min (IPS+P group, n=6). The ECGs were monitored for 60 min. The incidence and severity of ventricular arrhythmias were analyzed.</AbstractText>The IPS significantly decreased the frequency of premature ventricular contractions (control group: 9.1 &#177; 4.6/min, IPS group: 0.2 &#177; 0.4 /min, IPS+P group: 10.6 &#177; 4.2 / min; p&lt;0.05). The frequency of ventricular tachycardia was lower in IPS group (0 &#177; 0 /min) than in control group (0.15 &#177; 0.18 /min, p&lt;0.05) and than in IPS+P group (0.17 &#177; 0.12 /min, p<0.05). The incidence of ventricular fibrillation was lower in IPS group (0%) than in control group (33.3%) and than in IPS+P group (33.3%).</AbstractText>The IPS suppressed ventricular arrhythmias during acute ischemia mainly through its bradycardiac effect.</AbstractText> |
12 | 3D Heart Simulation And Recognition Of Various Events. | This paper presents a new way to solve the inverse problem of electrocardiography in terms of heart model parameters. The developed event estimation and recognition method is based on an optimization system of heart model parameters. An ANN-based preliminary ECG analyzer system has been created to reduce the searching space of the optimization algorithm. The optimal model parameters were determined by minimizing the objective functions, as relations of the observed and model-generated body surface ECGs. The final evaluation results, validated by physicians were about 86% correct. Starting from the fact that input ECGs contained various malfunction cases, such as Wolff-Parkinson-White (WPW) syndrome, atrial and ventricular fibrillation, these results suggest that this approach provides a robust inverse solution, circumventing most of the difficulties of the ECG inverse problem. |
13 | Adaptive ventricular rate smoothing during atrial fibrillation: a pilot comparison study. | An adaptive ventricular rate smoothing (VRS) algorithm is developed to regularize the ventricular rate during atrial fibrillation (AF) by means of ventricular pacing (VP). Using a quantitative AF-VP model, we conduct pilot study to compare its performance with three other VRS algorithms. Simulations show that all VRS algorithms are effective to stabilize the heart rate during AF when intrinsic ventricular rate is not higher than the maximum pacing rate. The effect of VRS is diminished as the intrinsic ventricular rate increases, whereas slower intrinsic ventricular rate renders more aggressive VP. Compared to other methods, the Adaptive-VRS algorithm tends to stabilize the ventricular rate during AF with less VP, while intrinsic ventricular responses with physiological rate and rhythm are preferably preserved. |
14 | The simultaneous multiple sites epicardial mapping of ventricular fibrillation. | Some recently researches have showed that cardiac electrical activities are chaotic during ventricular fibrillation (VF) [1]. It is very difficult to realize the originations and evolvements of these complex activities by used of non-simultaneous mapping techniques. Simultaneous multiple sites epicardial mapping is one of the precise mapping techniques developed in recent years. Fudan University has designed a novel 64/176-channel epicardial mapping system [2]. The new design includes a multi-electrodes patch, 64-channel ECG (electrocardiogram) signal amplifier, 80-channel A/D converter and a PC (personal computer). It uses finite hardware resources to detect depolarization wave from any way, any direction wherever in the whole mapping area. In this article we will discuss the characteristics of the mapping system and some interesting results we have obtained from the animal trials by use of this system. |
15 | Modeling magnetic catheters in external fields. | We develop a mechanical model for catheters and other interventional devices which are steered by externally applied magnetic fields. Each device contains a permanent magnet near its distal tip. The external magnetostatic field, whose direction and magnitude can be selectively varied, is applied to the vicinity of the tissue where the medical procedure is being performed, in order to orient the catheter tip. At the same time, the length of the catheter is varied by a motorized advancer. The position and orientation of the catheter tip is determined in real-time by electromagnetic means. This information can be fed into a closed-loop control algorithm which would decide how to change the magnetic field and the catheter length. The model includes closed-form solutions of the equilibrium equations, which facilitates accurate estimation of the catheter configuration and the contact force. Once the device is at a target point, the control algorithm can modify the contact force applied to the tissue. Common applications include navigation inside the heart and coronary vessels, electrophysiology (atrial fibrillation, flutter and tachycardia, ventricular tachycardia, etc.) and interventional cardiology (angioplasty). |
16 | A new quantitative analysis technique for cardiac arrhythmia using bispectrum and bicoherency. | Ventricular tachyarrhythmias, in particular ventricular fibrillation (VF), are the primary arrhythmic events in the majority of patients suffering from sudden cardiac death. Attention has focused upon these articular rhythms as it is recognized that prompt therapy can lead to a successful outcome. There has been considerable interest in analysis of the surface electrocardiogram (ECG) in VF centred on attempts to understand the pathophysiological processes occurring in sudden cardiac death, predicting the efficacy of therapy, and guiding the use of alternative or adjunct therapies to improve resuscitation success rates. Atrial fibrillation (AF) and ventricular tachycardia (VT) are other types of tachyarrhythmias that constitute a medical challenge. In this paper, a high order spectral analysis technique is suggested for quantitative analysis and classification of cardiac arrhythmias. The algorithm is based upon bispectral analysis techniques. The bispectrum is estimated using an AR model, and the frequency support of the bispectrum is extracted as a quantitative measure to classify atrial and ventricular tachyarrhythmias. Results show a significant difference in the parameter values for different arrhythmias. Moreover, the bicoherency spectrum shows different bicoherency values for normal and tachycardia patients. In particular, the bicoherency indicates that phase coupling decreases as arrhythmia kicks in. |
17 | Analysis of relation between coronary perfusion pressure and the extracted parameters from a ventricular fibrillation ECG signal. | This work presents an alternative return of spontaneous circulation (ROSC) estimate using indirectly induced presumption that coronary perfusion pressure (CPP) correlates with the extracted parameter from the ventricular fibrillation (VF) ECG signal. In past studies, it is revealed that successful cardiopulmonary resuscitation (CPR) needs at least 30 approximately 40 mmHg CPP during the aortic diastolic period. In 360 segments derived from 18 test dogs with experimental cardiac arrest of cardiac cause, we analyzed the ability of 4 spectral features of VF before countershock to discriminate or not between segments that correspond to CPP. The median frequency (MF), peak frequency (PF), average segment amplitude (ASA) and maximum segment amplitude (MSA) were studied. After preprocessing the raw data acquired from the specific experimental setup and protocol, we verified CPP is a serious estimate of ROSC, and then we analyzed the extracted parameters corresponding to CPP by multiple regression. In the specific conditional frequency domain (MF: 9.42 approximately 12.42 Hz, PF: 8.71 approximately 13.08 Hz, ASA: > 0.19 mV), CPP is correlated to the extracted parameter with 0.71 +/- 0.05 coefficient of multiple determination (R(2)). The combination of MF, PF, and ASA achieved a 79.47 +/- 3% sensitivity and 41.67 +/- 4% specificity in testing. |
18 | Asymmetry in dynamics of action potential duration transition between steady states: a simulation study. | Ventricular fibrillation (VF) contributes importantly to sudden cardiac death, however, exact mechanisms of VF remain elusive. Action potential duration (APD) restitution is widely used to predict dynamics of VF. Restitution of APD is a multi-modal phenomenon, with contributions from previous diastolic intervals (DI), as well as from activation history. We investigated dynamics of change in APD with contributions from memory by using a feedback-based protocol. A Luo-Rudy ionic model of cardiac activation was used to simulate activation. We used four levels of DI, 150, 450, 700, and 1000 msec, to compose a DI sequence which included all possible switches among these DIs. By abruptly changing the DI after APD reached a steady state, we analyzed the transient dynamics of change in APD. As expected, our results showed that for sufficiently long activation, the steady state of APD was unique for each DI. Transient changes in APD showed an asymmetric pattern that was dependent on direction of change in DI, the absolute level of change and the operating level of APD. These results further support the notion that restitution of APD is a multi-modal phenomenon, and that multiple factors need to be considered in using restitution to predict activation dynamics. |
19 | A three phase temporal model for cardiopulmonary resuscitation following cardiac arrest. | Data from a wide variety of studies suggests that survival from cardiac arrest is very much dependent on the implementation of therapeutic maneuvers in a sequence. Emphasis is on the time from the onset of cardiac arrest to the beginning of resuscitative maneuvers. For example, the optimal timing of defibrillation in a patient with ventricular fibrillation is one major issue, but is in part dependent upon having a defibrillating device available. As well, providing artificial circulation requires the presence of a bystander or a resuscitation team ready and willing to perform cardiopulmonary resuscitation. At some point resuscitation includes dealing with the metabolic consequences of prolonged cardiac arrest. This may require drugs or agents that mitigate the longer term consequences of metabolic factors that arise after cardiac arrest and a prolonged period of ischemia. |
20 | Vasopressin in shock states. | There is growing evidence that in end-stage shock or during cardiac arrest, inappropriately low endogenous vasopressin plasma levels may be responsible for pathologic vasodilatation, inadequate organ perfusion, and poor outcome. The purpose of this article is to review recent publications featuring arginine vasopressin as a potent vasoconstrictor in various shock states such as systemic vasodilatation, severe hypovolemia, or cardiac arrest.</AbstractText>Several retrospective investigations give evidence that vasopressin at a dosage of 2-6 U/h is effective in reversing catecholamine-resistant vasodilatory shock due to sepsis or after cardiopulmonary bypass, but prospective randomized controlled trials are warranted. In experimental hypovolemic cardiac arrest or therapy-resistant (irreversible) hypovolemic shock, vasopressin may be an intriguing therapy, although human evidence is not available. Animal data gives strong evidence that vasopressin given during cardiopulmonary resuscitation improves both return of spontaneous circulation and neurological outcome. Clinical experience on the use of vasopressin for in-hospital cardiopulmonary resuscitation with short response time showed equipotency with epinephrine; in patients with out-of-hospital ventricular fibrillation, vasopressin showed improved 24 h survival in comparison with epinephrine. After the large European multicenter study completed in summer 2002, we will hopefully be able to better determine the role of vasopressin versus epinephrine in the management of adult cardiac arrest.</AbstractText>Vasopressin administration is emerging as a rational and promising therapy in the management of various shock states and cardiac arrest.</AbstractText> |
21 | Pacemakers, recent directions and developments. | Pacemaker and implantable cardiovertor defibrillator utilization is evolving rapidly. Expanding indications are reviewed.</AbstractText>Current pacemakers are smaller, more dependable, longer lasting and have rate-adaptive features. Implantable cardiovertor defibrillators use transvenous leads and have advanced pacing abilities. Primary pacing indications remain sinus node dysfunction or atrioventricular conduction abnormalities. Dual-chamber pacemakers compared with single chamber ventricular pacemakers, have small quality of life advantages and result in less atrial fibrillation, but decrease stroke rates and mortality. In congestive heart failure patients with delayed ventricular conduction, cardiac resynchronization therapy (atrially timed biventricular pre-excitation) improves physiological parameters, performance indices and quality of life. Atrial arrhythmias may be prevented or treated with appropriate pacing strategies. Pacing-related improvements for symptomatic neurally mediated syncope and symptomatic hypertrophic obstructive cardiomyopathy have been demonstrated. For patients with coronary artery disease and low ejection fractions, implantable cardiovertor defibrillators are well established in the secondary prevention of sudden death, and may be helpful for primary prevention if there are inducible ventricular arrhythmias. Combining cardiac resynchronization and implantable cardiovertor defibrillators in similar patients is under investigation. The role of atrial defibrillators is being defined. Electromagnetic interference remains possible with these devices, particularly in electromagnetically hostile environments.</AbstractText>More pacemakers and implantable cardiovertor defibrillators will be encountered. Despite increasing sophistication, most often only basic anti-bradycardia modes are essential in the perioperative setting. Understanding the indications for implantation will help the anesthesiologist better support the physiological needs of the patient. Existing perioperative pacemaker-related guidelines for the anesthesiologist still apply.</AbstractText> |
22 | [Advanced cardiac life support in the prehospital setting in the Reykjavik area 1991-1996.]. | Since 1982 an emergency ambulance manned by a physician and two emergency medical technicians has been operated in the Reykjavik area. The physicians have followed guidelines from the American Heart Association (AHA). Until 1986 the AHA guidelines had bicarbonate and in some instances calcium as first line treatment in cardiopulmonary resuscitation (CPR).</AbstractText>The purpose of this study was to evaluate the influence of the advanced cardiac life-support (ACLS) service and of bystanders on survival after cardiopulmonary arrest. Also to compare the survival rates to results of previous studies of CPR outside the hospital in the Reykjavik area.</AbstractText>The data was collected prospectively according to the "Utstein Style" form. From 1991-1996 there were 361 attempted resuscitations by the emergency crew. Fifty-three cardiac arrests were secondary to trauma, suicide, drowning, drug overdose and sudden infantile death. In 308 cases of sudden cardiorespiratory arrest cardiac diseases were the presumed cause in accordance with the Utstein protocol.</AbstractText>In the 308 cases the mean age was 67.2 years and the male/female ratio was 233:75. The mean response time was 4.6 min. Patients admitted to the intensive or cardiac care units were 98 (31%) and 51 (17%) were discharged from the hospital. Ventricular fibrillation or ventricular tachycardia were the most common initial rhythms seen in 176 (57%) patients, asystole in 91 (30%) and other arrhythmias (EMD, agonal) in 41 (13%). Fourty-six patients (26%) with ventricular fibrillation on the first rhythm strip survived to be discharged from the hospital, three (3%) patients with asystole and two (5%) with other arrhythmias. Bystanders were present in 211 (68%) of cases and it fourfoulded the likelihood of discharge (OR 4.0; 95% CI 1.5-10.4; p=0.0025). There is no statistical difference in mean response time and survival rates between this study and previous studies from 1982-1986 and 1987-1990.</AbstractText>When sudden cardiorespiratory arrest is witnessed the probability of survival is multiplied. We conclude that the results of ACLS outside the hospital in Reykjavik and surrounding area continue to be among the best. Changes in ACLS guidelines do not appear to have increased survival.</AbstractText> |
23 | Non-pharmacological treatment of atrial fibrillation. | In selected patients with atrial fibrillation and severe symptoms, non-pharmacological treatment may be an alternative or supplement to drug therapy. Atrioventricular nodal radiofrequency ablation (requires pacemaker implantation), or atrial pacing for sick sinus syndrome, are established treatment modalities. All other non-pharmacological therapies for atrial fibrillation are still experimental. After the Maze operation, atrial depolarization has to follow one specific path determined by surgical scars in the myocardium. This prevents new episodes of atrial fibrillation, but at a cost of perioperative morbidity and mortality. Catheter-based "Maze-like" radiofrequency ablation is technically difficult, and thrombo-embolic complications may occur. Paroxysmal atrial fibrillation sometimes is initiated by spontaneous depolarizations in a pulmonary vein inlet. Radio frequency ablation against such focal activity has been reported with high therapeutic success, but the results await confirmation from several centres. For ventricular rate control, most electrophysiologists presently prefer ablation to induce a complete atrioventricular conduction block (with pacemaker) rather than trying to modify conduction by incomplete block. Atrial or dual chamber pacing may prevent atrial fibrillation induced by bradycardia. It remains to confirm that biatrial or multisite right atrial pacing prevents atrial fibrillation more efficiently than ordinary right atrial pacing. An atrial defibrillator is able to diagnose and convert atrial fibrillation. The equipment is expensive, and therapy without sedation may be unpleasant beyond tolerability. |
24 | Current concepts on ventricular fibrillation: a vicious circle of cardiomyocyte calcium overload in the initiation, maintenance, and termination of ventricular fibrillation. | Based on recent experimental studies, this review article introduces the novel concept that cardiomyocyte Ca2+ and ventricular fibrillation (VF) are mutually related, forming a self-maintaining vicious circle in the initiation, maintenance, and termination of VF. On the one hand, elevated myocyte Ca2+ can cause delayed afterdepolarizations, triggered activity, and consequently life-threatening ventricular tachyarrhythmias in various pathological conditions such as digitalis toxicity, myocardial ischemia, or heart failure. On the other hand, VF itself directly and rapidly causes progressive myocyte Ca2+ overload that maintains VF and renders termination of VF increasingly difficult. Accordingly, energy levels for successful electrical defibrillation (defibrillation thresholds) increase as both VF and Ca2+ overload progress. Furthermore, VF-induced myocyte Ca2+ overload can promote re-induction of VF after defibrillation and/or postfibrillatory myocardial dysfunction (postresuscitation stunning) due to reduced myofilament Ca2+ responsiveness. The probability of these adverse events is best reduced by early detection and rapid termination of VF to prevent or limit Ca2+ overload. Early additional therapy targeting transsarcolemmal Ca2+ entry, particularly during the first 2 min of VF, may partially prevent myocyte Ca2+ overload and thus, increase the likelihood of successful defibrillation as well as prevent postfibrillatory myocardial dysfunction. |
25 | The effects of right ventricular apical pacing on left ventricular function. Stimulation of the right ventricular apex: should it still be the gold standard? | Current pacing practice is undergoing continuous and substantial changes. Initially pacing had an exclusively palliative role, since it was reserved for patients developing complete heart block or severe symptomatic bradycardia. With the appearance of novel pacing indications such as pacing for heart failure and atrial fibrillation, the effect of pacing site on cardiac function has become a critically important issue and a subject for consideration. It seems that the classical pacing site in the right ventricular apex is no longer the gold standard because of possible disadvantageous effects on cardiac function. The aim of this review article is to discuss the effect of right ventricular apical pacing on cardiac function including cellular and hemodynamic changes. We also aim to discuss the role of alternative pacing sites in the light of cardiac function. |
26 | May fever trigger ventricular fibrillation? | The clinical precipitants of ventricular fibrillation (VF) remain poorly understood. Clinical factors such as hypoxemia, acidosis or electrolyte imbalance, drug-related toxicity, autonomic nervous system disorders as well as viral myocarditis have been proposed to be associated with sudden cardiac death particularly in patients with structural heart disease. However, In the Brugada syndrome, concurrent febrile illness has been reported to unmask the electrocardiographic features of the Brugada syndrome and be associated with an increased propensity for VF. More recently, a febrile illnesses of infectious etiology was associated to polymorphic ventricular tachycardia or VF in patients with normal hearts and without known repolarization abnormality. In this review we detail this phenomenon and its putative mechanisms. |
27 | Ventricular tachycardia in the absence of structural heart disease. | In up to 10% of patients who present with ventricular tachycardia (VT), obvious structural heart disease is not identified. In such patients, causes of ventricular arrhythmia include right ventricular outflow tract (RVOT) VT, extrasystoles, idiopathic left ventricular tachycardia (ILVT), idiopathic propranolol-sensitive VT (IPVT), catecholaminergic polymorphic VT (CPVT), Brugada syndrome, and long QT syndrome (LQTS). RVOT VT, ILVT, and IPVT are referred to as idiopathic VT and generally do not have a familial basis. RVOT VT and ILVT are monomorphic, whereas IPVT may be monomorphic or polymorphic. The idiopathic VTs are classified by the ventricle of origin, the response to pharmacologic agents, catecholamine dependence, and the specific morphologic features of the arrhythmia. CPVT, Brugada syndrome, and LQTS are inherited ion channelopathies. CPVT may present as bidirectional VT, polymorphic VT, or catecholaminergic ventricular fibrillation. Syncope and sudden death in Brugada syndrome are usually due to polymorphic VT. The characteristic arrhythmia of LQTS is torsades de pointes. Overall, patients with idiopathic VT have a better prognosis than do patients with ventricular arrhythmias and structural heart disease. Initial treatment approach is pharmacologic and radiofrequency ablation is curative in most patients. However, radiofrequency ablation is not useful in the management of inherited ion channelopathies. Prognosis for patients with VT secondary to ion channelopathies is variable. High-risk patients (recurrent syncope and sudden cardiac death survivors) with inherited ion channelopathies benefit from implantable cardioverter-defibrillator placement. This paper reviews the mechanism, clinical presentation, and management of VT in the absence of structural heart disease. |
28 | Role of implantable cardioverter defibrillators in the treatment of hypertrophic cardiomyopathy. | Hypertrophic cardiomyopathy (HCM) is an important cardiovascular disease with sudden cardiac death as the most devastating presentation. Implantable cardioverter defibrillators (ICD) are the optimal therapy for prevention of sudden death from ventricular tachycardia or fibrillation of any cause. While there is no controversy with implanting ICDs in patients who have already survived a cardiac arrest, identifying high-risk patients for primary prevention in this disease remains a challenge. Implanting ICDs in patients with HCM is an important clinical consideration since many individuals could achieve normal or near-normal lifespans with this protection. |
29 | Electrophysiological mechanisms of ventricular fibrillation induction. | Ventricular fibrillation (VF) is known as a main responsible cause of sudden cardiac death which claims thousands of lives each year. Although the mechanism of VF induction has been investigated for over a century, its definite mechanism is still unclear. In the past few decades, the development of new advance technologies has helped investigators to understand how the strong stimulus or the shock induces VF. New hypotheses have been proposed to explain the mechanism of VF induction. This article reviews most commonly proposed hypotheses that are believed to be the mechanism of VF induction. |
30 | Arrhythmias after tetralogy of fallot repair. | Tetralogy of Fallot is the most common cyanotic congenital heart disease, with a good outcome after total surgical correction. In spite of a low perioperative mortality and a good quality of life, late sudden death remains a significant clinical problem, mainly related to episodes of sustained ventricular tachycardia and ventricular fibrillation. Fibro-fatty substitution around infundibular resection, intraventricular septal scar, and patchy myocardial fibrosis, may provide anatomical substrates of abnormal depolarization and repolarization causing reentrant ventricular arrhythmias. Several non-invasive indices based on classical examination such as ECG, signal-averaging ECG, and echocardiography have been proposed to identify patients at high risk of sudden death, with hopeful results. In the last years other more sophisticated invasive and non-invasive tools, such as heart rate variability, electroanatomic mapping and cardiac magnetic resonance added a relevant contribution to risk stratification. Even if each method per se is affected by some limitations, a comprehensive multifactorial clinical and investigative examination can provide an accurate risk evaluation for every patient. |
31 | Atrial fibrillation and hyperthyroidism. | Atrial fibrillation occurs in 10 - 15% of patients with hyperthyroidism. Low serum thyrotropin concentration is an independent risk factor for atrial fibrillation. Thyroid hormone contributes to arrythmogenic activity by altering the electrophysiological characteristics of atrial myocytes by shortening the action potential duration, enhancing automaticity and triggered activity in the pulmonary vein cardio myocytes. Hyperthyroidism results in excess mortality from increased incidence of circulatory diseases and dysrhythmias. Incidence of cerebral embolism is more in hyperthyroid patients with atrial fibrillation, especially in the elderly and anti-coagulation is indicated in them. Treatment of hyperthyroidism results in conversion to sinus rhythm in up to two-third of patients. Beta-blockers reduce left ventricular hypertrophy and atrial and ventricular arrhythmias in patients with hyperthyroidism. Treatment of sub clinical hyperthyroidism is controversial. Optimizing dose of thyroxine treatment in those with replacement therapy and beta-blockers is useful in exogenous subclinical hyperthyroidism. |
32 | The role of biphasic shocks for transthoracic cardioversion of atrial fibrillation. | The modern generation of transthoracic defibrillators now employ impedance compensated biphasic waveforms. These new devices are superior to those with monophasic waveforms and practice is currently switching to biphasic defibrillators for the treatment of both ventricular and atrial fibrillation. However, there is no universal guideline for the use of biphasic defibrillators in direct current cardioversion of atrial fibrillation. This article reviews the use of biphasic defibrillation waveforms for transthoracic cardioversion of atrial fibrillation. |
33 | Effects of endocardial microwave energy ablation. | Until recently the treatment of atrial fibrillation (AF) consisted primarily of palliation, mostly in the form of pharmacological intervention. However because of recent advances in nonpharmacologic therapies, the current expectation of patients and referring physicians is that AF will be cured, rather than palliated. In recent years there has been a rapid expansion in the availability and variety of energy sources and devices for ablation. One of these energies, microwave, has been applied clinically only in the last few years, and may be a promising technique that is potentially capable of treating a wide range of ventricular and supraventricular arrhythmias. The purpose of this study was to review microwave energy ablation in surgical treatment of AF with special interest in histology and ultrastructure of lesions produced by this endocardial ablation procedure. |
34 | Automatic mode switching in atrial fibrillation. | Automatic mode switching (AMS) algorithms were designed to prevent tracking of atrial tachyarrhythmias (ATA) or other rapidly occurring signals sensed by atrial channels, thereby reducing the adverse hemodynamic and symptomatic consequences of a rapid ventricular response. The inclusion of an AMS function in most dual chamber pacemaker now provides optimal management of atrial arrhythmias and allows the benefit of atrioventricular synchrony to be extended to a population with existing atrial fibrillation. Appropriate AMS depends on several parameters: a) the programmed parameters; b) the characteristics of the arrhythmia; c) the characteristics of the AMS algorithm. Three qualifying aspects constitute an AMS algorithm: onset, AMS response, and resynchronization. Since AMS programs also provide data on the time of onset and duration of AMS episodes, AMS data may be interpreted as a surrogate marker of ATAs recurrence. Recently, stored electrograms corresponding to episodes of ATAs have been introduced, thus clarifying the accuracy of AMS in detecting ATAs Clinically this information may be used to assess the efficacy of an antiarrhythmic intervention or the risk of thromboembolic events, and it may serve as a valuable research tool for evaluating the natural history and burden of ATAs. |
35 | [Use of warfarin anticoagulation in patients with atrial fibrillation in Iceland.]. | Despite convincing evidence that warfarin anticoagulation reduces the risk of thromboembolism in patients with atrial fibrillation, recent data suggests that this therapy may be underutilized. Some patients are at higher risk than others and known risk factors for thromboembolism in nonvalvular atrial fibrillation include hypertension, diabetes, a prior history of a cerebrovascular accident or a transient ischemic attack and age over 65 years. Additionally, decreased left ventricular function and an enlarged left atrium increase the risk of emboli.</AbstractText>To study the use of anticoagulation in patients with nonvalvular atrial fibrillation in Iceland we looked at the pattern of warfarin use in two different settings, the emergency room at a University Hospital in Reykjavik and those followed at the Solvangur Health Center, a primary health clinic, in Hafnarfjordur.</AbstractText>Prospective data collection at the University Hospital and retrospective chart review at Solvangur Health Center.</AbstractText>A total of 68 patients (39 men, average age 73 years) with known preexisting atrial fibrillation were seen at the University Hospital during the 4 month study period. Thirty six (53%) were taking warfarin. Of the 32 not taking warfarin, 8 (25%) had a contraindication to anticoagulation. A large majority (96%) of the cohort had at least one risk factor for thromboembolism in atrial fibrillation. Fourteen (54%) of those not taking warfarin were on aspirin. At Solvangur Health Center, 40 of 71 patients (56%) (46 men, average age 72 years) with atrial fibrillation were taking warfarin while 4 of the 31 (13%) not on warfarin had a contraindication to the use of the medication. However, 14 (45%) of those not on warfarin were taking aspirin. In all 94% of the patients at Solvangur Health Center had at least one risk factor for thromboembolism.</AbstractText>The use of warfarin in patients with atrial fibrillation in Iceland was found to be less than optimal. We speculate that reluctance to use anticoagulants in the elderly and perhaps lack of awareness of the data showing benefit of anticoagulation may contribute to this. Given the relatively easy access of physicians to anticoagulation clinics, the added burden of following an anticoagulated patient is unlikely to be a factor.</AbstractText> |
36 | Congenital short QT syndrome. A review. | Sudden cardiac death in individuals with structurally normal hearts accounts for approximately 20% of sudden cardiac death cases. Patients in this subgroup suffer from what has been named "electrical diseases" which are gradually coming into focus as inherited ion channelopathies, diseases of anchoring proteins or of intracellular calcium regulating proteins. From 1993, the Short QT Syndrome (SQTS) came to our attention, as a new inherited "electrical disease" associated with increased risk of sudden cardiac death and atrial fibrillation. Mutations of Ikr, Iks, Ikl channels cause dysfunctional Iks, Ikr, Ikl channels with an increase in the net outward K current leading to shortening of repolarization. This in turn leads to a shorter QT interval on the ECG and shorter atrial and ventricular refractory periods with increased susceptibility to VF and AF. There seems to be an autosomal dominant mode of inheritance. The clinical profile of SQTS consists of: family history of sudden cardiac death, personal history of palpitations, syncope, dizziness, resuscitated SCD, history of AF and documented VF. It is important to emphasize that SQTS is symptomatic from early age (new-born) to old age. Therefore, it is possible that SQTS accounts for some of the sudden infant death syndrome cases and for some cases of AF, especially lone AF. The only efficient treatment for ventricular arrhythmias is ICD, associated with drugs (Quinidine or Propaphenone) for AF prophylaxis and for reducing the number of ventricular arrhythmic events (and ICD discharges). |
37 | [Recurrent hemoptysis following thienopyridines and amiodarone administration. therapeutic dilemma]. | The authors describe a case of a 74-year-old man with advanced coronary heart disease in whom pulmonary hemorrhagic complications during therapy with ticlopidine and subsequently with clopidogrel and amiodarone were observed. Fever and massive hemoptysis following five days of ticlopidine treatment, before elective coronary angiography, were noticed. Transient interstitial X-ray changes of the right lung were visible. Three months later a new episode on the third day of clopidogrel administration was manifested. He was after PCI, performed because of ACS complicated with ventricular fibrillation. Two days following clopidogrel discontinuation hemoptysis remitted but after ten days occurred again (this time with bilateral X-ray changes). Amiodarone, given after VF, was stopped. Spectacular improvement with steroid treatment was observed. Indobufen (reversible COX- 1 inhibitor) as an antiplatelet therapy was availed. The authors discuss therapeutic dilemma concerning the patient with coexisting different diseases. |
38 | [Value of electrocardiographic treadmill test for rate control strategy in permanent atrial fibrillation]. | of our study was to determine the correlation between physical activity tolerance assesed by exercise tolerance test (ETT) and dynamics of change of echocardiographic parameters of left atrium (LA) and left ventricle (LV) in standard transtoracic echocardiography (TTE) in long-term follow up of patients with persistent nonvalvular atrial fibrillation (AF).</AbstractText>We studied 67 patients (W/M: 23/44; mean age 63.2 +/- 7.1 years) with persistent AF lasting longer than 1 month. Rate control strategy targeted resting heart rate 70-90/min. All study subject underwent ETT in order to assess their exercise capacity. Before ETT we performed TTE in all patients and calculated the area of LA (LAar), longitudinal and saggital diameter of LA (LAlax, LAsax), LV end-diastolic diameter (LVEDD) and LV shortening fraction (FS). TTE was performed again in 2 and 12 months after beginning of observation.</AbstractText>Using variation analysis we established the correlation between time of ETT in patients with persistent AF and dynamics of change of specific echocardiographic parameters in 12 months follow-up. In patients with ETT time <60 sec we observed statistically significant rise of LAar from 26.5 +/- 6.1 to 29.6 +/- 4.9 cm2 (p < 0.05; ANOVA) and deterioration of LV function assessed with FS from 35.6 +/- 5.3% on the beginning to 31.7 +/- 7.4% at the end of study (p < 0.02; ANOVA). There was no correlation between time of ETT and dynamics of change of other echocardiographic parameters in patients with time of ETT >60 sec.</AbstractText>Time of exercise tolerance test limited with heart failure symptoms is an independent factor predicting dynamics of change of chosen echocardiographic parameters of left heart in long-term observation of patients with persistent atrial fibrillation.</AbstractText> |
39 | Antiarrhythmic activity of taurhythman. | Antiarrhythmic properties of taurhythman were demonstrated on experimental models of ventricular (early occlusion and calcium chloride-induced) and atrioventricular (aconitine-induced) arrhythmias. The preparation reduced or prevented episodes of paroxysmal tachycardia and ventricular fibrillation, decreased the incidence of arrhythmias, and increased the lethal dose (LD) of arrhythmogenic agents. By its efficiency, taurhythman was superior to procainamide and comparable to lidocaine. |
40 | Effect of a new ultrashort betalytic agent on aconitine-induced arrhythmia. | The anti-arrhythmic effect was tested on the model of aconitine-induced arrhythmia. The experiment was performed in vivo with 31 male Wistar laboratory rats. Group A was first administered aconitine and, after the onset of the first sinus rhythm disorders, the 44Bu compound was administered. Group B was first administered the 44Bu compound and only after that the aconitine. The control group was administered aconitine and saline as a replacement of the tested compound. In group A, there was a decrease in the ventricular fibrillation occurrence from 100 % to 8 % (p < 0.001) after the administration of the 44Bu compound. In the B group, the onsets of all monitored arrhythmia types were delayed by an average of 15.6 min. Ventricular rhythm occurrence was decreased from 100 to 20 %, as well as ventricular fibrillations, from 100 to 0 % (p < 0.001). |
41 | Simulated interactions between a Class III antiarrhythmic drug and a figure 8 reentry. | Ventricular Fibrillation is responsible for a majority of sudden cardiac death, but little is known about how ventricular tachycardia (VT) degenerates into ventricular fibrillation. Several clinical studies focused only on preventing VT with a class III antiarrhythmic drug resulted in many deaths. Our simulations investigate the interactions between an antiarrhythmic drug likely to suppress a VT and a Figure 8 reentry. A parameter AAR is introduced to increase the action potential duration and therefore simulate various Class III drugs. Simulations are ran under several conditions (phases of the reentry, values of AAR, durations). They show that a VT can be suppressed whatever the phase of the reentry but it strongly depends on the duration of the effect. It confirms that a drug which can suppress a reentry can also worsen it. It also shows a great variety of activation patterns and thus the complexity of antiarrhythmic drugs effects. Simulations also demonstrate that suppressing VT is an increasing function of AAR. |
42 | Does the abnormal signal-averaged electrocardiogram predict future appropriate therapy in patients with implantable cardioverter-defibrillators? | Several studies have documented the prognostic significance of the signal-averaged electrocardiogram (SAECG) both after myocardial infarction and nonischemic cardiomyopathy. However, whether the SAECG can identify patients with implantable cardioverter-defibrillator (ICD) who receive appropriate therapy has not been hitherto completely investigated.</AbstractText>Between August 2002 and August 2004, 83 consecutive ICD patients who had had SAECGs recorded were enrolled in this study. All patients were followed up in the outpatient ICD clinic, and interrogated electrograms were collected.</AbstractText>Over 9.0 +/- 2.8 months of follow-up, 27 (32%) patients had appropriate ICD therapy for ventricular tachycardia or fibrillation; 15 (55.6%) patients had abnormal; and the remaining 12 (44.4%) had normal SAECGs. Of the 56 patients with no appropriate therapy, 27 (48.2%) and 29 (51.8%) patients had abnormal and normal SAECGs, respectively. There were no statistically significant differences between the 2 groups in SAECG findings (P = .41). A Cox regression analysis showed that the left ventricular ejection fraction was the only predictor of appropriate therapy (P = .02). Subgroup analysis of the patients with coronary artery disease and spontaneous monomorphic ventricular tachycardia indicated that left ventricular ejection fraction (P = .03) and abnormal SAECG (P = .02) were predictors of appropriate therapy.</AbstractText>Our data demonstrate that except for the subgroup of patients with coronary artery disease presenting with monomorphic ventricular tachycardia, the SAECG did not predict ventricular tachyarrhythmia recurrence and, hence, appropriate ICD therapy. Thus, SAECG findings should generally not be a factor in decision for ICD implantation.</AbstractText> |
43 | Potential dangers of the Valsalva maneuver and adenosine in paroxysmal supraventricular tachycardia--beware preexcitation. | Paroxysmal supraventricular tachycardia (PSVT) is a common clinical problem. Valsalva maneuver and adenosine are effective therapies for many patients with PSVT, although any conversion to an irregular or wide complex tachycardia should prompt consideration of a preexcitation syndrome. We report a case where the Valsalva maneuver and adenosine, in a patient with PSVT and previously undiagnosed Wolff-Parkinson-White syndrome, caused atrial fibrillation and led to a haemodynamically unstable wide complex tachycardia and ventricular fibrillation. In PSVT, where preexcitation has not been excluded, the Valsalva maneuver and adenosine can be potentially dangerous. |
44 | Cardiac arrhythmias: diagnosis and management. The tachycardias. | To review the diagnosis and management of cardiac arrhythmias in a two-part presentation.</AbstractText>Articles and published peer-review abstracts on tachycardias and bradycardias.</AbstractText>Normal cardiac rhythm originates from impulses generated within the sinus node. These impulses are conducted to the atrioventricular node where they are delayed before they are distributed to the ventricular myocardium via the His-Purkinje system. Abnormalities in cardiac rhythm are caused by disorders of impulse generation, conduction or a combination of the two and may be life threatening due to a reduction in cardiac output or myocardial oxygenation. Cardiac arrhythmias are commonly classified as tachycardias (supraventricular or ventricular) or bradycardias. The differentiation between supraventricular and ventricular tachycardias usually requires an assessment of atrial and ventricular rhythms and their relationship to each other. In the critically ill patient the commonest tachycardia is sinus tachycardia and treatment generally consist of management of the underlying disorder. Other supraventricular tachycardias (SVTs) include, atrial flutter, atrial fibrillation and paroxysmal supraventricular tachycardia (PSVT) all of which may require cardioversion, although to maintain sinus rhythm, antiarrhythmic therapy is often needed. Adenosine is useful in management and treatment many SVTs although its use in PSVT with Wolff-Parkinson-White syndrome is hazardous. Multifocal atrial tachycardia is a characteristic supraventricular tachycardia found in the critical ill patient. While it usually responds to intravenous magnesium sulphate, its management also requires removal of various precipitating factors. Ventricular tachycardia (VT) and ventricular fibrillation (VF) require urgent cardioversion and defibrillation respectively. Torsade de pointes should be differentiated from these ventricular arrhythmias as antiarrhythmic therapy may be contraindicated.</AbstractText>Supraventricular and ventricular tachycardias in the critically ill patient often have underlying disorders that precipitate their development (e.g. hypokalaemia, hypomagnesaemia, anti-arrhythmic proarrhythmia, myocardial ischaemia, etc). While antiarrhythmic therapy and cardioversion or defibrillation may be required to achieve sinus rhythm, correction of the associated abnormalities is also required.</AbstractText> |
45 | Hypothermia does not improve outcome from traumatic brain injury. | Therapeutic hypothermia is a potentially dangerous treatment with a very narrow therapeutic index. It is of proven benefit in certain conditions, including post ventricular fibrillation cardiac arrest and intermediate severity neonatal asphyxia. It is of no benefit and may cause harm in other contexts, such as elective neurovascular surgery. In traumatic brain injury there has been much provocative early evidence. While it is clear that hypothermia decreases intracranial pressure, a major phase III trial demonstrated no improvement in neurological outcomes with hypothermia, in an unselected group of patient with severe head injury. More focused phase III trials are underway but until the results are known this treatment should not be offered to patients outside the context of a clinical trial. |
46 | Hypothermia improves outcome from cardiac arrest. | Out-of-hospital cardiac arrest is common and patients who are initially resuscitated by ambulance officers and transported to hospital are usually admitted to the intensive care unit (ICU). In the past, the treatment in the ICU consisted of supportive care only, and most patients remained unconscious due to the severe anoxic neurological injury. It was this neurological injury rather than cardiac complications that caused the high rate of morbidity and mortality. However, in the early 1990's, a series of animal experiments demonstrated convincingly that mild hypothermia induced after return of spontaneous circulation and maintained for several hours dramatically reduced the severity of the anoxic neurological injury. In the mid-1990's, preliminary human studies suggested that mild hypothermia could be induced and maintained in post-cardiac arrest patients without an increase in the rate of cardiac or other complications. In the late 1990's, two prospective, randomised, controlled trials were conducted and the results confirmed the animal data that mild hypothermia induced after resuscitation and maintained for 12 - 24 hours dramatically improved neurological and overall outcomes. On the basis of these studies, mild hypothermia was endorsed in 2003 by the International Liaison Committee on Resuscitation as a recommended treatment for comatose patients with an initial cardiac rhythm of ventricular fibrillation. However, the application of this therapy into routine clinical critical care practice has been slow. The reasons for this are uncertain, but may relate to the relative complexity of the treatment, unfamiliarity with the pathophysiology of hypothermia, lack of clear protocols and/or uncertainty of benefit in particular patients. Therefore, recent research in this area has focused on the development of feasible, inexpensive techniques for the early, rapid induction of mild hypothermia after cardiac arrest. Currently, the most promising strategy is a rapid infusion of large-volume (40 mL/kg) ice cold intravenous fluid. Also, newer automated surface cooling/warming devices have been developed which allow tight control of body temperature in the ICU. On the other hand, a number of questions remain. The benefit of hypothermia in non-ventricular fibrillation cardiac arrest remains uncertain. Also, the best timing of induction and the duration of hypothermia after cardiac arrest are uncertain. Clinical trials are currently underway to assess these issues. |
47 | Automated external defibrillators on board merchant vessels? Preliminary report article for discussion. | Acute heart diseases are the most frequent causes for fatalities on merchant vessels. Presently there is no sufficient therapy available to treat ventricular fibrillation. The aim of this study was to test whether common automated external defibrillators [AED] may be appropriate for the use aboard merchant vessels.</AbstractText>In 2005, nine seafarers were introduced to four common models of AED (HeartStartFR2+, Lifepak500, AEDplus, FREDeasy) using standard video or DVD presentations. AED handling by the subjects was tested in standardized simulated emergency scenarios. After training, they subjectively rated each AED on 24 factors involved in the introduction and handling of the device. An actual ECG was then obtained with each AED at a site located beside the ship's main engine to test under maximum vibration. The ECG data were extracted and sent as an e-mail attachment via satellite to the German Telemedical Maritime Assistance Service [TMAS] in Cuxhaven.</AbstractText>All subjects handled the AED correctly. The AED received a total amount of points in the range between 2125 to 2241 (of 2400 possible). The subjects preferred AED with coloured as well as light marked buttons which gave a feedback (e.g. audible tones) when they were pressed. All AED were able to register an ECG in the vibrating ambient. Due to interface problems it was only possible to extract three ECG files, and only two files (data < 300 kB) could be sent as e-mail attachment via satellite to the German TMAS. In noisy areas the AED must guide the user, e.g. by screen massages and/or pictograms. Displays should provide additional data to help assess resuscitation effectiveness. A special procedure is necessary to ensure that ships and TMAS own the same software to read the transmitted ECG files, which are not allowed to exceed a size of 300 kB.</AbstractText> |
48 | Implantable cardioverter defibrillatory implantation in a patient with persistent left superior vena cava and right superior vena cava atresia. | Persistence of a left superior vena cava has been observed in 0.3% of the general population as established by autopsy findings. In the adult population. it is an important anatomic finding if a left or right superior vena cava approach to the heart is considered for device implantation. We present a case with persistent left superior vena cava and right superior vena cava atresia in whom a dual chamber implantable cardioverter defibrillator was implanted and was technically challenging. |
49 | [The network for the management of acute coronary syndromes in Milan: results of a four-year experience and perspectives of the prehospital and interhospital cardiological network]. | In patients with acute ST-elevation myocardial infarction (STEMI), in order to shorten the time to definitive treatment, it is essential to coordinate the intervention between the local healthcare system and the hospitals. In 1999, a Working Group for Prehospital Emergency in Cardiology was established in Milan, and a network for 12-lead ECG transmission between advances life support (ALS) ambulances, the headquarter of 118 Rescue Service and the Coronary Care Units (CCU) or Divisions of Cardiology was developed: between February 1, 2001 and May 1, 2005, 6821 patients with suspected heart attack were rescued and their ECG recorded and transmitted (177 patients/month, 20% of them with an ST-segment shift, 11% ST-segment elevation, 9% non-ST-segment elevation, 24% with normal ECG). The rate of false positive automatic diagnosis of acute myocardial infarction was 0.3%, the rate of false negative was 0.8%. Forty-six patients with ventricular fibrillation underwent DC-shock. After May 1, 2004, clinical data of patients with STEMI transferred to the hospitals by ALS ambulances were reported in a database: 82% of the 89 patients were treated with primary angioplasty. The time (median, interquartile ranges) between ECG arrival to the CCU and the ECG report was 2 min (1-5), between ECG arrival to the CCU and patient arrival to the hospital was 34 min (24-42), between ECG arrival to the CCU and primary angioplasty was 69 min (50-93); the door-to-balloon time was 33 min (22-60). The telephone ECG transmission has been demonstrated to be a useful and rapid tool, easy to use; the automatic ECG diagnosis was accurate. In patients with STEMI the telephone ECG transmission shortened the time of delivery of therapy, helped to recover arrhythmic complications, allowed both the coordination between the 118 System and the Divisions of Cardiology and the implementation of the triage for primary angioplasty. Increasing the technological level of the service will be the next step of the program: the protocol will be upgraded in order to increase the number of patients rescued, to shorten the time of operation and to administer prehospital fibrinolytic therapy in selected patients. |
50 | The role of NO in ischemia/reperfusion injury in isolated rat heart. | Nitric oxide (NO) is an important regulator of myocardial function and vascular tone under physiological conditions. However, its role in the pathological situations, such as myocardial ischemia is not unequivocal, and both positive and negative effects have been demonstrated in different experimental settings including human pathology. The aim of the study was to investigate the role of NO in the rat hearts adapted and non-adapted to ischemia. Isolated Langendorff-perfused hearts were subjected to test ischemic (TI) challenge induced by 25 min global ischemia followed by 35 min reperfusion. Short-term adaptation to ischemia (ischemic preconditioning, IP) was evoked by 2 cycles of 5 min ischemia and 5 min reperfusion, before TI. Recovery of function at the end of reperfusion and reperfusion-induced arrhythmias served as the end-points of injury. Coronary flow (CF), left ventricular developed pressure (LVDP), and dP/dt(max) (index of contraction) were measured at the end of stabilization and throughout the remainder of the protocol until the end of reperfusion. The role of NO was investigated by subjecting the hearts to 15 min perfusion with NO synthase (NOS) inhibitor L-NAME (100 mmol/l), prior to sustained ischemia. At the end of reperfusion, LVDP in the controls recovered to 29.0 +/- 3.9 % of baseline value, whereas preconditioned hearts showed a significantly increased recovery (LVDP 66.4 +/- 5.7 %, p < 0.05). Recovery of both CF and dP/dt(max) after TI was also significantly higher in the adapted hearts (101.5 +/- 5.8 % and 83.64 +/- 3.92 % ) as compared with the controls (71.9 +/- 6.3 % and 35.7 +/- 4.87 %, respectively, p < 0.05). NOS inhibition improved contractile recovery in the non-adapted group (LVDP 53.8 +/- 3.1 %; dP/dt(max) 67.5 +/- 5.92 %) and increased CF to 82.4 +/- 5.2 %. In contrast, in the adapted group, it abolished the protective effect of IP (LVDP 31.8 +/- 3.1 %; CF 70.3 +/- 3.4 % and dP/dt(max) 43.25 +/- 2.19 %). Control group exhibited 100 % occurrence of ventricular tachycardia (VT), 57 % incidence of ventricular fibrillation (VF) - 21 % of them was sustained VF (SVF); application of L-NAME attenuated reperfusion arrhythmias (VT 70 %, VF 20 %, SVF 0 %). Adaptation by IP also reduced arrhythmias, however, L-NAME in the preconditioned hearts increased the incidence of arrhythmias (VT 100 %, VF 58 %, SVF 17 %).</AbstractText>our results indicate that administration of L-NAME might be cardioprotective in the normal hearts exposed to ischemia/reperfusion (I/R) alone, suggesting that NO contributes to low ischemic tolerance in the non-adapted hearts. On the other hand, blockade of cardioprotective effect of IP by L-NAME points out to a dual role of NO in the heart: a negative role in the non-adapted myocardium subjected to I/R, and a positive one, due to its involvement in the mechanisms of protection triggered by short-term cardiac adaptation by preconditioning.</AbstractText> |
51 | [Juvenile haemochromatosis presenting as intractable congestive heart failure]. | Juvenile haemochromatosis is an autosomal, recessive inherited iron metabolism disorder. The rapid deterioration and malignant prognosis differentiate juvenile haemochromatosis from hereditary haemochromatosis. The authors summarize the history of a 25 year old man, who worked in Hungary as a guest worker living in Romania. No significant illness has occurred in his previous history. The abdominal pain was his first symptom and he was treated in different institutions, where cholecystitis, alcoholic hepatic disease, hepatic cirrhosis were considered as a cause of his symptoms. Some weeks later atrial tachycardia, and congestive heart failure were observed and he was sent to our Cardiology Department. The echocardiography revealed diffuse hypokinesis, serious systolic dysfunction (ejection fraction: 21%), grade II mitral and tricuspid insufficiency with pulmonary hypertension. Considering the rapid deterioration of his cardiac function, myocarditis was suspected. Myocardial biopsy and coronary arteriography were performed. Coronary arteries were normal. Ventricular fibrillation occurred during coronary arteriography. Myocardial biopsy revealed juvenile haemochromatosis. Special laboratory examinations (transferrin saturation) were made after biopsy, that also confirmed the diagnosis of juvenile haemochromatosis. Cardiac transplantation was planned. Some days after the diagnosis was made the patient died of cardiogenic shock and intractable heart failure. Autopsy revealed hypogonadism and serious haemochromatosis in different parenchymal organs. Juvenile haemochromatosis should be considered in every young patient with congestive heart failure of unknown etiology. |
52 | Cardiac gas embolism after central venous catheter removal. | Clinical images reporting intracardiac gas level are sparce and, to our knowledge, the presence of gas embolism into the coronary arteries has never been reported. We describe the case of a young man who experiences life-threatening gas embolism with the presence of gas bubbles into cardiac cavities and coronary arteries. |
53 | The antiarrhythmic effect of n-3 polyunsaturated fatty acids: modulation of cardiac ion channels as a potential mechanism. | Sudden cardiac death remains one of the most serious medical challenges in Western countries. Increasing evidence in recent years has demonstrated that the n-3 polyunsaturated fatty acids (PUFAs) can prevent fatal ventricular arrhythmias in experimental animals and probably in humans. Dietary supplement of fish oils or intravenous infusion of the n-3 PUFAs prevents ventricular fibrillation caused by ischemia/reperfusion. Similar antiarrhythmic effects of these fatty acids are also observed in cultured mammalian cardiomyocytes. Based on clinical observations and experimental studies in vitro and in vivo, several mechanisms have been postulated for the antiarrhythmic effect of the n-3 PUFAs. The data from our laboratory and others have shown that the n-3 PUFAs are able to affect the activities of cardiac ion channels. The modulation of channel activities, especially voltage-gated Na(+) and L-type Ca(2+) channels, by the n-3 fatty acids may explain, at least partially, the antiarrhythmic action. It is not clear, however, whether one or more than one mechanism involves the beneficial effect of the n-3 PUFAs on the heart. This article summarizes our recent studies on the specific effects of the n-3 PUFAs on cardiac ion channels. In addition, the effect of the n-3 PUFAs on the human hyperpolarization-activated cyclic-nucleotide-modulated channel is presented. |
54 | Membrane basis for fish oil effects on the heart: linking natural hibernators to prevention of human sudden cardiac death. | The concept that diet-induced changes in membrane lipids could modify heart function partly arose from observations that membrane composition and physical properties were closely associated with the capacity of the heart to respond appropriately to torpor and hibernation. Observations of natural hibernators further revealed that behavior of key membrane-bound enzymes could be influenced through the lipid composition of the cell membrane, either by changing the surrounding fatty acids through reconstitution into a foreign lipid milieu of different composition, or by alteration through diet. Myocardial responsiveness to beta-adrenoceptor stimulation, including initiation of spontaneous dysrhythmic contractions, was altered by both hibernation and dietary modulation of membrane fatty acids, suggesting modified vulnerability to cardiac arrhythmia. Subsequent studies using whole-animal models recognized that vulnerability to ventricular fibrillation decreased as the polyunsaturated: saturated fat (P:S) ratio of the diet increased. However, dietary fish oils, which typically contain at least 30% saturated fatty acids and only 30% long-chain n-3 (omega-3) polyunsaturated fatty acids (PUFA), exhibit antiarrhythmic effects that exceed the predicted influence of the P:S ratio, suggesting properties unique to the long-chain n-3 PUFA. Large-scale clinical trials and epidemiology have confirmed the arrhythmia prevention observed in vitro in myocytes, papillary muscles, and isolated hearts and in whole-animal models of sudden cardiac death. Some progress has been made towards a biologically plausible mechanism. These developments highlight nature's ability to provide guidance for the most unexpected applications. |
55 | Epidemiology and stratification of risk for sudden cardiac death. | Sudden cardiac death (SCD) is a major cause of mortality in the United States. Approximately 65% of cases of SCD occur in patients with underlying acute or chronic ischemic heart disease. The incidence of SCD increases 2- to 4-fold in the presence of coronary disease and 6- to 10-fold in the presence of structural heart disease. Ventricular fibrillation (VF) precipitated by ventricular tachycardia (VT) is a common mechanism of cardiac arrest leading to SCD. Triggers for SCD include electrolyte disturbances, heart failure, and transient ischemia. Although a large percentage of patients with out-of-hospital SCD do not survive, successful resuscitation to hospitalization has improved in recent years. One of the challenges for preventing SCD lies in identifying individuals at highest risk for SCD within a lower-risk population. The progression from conventional risk factors of coronary artery disease to arrhythmogenesis and SCD can be represented as a cascade of changes associated with levels of increasing risk. At the first level is atherogenesis, followed by changes in atherosclerotic plaque anatomy, which may be mediated by inflammatory processes. Disruption of active plaque formed during a transitional state initiates the thrombotic cascade and acute occlusion, after which acute changes in myocardial electrophysiology become the immediate trigger for arrhythmogenesis and SCD. Each level of the cascade offers different opportunities for risk prediction. Among the classes of risk predictors are clinical markers, such as ECG measures and ejection fraction. Transient risk markers, such as inflammatory markers, are potentially useful for identifying triggers for SCD. In the future, genetic profiling is expected to allow better assessment of individual risks for SCD. |
56 | Successful management of air embolism-induced ventricular fibrillation in orthotopic liver transplantation. | Ventricular fibrillation (VF) although less common during noncardiac surgery often brings about severe complication as an aftermath. We report a case of VF which was highly suspected to be induced by air embolism at the moment when the surgeon was dissecting the collateral vessels of portal vein in liver transplantation surgery. The outcome of this patient was excellent due to aggressive resuscitative measures including open-chest cardiac massage. Transesophageal echocardiogram (TEE) was not applied in this patient in fear of increased risk of esophageal varicose bleeding in a liver cirrhotic patient. However, some reports described the use of TEE in cirrhotic patients without obvious complications. In this case, venous air embolism (VAE) happened during the dissection of collateral vessels of the portal vein, which to our knowledge was ever been reported in liver transplantation surgery. The related literature has been reviewed and the success of the resuscitation is also herein discussed. |
57 | [Angiotensin-converting enzyme inhibition and cardiovascular prevention: more than twenty years of clinical success]. | Angiotensin-converting enzyme (ACE) inhibitors are widely used for the treatment of cardiovascular disease since they improve blood pressure control in patients with hypertension and prolong survival in patients with acute myocardial infarction, asymptomatic left ventricular dysfunction and congestive heart failure. Most of the information about the therapeutic role of ACE-inhibitors has been achieved during the last 20 years since the publication of some pivotal trials mostly involving the use of ACE-inhibitors like captopril and enalapril. In particular the treatment with enalapril has considerably improved the clinical outcome of patients with either mild-to-moderate (SOLVD studies) or severe (CONSENSUS trial) congestive heart failure. The benefit of ACE-inhibitors in patients with congestive heart failure has also involved a remarkable reduction in the rate of hospitalization, thus contributing to improve the pharmaco-economic approach to the disease. Most of the beneficial effect of ACE-inhibitors in clinical practice is dependent on their capacity of inhibiting the renin-angiotensin system, although some recent trials have supported a primary role for such drugs (in particular enalapril) in the prevention of atrial fibrillation. After more than 25 years from their discovery, ACE-inhibitors must be again considered among the first-line treatment in many patients with cardiovascular disease. |
58 | Transthoracic echocardiographic predictors of left atrial appendage thrombus. | Transesophageal echocardiography (TEE) is commonly performed to detect the presence of a left atrial appendage (LAA) thrombus in the setting of an embolic event or before an anticipated electrical cardioversion for atrial fibrillation. The predictive value of transthoracic echocardiographic (TTE) findings in these patients has not been well defined. This study evaluated whether TTE findings can predict LAA thrombi using TEE as the gold standard for the identification of LAA thrombi. From November 1995 to March 2003, 10,753 patients underwent TEE to exclude LAA thrombi after embolic events or before cardioversion. Of these, 3,768 patients had complete TTE examinations performed <2 weeks before undergoing TEE. Demographics, TTE, and cardiac rhythm variables were analyzed using univariate and multivariate logistic regression to identify predictors of LAA thrombi diagnosed on subsequent TEE. LAA thrombi were identified by TEE in 199 patients (5.3%). Several TTE variables predicted LAA thrombi by TEE, including mitral stenosis, atrial fibrillation, tricuspid regurgitation, valvular prosthesis, left ventricular dysfunction, and right ventricular dysfunction. Mitral regurgitation was associated with a reduced risk for LAA thrombi (odds ratio 0.61, p = 0.003). A structurally normal heart in sinus rhythm (n = 247, 6.9%) had a 100% negative predictive value for LAA thrombi. In conclusion, several TTE variables were found to be predictive of LAA thrombi. The likelihood of LAA thrombi being found on TEE was infinitely small in the absence of these variables and the presence of sinus rhythm. |
59 | Effects of thrombolysis during out-of-hospital cardiopulmonary resuscitation. | In this post hoc analysis, we assessed effects of thrombolysis during out-of-hospital cardiopulmonary resuscitation. The original study was designed as a double-blinded, prospective, multicenter, randomized, controlled clinical trial. In this report, 1,219 patients were randomized, but 33 patients were excluded due to missing study drug codes. Thus, 1,186 patients were analyzed based on receipt (n = 99) versus nonreceipt (n = 1,087) of thrombolysis; the primary end point was hospital admission, and the secondary end point was hospital discharge. Patients who received thrombolysis versus those who did not were significantly younger (mean +/- SD 62.7 +/- 13.3 vs 66.5 +/- 14.3 years of age, p = 0.01) and more likely to have had an acute myocardial infarction (75.3% vs 54.6%, p < 0.01) or pulmonary embolism (20.2% vs 12.0%, p = 0.03) as the suspected underlying cause for cardiac arrest. In patients who underwent thrombolysis versus those who did not, cardiac arrest was more often witnessed (86.9% vs 77.5%, p = 0.03), initial ventricular fibrillation was more likely (59.6% vs 38.0%, p < 0.01), and a short estimated interval (0 to 5 minutes) between collapse and initiation of basic life support was more likely (51.3% vs 29.2%, p < 0.01). In patients who received thrombolysis, sodium bicarbonate (45.5% vs 33.0%, p = 0.01), lidocaine (32.3% vs 18.1%, p < 0.01), and amiodarone (30.3% vs 12.2%, p < 0.01) were administered significantly more often. Hospital admission rates were significantly higher in patients who underwent thrombolysis than in patients who did not (45.5% vs 32.7%, p = 0.01), and there was a trend to higher hospital discharge rates (14.1% vs 9.5%, p = 0.14). In patients who had suspected myocardial infarction, hospital admission and discharge rates were significantly higher in patients who underwent thrombolysis than in patients who did not. In logistic regression models after adjusting for confounding variables (e.g., age, initial electrocardiographic rhythm, and initiation of basic life support), hospital admission and discharge rates did not differ significantly. In conclusion, even when being employed in patients with a potentially better chance to survive, thrombolysis in patients with cardiac arrest resulted in an increased hospital admission but not discharge rate in this post hoc analysis. |
60 | Intake of tuna or other broiled or baked fish versus fried fish and cardiac structure, function, and hemodynamics. | Fish intake is associated with improved cardiovascular health, including a lower risk of arrhythmic death, atrial fibrillation, and heart failure. However, the physiologic effects that may produce these cardiovascular benefits are not well-established. We investigated the cross-sectional associations between a usual dietary intake of fish during the previous year and cardiac structure, function, and hemodynamics as determined by physical examination and 2-dimensional, Doppler, and M-mode transthoracic echocardiography among 5,073 older adults enrolled in the Cardiovascular Health Study. On multivariate-adjusted analyses, consumption of tuna or other broiled or baked fish was associated with a lower heart rate (p < 0.001), lower systemic vascular resistance (p = 0.002), and greater stroke volume (p < 0.001). Tuna/other fish intake was also associated with a higher E/A ratio (p = 0.004), a measure of more normal diastolic function. In contrast, fried fish or fish sandwich (fish burger) intake was associated with left ventricular wall motion abnormalities (p = 0.02), a reduced ejection fraction (p < 0.001), lower cardiac output (p = 0.04), a trend toward a larger left ventricular diastolic dimension (p = 0.07), and higher systemic vascular resistance (p = 0.003). In conclusion, in this large population-based study, the intake of tuna or other broiled or baked fish was associated with improved cardiac hemodynamics, but fried fish intake was associated with structural abnormalities indicative of systolic dysfunction and potential coronary atherosclerosis. These findings suggest potential specific physiologic mechanisms that may, in part, account for the effects of fish intake on cardiovascular health. |
61 | [Evaluation and surveillance of patients with an implantable defibrillator]. | The implantable cardioverter-defibrillator became in some years the reference treatment of ventricular arrhythmias in association with heart disease. Recently, this technique showed its efficiency in primary prevention for patients at high risk of sudden death. The follow-up of patients with automatic defibrillator requires a detailed knowledge of both electrophysiology and stimulation. This training is based on a practical and theoretical formation. In France, a specific diploma validation is necessary and centres organisation is required. The purpose of this general review is to supply a set of updated data necessary for the coverage and the follow-up of patients with an implantable cardioverter-defibrillator. |
62 | [Arrhythmia and sport]. | Sports arrhythmia has gained wide attention with the mediatization of the death of famous sports stars. Sport strongly modifies the structure of the heart with the development of left ventricular hypertrophy which may be difficult to differentiate from that due to doping. Intense training modifies also the resting electrocardiogram with appearance of signs of left ventricular hypertrophy whereas resting sinus bradycardia and atrioventricular conduction disturbances usually reverts upon exertion. Accordingly, arrhythmia may develop ranging from extrasystoles to atrial fibrillation and even sudden death. Recent data suggest that if benign arrhythmia may be the result of the sole intense training and are reversible, malignant ventricular arrhythmia and sudden death mostly occur in unknown structural heart disease. Hypertrophic cardiomyopathy is amongst the most frequent post mortem diagnosis in this situation. Doping is now present in many sports and further threatens the athlete in the safe practice of sport. |
63 | [Sick sinus syndrome]. | Sick sinus syndrome is an association of sinus node dysfunction with bradycardia, pauses, sino-atrial block, chronotropic insufficiency and atrial arrhythmias. The diagnosis is essentially clinical and electrocardiographic. Prolonged ECG recordings allow a better assessment of the severity of the condition whereas electrophysiological investigations only provide complementary information which is rarely decisive in the therapeutic indications. Cardiac pacing is the treatment of choice for symptomatic patients: significant improvement in symptoms may be expected but there is no significant change in survival. Single chamber atrial stimulation or dual chamber pacing is preferable to single chamber ventricular pacing, especially with regards to the incidence of atrial fibrillation and the impact on quality of life. |
64 | [Mapping and ablation of malignant ventricular arrhythmias]. | Endocavitary investigations showed that the ventricular extrasystoles originated in the common ventricular myocardium (pulmonary infundibulum) in only 9 cases whereas the majority arose from the Parkinje system either on the anterior wall of the right ventricle or in septal region of the left ventricle. The extrasystoles arising from the Parkinje system and pulmonary infundibulum differed in their duration and polymorphism (128 +/- 18 ms vs 145 +/- 13 ms, p = 0.05; 3.3 +/- 2.7 morphologies vs 1.1 +/- 0.4, p < 0.001, respectively). During the extrasystoles, the local Pukinje potential preceded the ventricular activation by variable intervals, some of which were very long, up to 150 ms. Seven applications of radiofrequency were delivered on average per patient on the most distal part of the Purkinje system leading to ablation of the specific activation. The clinical results were spectacular: 88% of patients had no further episodes of ventricular fibrillation as demonstrated by analysis of the defibrillator with an average follow-up period of more than 34 months. |
65 | [Primary anomalies of ventricular repolarisation]. | The duration of repolarisation is the main determinant of the refractory period and therefore plays a major electrophysiological role. Ventricular repolarisation can be influenced or modified by very many extrinsic factors responsible for so-called secondary changes or anomalies. On the contrary, primary anomalies of ventricular repolarisation correspond to intrinsic anomalies of ionic conduction which in turn affect repolarisation. Primary anomalies of ventricular repolarisation are the consequences of vascular disease, which is the origin of both electrocardiographic anomalies and rhythm disorders, and which can result in sudden death from ventricular fibrillation. Three clinical syndromes correspond with these definitions: long QT syndrome, short QT syndrome, and Brugada syndrome. Much of the experimental work seems to show that arrhythmogenic action results mostly from an increase in the heterogeneity of the refractory periods, whether this involves a prolonged, short or even normal repolarisation time. The various experimental models also give a better understanding of the repolarisation changes observed on the electrocardiogram. Knowledge of the mechanisms responsible for arrhythmias due to primary anomalies of ventricular repolarisation could provide a model for secondary anomalies. |
66 | Postoperative atrial fibrillation independently predicts prolongation of hospital stay after cardiac surgery. | Postoperative atrial fibrillation (AF) occurs in up to 50% of cardiac surgery patients and represents the most common postoperative arrhythmic complication. A reduction of the length of hospital stay is a desirable goal in preventive strategies of postoperative AF. The aim of the present investigation was to determine whether prolonged postoperative hospital stay associated with AF after cardiac surgery surgery is attributable to the arrhythmia itself or to baseline characteristics of patients who develop AF.</AbstractText>Patients undergoing elective cardiac surgery in the absence of heart failure and significant left ventricular dysfunction (n = 253; average age 65+/-11 years) were recruited to the present prospective study. Midline sternotomy procedures with standard surgical techniques for normothermic cardiopulmonary bypass in coronary artery bypass grafting and valvular surgery were used.</AbstractText>A total of 99 patients (39.1%) of the study population developed AF during the postoperative period. AF patients were older and more likely to have surgery for valvular heart disease and less likely to have antiarrhythmic drugs including beta-adrenergic blockers than patients without AF, but both patients with and without AF had similar body mass index and duration of surgery. Postoperative hospital stays were longer in patients with AF compared to those without AF (14.9+/-5.7 vs 10.6+/-3.6, respectively; P = 0.001). Multivariate analysis, adjusted for age and postoperative complications, demonstrated that postoperative hospital stay was 14.2+/-5.3 days in patients with AF and 10.8+/-3.8 days in patients without AF (P < 0.01). Treatment with oral antiarrhythmic drugs that reduce AF is associated with a reduction of postoperative hospital stay.</AbstractText>Despite baseline characteristics differed between patients with and without postoperative AF, most of the prolongation of hospital stay can be attributed to the rhythm disturbance itself.</AbstractText> |
67 | Myocardial protection with insulin cardioplegia: who can really benefit? | The aim of the study was to evaluate the effects on myocardial protection of insulin-enriched warm blood cardioplegia (IWBC) in coronary artery bypass grafting (CABG) and in subgroups of patients with associated cardiac co-morbidities.</AbstractText>Between May 2000 and December 2002, 268 consecutive patients underwent CABG with warm blood cardioplegia (group A) or IWBC (10 UI/L) (group B). Hospital outcome, ECG, echocardiography and biochemical markers of ischemia were compared. Differences between subgroups of patients with unstable angina (UA), ventricular hypertrophy (VH) and diabetes were assessed.</AbstractText>Hospital mortality, incidence of postoperative myocardial infarction and low output syndrome, IABP requirement, postoperative atrial fibrillation, in-hospital and in-ITU stay, postoperative recovery of left ventricular function and enzyme leakage did not show differences between the 2 groups; inotropic support was lower in IWBC. Moreover, patients with UA and IWBC showed a lower troponin I (TnI) (12 h: 0.82+/-0.57 ng/mL vs 2.56+/-1.18, P < 0.0001; 24 h: 0.71+/-0.64 vs 2.16+/-1.52, P < 0.0001; 48 h: 0.69+/-1.13 vs 1.79+/-1.43, P = 0.001; 72 h: 0.44+/-0.83 vs 1.01+/-1.02, P = 0.001), lower incidence of atrial fibrillation (4.2% versus 60.6%; P < 0.0001) and intraoperative defibrillation (0% versus 27.3%; P = 0.007). Furthermore, patients with VH treated with IWBC showed lower level of TnI (12 h: 0.41+/-0.32 ng/mL vs 2.93+/-0.67, P < 0.0001; 24 h: 0.37+/-0.45 vs 2.40+/-1.28, P < 0.0001; 48 h: 0.22+/-0.18 vs 1.95+/-1.33, P < 0.0001; 72 h: 0.12+/-0.12 vs 1.31+/-1.56, P < 0.0001), lower atrial fibrillation (6.5% vs 48%, P < 0.0001) and ventricular defibrillation (0% vs 20%, P = 0.011).</AbstractText>Insulin addiction to blood cardioplegia does not show any benefit in the global population and in diabetics; nevertheless, better myocardial protection can be demonstrated in patients with unstable angina and left ventricular hypertrophy.</AbstractText> |
68 | Thoracic epidural anesthesia preserves myocardial function during intraoperative and postoperative period in coronary artery bypass grafting operation. | The purpose of this study was to investigate the effect of thoracic epidural anesthesia (TEA) in patients with poor ventricular function undergoing conventional coronary artery bypass graft surgery (CABG) during the intraoperative and the postoperative period.</AbstractText>Eighty patients (n = 80) undergoing elective CABG surgery with cardiopulmobary bypass (CPB) were divided into 4 groups: 1) General anesthesia (GA) plus poor ventricular (PV) function patients (Group GA plus PV) (n = 20), ejection fraction (EF) = or <40%; 2) GA plus good ventricular (GV) function patients (Group GA plus GV) (n = 20), EF >40%; 3) Thoracic epidural anaesthesia (TEA)+GA, poor ventricular function patients (Group TEA+GA plus PV) (n = 20), EF = or <40%; 4) TEA+GA, good ventricular function patients (Group TEA+GA plus GV) (n = 20), EF >40%.</AbstractText>Within groups, at 4 h after the end of CPB, in the Group TEA+GA plus PV and Group TEA+GA plus GV, the cardiac index values were significantly higher than baseline values; P < 0.05, whereas no difference was found in the Group GA plus PV and Group GA plus GV. According to Tukey test, using repeated measures, between trend of groups, the cardiac index values were significantly different P < 0.05. In the Group TEA+GA plus PV, cardiac index values were significantly higher than the Group GA plus PV, P < 0.05. But in the Group GA plus GV, cardiac index values were not significantly different than the Group TEA+GA plus GV. The incidence of reperfusion ventricular fibrillation (VF) after release of aortic cross-clamp, in the Group TEA+GA plus PV (4 of 20 patients: 20%) was significantly lower than in the Group GA plus PV (11 of 20 patients: 55%); P < 0.05. The incidence of reperfusion VF after release of aortic cross-clamp, in the Group TEA+GA plus GV (5 of 20 patients: 25%) was not significantly different than in the Group GA plus GV (10 of 20 patients: 50%); NS.</AbstractText>TEA seems to be effective in patients with poor left ventricular function. Our results (improved cardiac index, reduced arrhythmias after release of aortic clamp and decreased inotropic requirement) are better with TEA, particularly in patients with poor left ventricular function.</AbstractText> |
69 | Etiology of cerebrovascular accidents in octogenarians. | Stroke is the third leading cause of death in the United States, after coronary heart disease and cancer. Many survivors are left with mental and physical impairment and require assistance with activities of daily living. Twenty-eight percent of patients with stroke are under 65 years of age. We analyzed retrospectively 213 elderly patients with the diagnosis of ischemic cerebrovascular event that were consecutively admitted to the stroke unit of our institution between January 2002 and December 2004. Patient age varied from 65 to 100 years (mean = 79.8 years), and there were 66.19% females and 33.81% males. We analyzed the head CT findings of all the patients and separated the patients into two groups based on the results. Patients in Group I had large infarcts on CT and extensive neurological deficits, while patients in Group II had small lacunar infarcts and minor neurological findings. The charts of all the patients were reviewed retrospectively and data on hypertension, diabetes mellitus, carotid stenosis, atrial fibrillation, left ventricular hypertrophy and anticoagulation were retrieved and analyzed. Our results showed that 35.6% (76) of the patients suffered a major stroke (Group 1) and the remainder 64.4% (137) suffered small lacunar strokes (Group 2). More than half (57.9%) of the patients in Group I were found to have atrial fibrillation and significant carotid stenosis (35.5%) and 22.4%), respectively. The remaining patients (28) were hypertensive and 12% had diabetes mellitus, but no extracerebral source of embolism was found. In Group II, only 13.1% were found to have atrial fibrillation or significant carotid stenosis, but all were hypertensive and 86% suffered from diabetes. Our results indicate that major strokes are less prevalent in the geriatric population than small lacunar strokes and tend to be more related to hypertension and diabetes. |
70 | [Cardiac resynchronization therapy: who is suitable? Who requires an additional ICD as a backup?]. | Cardiac resynchronization therapy (CRT) has significant positive effects on the quality of life, enables patients to cope more efficiently with cardiopulmonary stress and leads to a reduction of total mortality in patients suffering from congestive heart failure NYHA classes III and IV, reduced ventricular function and left bundle branch block with a QRS complex wider than 150 ms. In a large number of patients suited for CRT, an additional defibrillator function seems to work out well concerning an additional prognostic improvement by means of reducing sudden cardiac death. Due to partially contradictory study outcomes, it still remains to be discussed whether all patients suited for CRT really need an ICD. |
71 | Progressive facilitation of antegrade conduction via an accessory pathway in a patient with Wolff-Parkinson-White syndrome and permanent atrial fibrillation. | The case of a 64-year-old man with Wolff-Parkinson-White syndrome and permanent atrial fibrillation (AF) is reported. The patient was admitted due to electrocardiographic feature of AF with rapid conduction over the left-sided accessory pathway. Administration of pirmenol effectively suppressed the ventricular response via an accessory pathway. A transesophageal echocardiography detected an uncertain thrombus in the left atrial appendage. During the 33-month follow-up period, the ventricular response via an accessory pathway was progressively facilitated. Radiofrequency catheter ablation using a transseptal approach was performed during AF, resulting in complete elimination of the antegrade accessory pathway conduction. |
72 | The Brugada syndrome--an update. | Brugada syndrome is characterized by ST-segment elevation in the right precordial leads (V1-V3) and an episode of ventricular fibrillation (VF) in the absence of structural heart disease. A number of reports from the world have unveiled the clinical, electrocardiographic, electrophysiologic and prognostic features of Brugada syndrome, and two recent consensus reports have suggested the diagnostic criteria of Brugada syndrome and the risk stratification for the identification of high risk Brugada patients for sudden cardiac death. SCN5A, the gene encoding the alpha subunit of the sodium channel, is the only gene thus far linked to Brugada syndrome; its prognostic value remains unclear. On the other hand, advances in the understanding of the cellular mechanism for Brugada phenotype derived from experimental studies have suggested possibilities for the development of strategies for managing and treating patients with Brugada syndrome. In this review, the recent understanding and knowledge of Brugada syndrome will be updated. |
73 | Microvolt T-wave alternans and the risk of death or sustained ventricular arrhythmias in patients with left ventricular dysfunction. | This study hypothesized that microvolt T-wave alternans (MTWA) improves selection of patients for implantable cardioverter-defibrillator (ICD) prophylaxis, especially by identifying patients who are not likely to benefit.</AbstractText>Many patients with left ventricular dysfunction are now eligible for prophylactic ICDs, but most eligible patients do not benefit; MTWA testing has been proposed to improve patient selection.</AbstractText>Our study was conducted at 11 clinical centers in the U.S. Patients were eligible if they had a left ventricular ejection fraction (LVEF) < or =0.40 and lacked a history of sustained ventricular arrhythmias; patients were excluded for atrial fibrillation, unstable coronary artery disease, or New York Heart Association functional class IV heart failure. Participants underwent an MTWA test and then were followed for about two years. The primary outcome was all-cause mortality or non-fatal sustained ventricular arrhythmias.</AbstractText>Ischemic heart disease was present in 49%, mean LVEF was 0.25, and 66% had an abnormal MTWA test. During 20 +/- 6 months of follow-up, 51 end points (40 deaths and 11 non-fatal sustained ventricular arrhythmias) occurred. Comparing patients with normal and abnormal MTWA tests, the hazard ratio for the primary end point was 6.5 at two years (95% confidence interval 2.4 to 18.1, p < 0.001). Survival of patients with normal MTWA tests was 97.5% at two years. The strong association between MTWA and the primary end point was similar in all subgroups tested.</AbstractText>Among patients with heart disease and LVEF < or =0.40, MTWA can identify not only a high-risk group, but also a low-risk group unlikely to benefit from ICD prophylaxis.</AbstractText> |
74 | Estimation of atrial fibrillatory wave from single-lead atrial fibrillation electrocardiograms using principal component analysis concepts. | A new method for the assessment of the atrial fibrillatory wave (AFW) from the ECG is presented. This methodology is suitable for signals registered from Holter systems, where the reduced number of leads is insufficient to exploit the spatial information of the ECG. The temporal dependence of the bio-electrical activity were exploited using principal component analysis. The main features of ventricular and atrial activity were extracted, and several basis signals for each subspace were determined. Hence, the estimated (AFW) are reconstructed exclusively from the basis signals that formed the atrial subspace. Its main advantage with respect to adaptive template subtraction techniques was its robustness to variations in the QRST morphology, which thus minimised QRST residua. The proposed approach was first validated using a database of simulated recordings with known atrial activity content. The estimated AFW was compared with the original AFW, obtaining correlation indices of 0.774 +/- 0.106. The suitability of this methodology for real recordings was also proven, though its application to a set of paroxysmal AF ECGs. In all cases, it was possible to detect the main frequency peak, which was between 4.6 Hz and 6.9 Hz for the patients under study. |
75 | Massive cardiac thrombosis in a patient with Sheehan's syndrome. | Growth hormone deficiency (GHD) is a risk factor for increased cardiovascular disease, and it has been recently demonstrated that abnormalities in coagulation system might contribute to the increased cardiovascular morbidity and mortality. However, there is not enough data related to the major thrombotic events in GH-deficient patients. We describe the case of a 62-year-old woman with Sheehan's syndrome who developed massive cardiac thrombosis. She was hospitalized with acute pulmonary edema. ECG revealed high ventricular responsive atrial fibrillation (AF) and T-wave inversion on precordial leads. The ejection fraction of left ventricle (LVEF) was measured as 60% by transthoracic echocardiography (TTE) and there was 2nd degree mitral regurgitation with concentric hypertrophic LV walls. Transesophagial echocardiography (TEE) established thrombi both at right atrium and left atrial appendix. Before anticoagulant therapy several hemostatic and fibrinolytic markers were measured. Except increased D-dimer concentration (763.14 mug/L (0-325)) we did not observe any pathological finding in these parameters. After 14 days of discharge, the patient was admitted to the intensive care unit with upper gastrointestinal bleeding. The warfarin and salicylate were stopped for two months. At the end of two months, the patient was again hospitalized with congestive heart failure and there was a high ventricular responsive AF on ECG. TEE was performed and three thrombi were demonstrated at right atrium (RA), left atrium (LA) and left ventricle (LV). There was no active bleeding on upper GIS endoscopy and anticoagulant therapy was restarted. In this particular case massive cardiac thrombi involving three chambers (LA, RA, LV) were more extensive than expected in AF. Moreover, there was a 2nd degree mitral regurgitation in the patient, and based on previous studies mitral regurgitation has been associated with less prevalent LA spontaneous echo contrast and fewer thromboembolic events. Therefore we hypothesized that severe GHD in the present case might be the major contributing factor in massive cardiac thrombosis. In summary, based on previous data there is increased risk of thromboembolic events in GHD although the mechanism is unclear yet. Our case is the first case showing massive cardiac thrombosis in a severe GH-deficient patient with Sheehan's syndrome. Therefore, patients with GHD should be screened carefully for thrombus in clinical practice, and further studies need to be done to understand the relation between GHD and coagulation system. |
76 | [Comparative study of the antiarrhythmic activity of mu- and delta-opioid receptor agonists during acute cardiac ischemia and reperfusion models in rats]. | It has been established that pretreatment with the selective mu-opioid receptor (OR) agonist DALDA (0.1 mg/kg, i.v.) or the selective delta1-OR agonists DPDPE (0.09 mg/kg) and/or (-)-TAN-67 (0.08 mg/kg) has no effect on the incidence of ventricular arrhythmias induced by a 10-min coronary artery occlusion and a 10-min reperfusion in ketamine-anesthetized rats. In contrast, the pretreatment with the selective delta2-OR agonist deltorphin II (0.12 mg/kg) and the proposed delta2-OR agonists deltorphin D (0.3 mg/kg) and/or dermorphin H (0.23 mg/kg) increases cardiac resistance to the arrhythmogenic action of acute ischemia and reperfusion. Administration of the mixed mu- and delta-OR agonist dalargin (0.12 mg/kg) 15 min before the coronary artery ligation abolished only the reperfusive ventricular fibrillation. It is concluded that peptidergic stimulation of delta2-ORs can be used as a new means of increasing cardiac tolerance to the arrhythmogenic effects of acute ischemia and reperfusion. |
77 | Atrial fibrillation and recurrent ventricular fibrillation during hypokalemia in Brugada syndrome. | A 41-year-old man with Brugada syndrome (BS) and no previous episodes of aborted sudden death or syncope referred to local emergency room for an episode of symptomatic atrial fibrillation. Blood chemistry results showed hypokalemia (2.9 mEq/L). The other parameters were within the normal range. After few minutes, an episode of ventricular fibrillation treated with biphasic DC shock 150 J occurred. In successive 2 hours, the patient experienced recurrent episodes of ventricular tachycardia and fibrillation. Each biphasic DC shock 150 J was effective to restore sinus rhythm. No further episodes occurred after normalization of serum levels of potassium. Before discharge, an implantable cardioverter defibrillator was inserted to prevent sudden cardiac death. Hypokalemia increases the risk of arrhythmic events in BS. |
78 | Ventricular fibrillation in two cases with dilated cardiomyopathy and mechanical alternans. | Clinical implication of mechanical alternans is yet unclear. It may suggest the risk for sudden death in patients with chronic heart failure. Two cases with dilated cardiomyopathy showed mechanical alternans during diagnostic cardiac catheterization. They suddenly died due to ventricular fibrillation before the induction of beta-blocker therapy. Patients with mechanical alternans should be treated under intense monitoring until the induction of beta-blocker therapy. |
79 | Determinants of mortality in patients undergoing cardiac resynchronization therapy: baseline clinical, echocardiographic, and angioscintigraphic evaluation prior to resynchronization. | In dilated cardiomyopathy (DCM) patients (pts) with cardiac resynchronization therapy (CRT) for ventricular dyssynchrony, long-term predictors of mortality and morbidity remain poorly investigated.</AbstractText>We reviewed data of 102 pts, 68 +/- 10 years, NYHA Class II-IV (14 Class II, 67 Class III, 21 Class IV), who benefited from CRT (69 CRT, 33 CRT-ICD). Fifty-two patients had an ischemic DCM, 36 a previously implanted conventional PM/ICD, 29 a permanent atrial fibrillation, and 19 needed dobutamine in the month preceding implant. QRS duration was 187 +/- 35 ms, left ventricular end-diastolic diameter 72 +/- 10 mm, mitral regurgitation severity 1.9 +/- 0.8, echographic aorto-pulmonary electromechanical delay 61.5 +/- 25 ms and septo-lateral left intraventricular delay 86 +/- 56 ms, pulmonary artery pressure (PAP) 43 +/- 11 mmHg, angioscintigraphic left ventricular ejection fraction (EF) 20 +/- 9%, and right ventricular EF 30.5 +/- 14%. Over a mean follow-up of 23 +/- 20 months, 26 pts died (18 heart failures (HFs), 1 arrhythmic storm, 7 noncardiac deaths). Positive univariate predictors of death from any cause were NYHA Class IV (P < 0.001), and need for dobutamine the month preceding CRT (P < 0.008), while use of beta-blocking agents (P < 0.08) and left ventricular EF (P < 0.09) were negative ones. NYHA Class IV was the only independent predictor at multivariate analysis (P < 0.01). Survival at 24 months was 85% in Class II, 80% in Class III, and 37% in Class IV (II vs III, P = ns; III vs IV, P < 0.001). When using a composite endpoint of death from any cause and unplanned rehospitalization for a major cardiovascular event, there were 48 events (14 HF deaths, 3 noncardiac deaths, 26 HF rehospitalizations, 2 paroxysmal atrial fibrillation, 2 sustained ventricular tachycardia, 1 nonfatal pulmonary embolism). Predictors of death from any cause/unplanned rehospitalization for a major cardiovascular event in the follow-up were NYHA Class IV (P < 0.001), need for dobutamine during the month preceding CRT (P < 0.002), and PAP (<0.02). NYHA Class IV was the only independent predictor at multivariate analysis (P < 0.05). Event-free proportion at 24 months was 70% in Class II, 64% in Class III, and 37% in Class IV (II vs III, P = ns; III vs IV, P < 0.01). When considering determinants of mortality only in NYHA Class IV patients, no variable was significantly correlated to mortality. Need for dobutamine during the last month preceding CRT did not add an adjunctive mortality risk.</AbstractText>Baseline NYHA Class IV at implantation appears as the most important determinant of a poor clinical outcome in terms of both mortality and morbidity. No predictive criteria seem available for NYHA Class IV patients, in order to discriminate who will die after CRT and who will not. NYHA Class IV strongly influences the clinical outcome, suggesting that, in future studies planned on mortality and rehospitalization as major endpoints, baseline NYHA Class IV should be separately taken into account.</AbstractText> |
80 | Determinants and effects of electrical stimulation of the inferior interatrial parasympathetic plexus during atrial fibrillation. | Catheter stimulation of the inferior interatrial ganglionated parasympathetic plexus decreases the ventricular rate during atrial fibrillation (AF) in humans. However, the relatively high stimulation voltages might prevent implementation of neurostimulation in chronic implantable devices. From myocardial electrostimulation it is known that the required impulse energy and charge is lowest at the chronaxie time. In order to lower energy requirements for cardiac neurostimulation, the present study evaluates the impulse-strength versus impulse-duration relationship for a neurostimulation lead that was implanted into the inferior interatrial ganglionated plexus.</AbstractText>In nine dogs, permanent epicardial bipolar screw-in electrodes were fixed in the inferior interatrial ganglionated plexus. AF was maintained via rapid atrial pacing. During AF, neural stimulation was performed at various frequencies (1-100 Hz), impulse durations (0.05-2 msec), and voltages (0.02-11.5 V). There was a linear correlation between R-R interval lengthening and stimulus voltage (R = 0.99; P < 0.001) and a bell-shaped relationship between stimulation frequency and negative dromotropic effect with maximum rate slowing at 30-50 Hz. The rheobase for a 50% R-R interval prolongation during AF was 1.81 V and 2.72 V for high-grade AVB yielding a chronaxie time of 0.14 msec and 0.18 msec, respectively. The impulse energy (charge) at the chronaxie time was 4-6 microJ (6-8 microC).</AbstractText>Cardiac neurostimulation follows a chronaxie/rheobase behavior. Energy, charge, and voltage values needed to achieve significant negative dromotropic effects are within the limits of conventional cardiac pacemaker outputs, which may allow implementation of neurostimulation capabilities in current pacemaker technology.</AbstractText> |
81 | Mapping of atrial activation during sustained atrial fibrillation in dogs with rapid ventricular pacing induced heart failure: evidence for a role of driver regions. | Dogs with rapid ventricular pacing (RVP)-induced congestive heart failure (CHF) have inducible atrial tachycardia, flutter, and fibrillation (AF). We tested the hypothesis that rapid atrial activation in multiple regions and at different rates is responsible for sustained AF in this CHF model.</AbstractText>We studied 12 episodes of sustained (>10 minutes) AF induced in 12 dogs with CHF produced by 3-6 weeks of RVP at 230 beats/minute. High-density mapping of AF was performed using 382 unipolar atrial electrograms recorded simultaneously from epicardial electrodes on the right (RA) and left atria (LA) and Bachmann's bundle. AF mechanisms were based on Fast Fourier Transform (FFT) analysis and activation sequence mapping. A driver was defined as a rapid stable activation region with a single dominant frequency peak in FFT analysis. During AF, three FFT and activation patterns were seen: (1) a single LA driver (7.8 +/- 1.1 Hz) near the pulmonary veins (PVs) with irregular activation in the rest of the atria (n = 4); (2) simultaneous, multisite, biatrial drivers at differing frequencies (LA vs RA dominant frequency gradient: 1.3 +/- 0.8 Hz) near the PVs (8.4 +/- 0.3 Hz) and high RA (8.5 +/- 1.5 Hz) (n = 7); and (3) biatrial irregular activation with multiple and/or broadband frequency peaks without a dominant frequency. (LA: 7.1-11.4 Hz; RA: 5.9-7.7 Hz) (n = 1). Atrial drivers had either a focal activation pattern or were due to a macroreentrant circuit around the PVs.</AbstractText>In this CHF model, FFT analysis and activation sequence mapping demonstrate that sustained AF is characterized by single and multiple, stable LA and RA drivers with predominant sources in the PVs and high RA causing fibrillatory conduction.</AbstractText> |
82 | Atrial natriuretic peptide has dose-dependent, autonomically mediated effects on atrial refractoriness and repolarization in anesthetized dogs. | Atrial natriuretic peptide (ANP) may alter electrophysiological properties of the heart and possibly have a role in arrhythmogenesis. However, previous studies have yielded conflicting results and have not fully considered whether ANP's cardiac electrophysiological effects are mediated via direct actions and/or indirectly via the autonomic nervous system. This study's aim was to establish whether ANP infused at pathophysiological and pharmacological doses has significant in vivo cardiac electrophysiological effects and to determine whether these effects are directly or autonomically mediated.</AbstractText>Electrophysiologic and hemodynamic effects of ANP infusion (human ANP at 15-600 ng/kg per minute) were examined in chloralose-anesthetized dogs under conditions of varying autonomic blockade. In autonomically intact dogs (n = 12), low-dose ANP (15 ng/kg per minute) shortened atrial effective refractory period (ERP) (P < 0.001) and monophasic action potential duration (MAPD90) (P < 0.05) at 600, 500, and 400 msec atrial paced cycle lengths and reduced right atrial pressure (P < 0.05) but did not alter mean arterial pressure. After either combined vagal and beta-adrenergic blockade (vagotomy plus atropine plus propranolol, n = 7) or selective vagal blockade (n = 9), low-dose ANP no longer altered atrial ERP or MAPD90. Higher ANP doses (150 and 600 ng/kg per minute) decreased mean arterial and right atrial pressures (P < 0.001) but did not alter atrial ERP, MAPD90, or other electrophysiological parameters including atrial fibrillation threshold, ventricular ERP, and MAPD90.</AbstractText>ANP has dose-dependent, autonomically mediated effects on atrial refractoriness and repolarization.</AbstractText> |
83 | Clinical predictors of noninducibility of sustained atrial fibrillation after pulmonary vein isolation. | Noninducibility of sustained atrial fibrillation (AF) after pulmonary vein isolation (PVI) has been shown to be associated with a better clinical outcome. We evaluated the role of clinical variables that could predict noninducibility of sustained AF after PVI.</AbstractText>Data were collected prospectively from 181 patients (153 male; age 54 +/- 9 years) referred for ablation of drug-refractory symptomatic paroxysmal AF (duration < or =7 days). Clinical variables were evaluated with regard to their ability of predicting noninducibility of sustained AF (< or =10 minutes) after PVI. Univariate analysis was performed on all collected variables followed by multivariate analysis for variables showing a P value <0.1. After PVI, sustained AF was noninducible in 97 (54%) patients. The following clinical variables showed a significant difference between the groups: body weight, longest AF episode, duration of AF history, presence or absence of structural heart disease, left ventricular (LV) hypertrophy, prior cardioversion, left atrial (LA) parasternal, and longitudinal diameters and LV diameters. On multivariate analysis, three independent predictors of noninducibility were identified: a shorter duration of AF episodes (AF <12 hours: RR 0.01 (0.002-0.06), P < 0.001; AF 12-48 hours: RR 0.07 (0.01-0.37), P = 0.001); LA longitudinal diameter <57 mm (RR 0.33 (0.13-0.82), P = 0.016); and absence of LV hypertrophy (RR 0.15 (0.04-0.63), P = 0.01).</AbstractText>Shorter AF episodes, smaller LA longitudinal diameter, and absence of LV hypertrophy are independent predictors of noninducibility of sustained AF after PVI.</AbstractText> |
84 | [Progress in diagnostic and management of cardiac arrhythmias]. | The era of catheter ablation for the treatment of arrhythmias began in 1981 when Dr Scheinman performed the first atrioventricular junction ablation using direct current shocks in a patient with drug refractory atrial fibrillation and an uncontrolled ventricular rate. With the progress of radiofrequency catheter ablation, the range of arrhythmias amenable to catheter ablation and the number of patients that could be treated safely by this procedure expanded enormously. Lastly, although still in an evolutionary phase, catheter ablation to eliminate atrial fibrillation has been demostrated in the past years to be feasible and clinically useful. On the other hand, innovations in technology and pharmacology, and better preventive and diagnostic tools, have provided our patients with an important improvement in their prognosis. The new developments in molecular genetics and biology are likely to change the way we approach a cardiac patient in the future. The diseases are now being deciphered at the most basic level, and the information obtained opens new possibilities not only for better therapeutic and diagnostic measures but also for prevention of the disease. |
85 | Atrial fibrillation as a cause of left ventricular dysfunction after cardiac transplantation. | We report 3 cases of late-onset atrial fibrillation several years after cardiac transplantation, each involving left ventricular systolic dysfunction in the absence of cardiac rejection or cardiac allograft vasculopathy. Although the etiology of late-onset atrial fibrillation in cardiac transplant recipients is not clear, its presence in the absence of cardiac rejection or coronary allograft vasculopathy can result in left ventricular systolic dysfunction, and therefore should be considered in the differential diagnosis of cardiac allograft failure. The onset of atrial fibrillation years after a heart transplant is not necessarily an indication of rejection. Aggressive rate control and restoration of normal sinus rhythm may improve allograft function in such cases. |
86 | Prevalence, pathophysiology, and clinical significance of post-heart transplant atrial fibrillation and atrial flutter. | Atrial rhythm disturbances, in particular atrial fibrillation (AF) and flutter (AFL), are common in the denervated transplanted heart. However, there is a relative paucity of data in the prevalence, mechanism of arrhythmia, and long-term significance.</AbstractText>(1) Determine the prevalence of AF and AFL in heart transplant patients, (2) define the echo/Doppler features associated with arrhythmia, and (3) evaluate the impact of arrhythmia on long-term survival.</AbstractText>All patients who received an orthotopic heart transplant at the Mayo Clinic, Rochester, Minnesota, between 1988 and 2000 were included. Analysis of serial electrocardiograms and Holter monitor records provided evidence of AF or AFL development. Variables including general patient demographics, histology-proven rejection numbers and grades, results of serial coronary angiography, endomyocardial biopsy specimens, and echocardiographic studies performed at 6 weeks and 3 years after transplant were obtained to determine variables predictive of arrhythmia development.</AbstractText>There were 167 heart transplant recipients, of which 16 (9.5%) developed AF and another 25 (15.0%) developed AFL over 6.5 +/- 3.4 years. Patients who developed AF or AFL had lower left ventricular (LV) ejection fractions (56.6% +/- 1.6% vs 62.5% +/- 1.5%, p < 0.05), higher LV end-systolic dimensions (LVESD) (33.6 +/- 1.12 mm vs 29.7 +/- 0.97 mm, p < 0.01), higher right atrial volume indexes (43.2 +/- 12.3 ml vs 35 +/- 5.3 ml, p < 0.03), lower mitral deceleration time (145 +/- 8 msec vs 160 +/- 12 msec, p < 0.05), and lower late mitral annulus tissue a' velocities (0.06 +/- 0.005 cm/sec vs 0.08 +/- 0.01 cm/sec, p < 0.02) compared with an age- and gender-matched Sinus Rhythm Group. Grade 3 rejection was a time-dependent covariate predictor of AFL risk (hazard ratio [HR], 2.95; 95% confidence interval [CI], 1.3-6.6, p < 0.008) but not AF (HR, 2.264; 95% CI, 0.72-7.1; p = 0.10). Thirty-nine of 167 patients died: 13 in the arrhythmia group and 26 in the normal sinus rhythm group. Development of atrial dysrhythmia adversely affected the outcome in the first 5 years (p < 0.001) compared with normal sinus rhythm. Predictors of long-term mortality included AF/AFL (HR, 2.88; 95% CI, 1.38-5.96; p < 0.004), age at transplant (HR, 1.04; 95% CI, 1.00-1.07, p < 0.03), coronary artery disease (HR, 2.655; 95% CI, 1.25-5.64; p = 0.01), pre-transplant cardiac amyloidosis (HR, 5.02; 95% CI 2.37-10.62; p < 0.001), right atrial volume index (HR, 1.03; 95% CI, 1.00-10.7; p = 0.03), mitral deceleration time <160 msec (p < 0.01), and LVESD >30 mm (p < 0.04).</AbstractText>Development of AF/AFL post-heart transplantation is not uncommon and is associated with decreased long-term survival. Cumulative effects of repeated moderate-to-severe (grade 3 or more) rejections that result in increased cardiac fibrosis are associated with the development of AFL, but not AF. Similarly advanced restrictive diastolic dysfunction caused by fibrosis from repeated moderate-to-severe (grade 3 or more) rejections was predominant in the patients with arrhythmia and was a marker of poor long-term outcome.</AbstractText> |
87 | Therapies for ventricular cardiac arrhythmias. | During recent years, engineers and physicists have become increasingly interested in studying the electrical activity of the heart. Despite the fact that the heart is a complex and highly nonlinear system, its electrical behavior can be studied using a variety of experimental and clinical techniques, and can be modeled mathematically using relatively simple systems of differential equations, allowing scientists to perform both real and virtual (in silico) experiments to gain insights into its physiology and pathophysiology. Although these approaches have in recent years allowed great headway to be made into understanding the dynamic behavior of the heart, cardiac arrhythmias such as ventricular fibrillation still claim the lives of hundreds of thousands of people each year in the United States alone. Bridging the gap between understanding the mechanistic bases of arrhythmias and applying such knowledge to improving therapy presents one of the greatest challenges in the field of cardiac electrophysiology. In this review, we describe the basic electrical properties and dynamic behavior of the heart and review the current state of the art in ventricular arrhythmia therapy. We also discuss some possibilities for future therapies, with the hope that such informed speculation will promote new investigations in these areas. |
88 | [Relationship between efficacy of antiarrhythmic drug therapy and structural remodeling in patients with paroxysmal atrial fibrillation]. | To evaluate whether the response to antiarrhythmic drug therapy in patients with paroxysmal atrial fibrillation affects the development of structural remodeling in the left atrium and ventricle.</AbstractText>This study included 230 patients (158 men and 72 women, mean age 67 +/- 11 years) in whom antiarrhythmic drug therapy was attempted for > or = 12 months to maintain sinus rhythm (mean follow-up period 45 +/- 27 months). The patients were divided into three groups according to the response to antiarrhythmic drug therapy: group A consisted of 78 patients without recurrence of atrial fibrillation, group B consisted of 87 patients with recurrence of atrial fibrillation and electrical and/or pharmacological cardioversion to restore sinus rhythm, and group C consisted of 65 patients with permanent conversion despite antiarrhythmic drug therapy.</AbstractText>In group A, left atrial dimension (LAD), left ventricular end-diastolic dimension (LVDd), and left ventricular ejection fraction (LVEF) did not change after antiarrhythmic drug therapy. In group B, LAD increased significantly after antiarrhythmic drug therapy (from 32.6 +/- 6.4 to 36.0 +/- 6.5 mm, p < 0.01), Whereas either LVDd or LVEF did not change after antiarrhythmic drug therapy. In group C, LAD increased significantly after antiarrhythmic drug therapy (from 37.3 +/- 7.0 to 40.5 +/- 7.9 mm, p < 0.01) and LVEF was significantly reduced after antiarrhythmic drug therapy (from 69.4 +/- 6.2% to 66.5 +/- 8.9%, p < 0.05). LVDd did not change after antiarrhythmic drug therapy. The plasma concentration of human atrial natriuretic peptide during sinus rhythm at the initiation of antiarrhythmic drug therapy in group A (30.5 +/- 26.7 pg/ml) was significantly lower than those in group B (48.0 +/- 49.7 pg/ml) and group C (49.7 +/- 39.5 pg/ml).</AbstractText>The development of structural remodeling in human myocardium can be prevented with antiarrhythmic drug therapy if sinus rhythm is maintained without recurrence of atrial fibrillation in patients with paroxysmal atrial fibrillation.</AbstractText> |
89 | Declining case fatality rates for acute myocardial infarction in South Asian and white patients in the past 15 years. | To determine whether case fatality rates in South Asian (Bangladeshi, Indian and Pakistani) patients with acute myocardial infarction have shown similar declines to those reported for white patients during the past 15 years.</AbstractText>Cross-sectional, observational study.</AbstractText>Coronary care unit in east London.</AbstractText>2640 patients-29% South Asian-admitted with acute myocardial infarction between January 1988 and December 2002.</AbstractText>Differences over time in rates of in-hospital death, ventricular fibrillation and left ventricular failure.</AbstractText>The proportion of South Asians increased from 22% in 1988-92 to 37% in 1998-2002. Indices of infarct severity were similar in South Asian and white patients, with declining frequencies of ST elevation infarction (88.2% to 77.5%, p < 0.0001), Q wave development (78.1% to 56.9%, p < 0.0001) and mean (interquartile range) peak serum creatine kinase concentrations (1250 (567-2078) to 1007 (538-1758) IU/l, p < 0.0001) between 1988-92 and 1998-2002. Rates of in-hospital death (13.0% to 9.4%, p < 0.01), ventricular fibrillation (9.2% to 6.0%, p < 0.001) and left ventricular failure (33.2% to 26.5%, p < 0.0001) all declined; these changes did not interact significantly with ethnicity. Odds ratios for the effect of time on risk of death increased from 0.81 (95% CI 0.70 to 0.93) to 1.02 (95% CI 0.87 to 1.21) after adjustment for ethnicity and indices of infarct severity (ST elevation, peak creatine kinase, Q wave development and treatment with a thrombolytic).</AbstractText>In the past 15 years, death from acute myocardial infarction among South Asians has declined at a rate similar to that seen in white patients. This is largely caused by reductions in indices of infarct severity.</AbstractText> |
90 | Intracoronary infusion of Gd3+ into ischemic region does not suppress phase Ib ventricular arrhythmias after coronary occlusion in swine. | Increased mechanical tension in the ischemic region during acute coronary occlusion might favor the occurrence of phase Ib ventricular arrhythmias. We aimed to investigate whether intracoronary administration of Gd(3+), a stretch-activated channel blocker, into the ischemic zone reduces the incidence of these arrhythmias. In thiopental-anesthetized, open-chest pigs, the left anterior descending coronary artery (LAD) was ligated for 45 or 48 min. Phosphate-free, HEPES-buffered saline bubbled with 100% N(2) was infused into the ischemic region for 4 min, starting 5 min (series A; n = 16) or 20 min (series B; n = 16) after coronary occlusion, at a rate doubling the baseline blood flow. Animals were blindly allocated to receive 40 muM Gd(3+) or only the buffer during the final 2 min of the infusion. There were no differences between groups with respect to hemodynamic variables, plasma K(+) levels, or size of the ischemic region. In neither series was the number of phase Ib premature ventricular beats reduced by Gd(3+) (46 +/- 20 in untreated vs. 91 +/- 37 in Gd(3+)-treated animals in series A and 19 +/- 7 vs. 22 +/- 13, respectively, in series B; both P = not significant). The occurrence of ventricular tachycardia or fibrillation was significantly associated with the magnitude of early ischemic expansion of the LAD region, as measured by ultrasonic crystals, but was also not prevented by Gd(3+). These results argue against a major role of stretch-activated channels inside the area at risk in the genesis of phase Ib ischemic ventricular arrhythmias. |
91 | Endurance exercise training attenuates cardiac beta2-adrenoceptor responsiveness and prevents ventricular fibrillation in animals susceptible to sudden death. | Enhanced cardiac beta(2)-adrenoceptor (beta(2)-AR) responsiveness can increase susceptibility to ventricular fibrillation (VF). Exercise training can decrease cardiac sympathetic activity and could, thereby, reduce beta(2)-AR responsiveness and decrease the risk for VF. Therefore, dogs with healed myocardial infarctions were subjected to 2 min of coronary occlusion during the last minute of a submaximal exercise test; VF was observed in 20 susceptible, but not in 13 resistant, dogs. The dogs were then subjected to a 10-wk exercise-training program (n = 9 susceptible and 8 resistant) or an equivalent sedentary period (n = 11 susceptible and 5 resistant). Before training, the beta(2)-AR antagonist ICI-118551 (0.2 mg/kg) significantly reduced the peak contractile (by echocardiography) response to isoproterenol more in the susceptible than in the resistant dogs: -45.5 +/- 6.5 vs. -19.2 +/- 6.3%. After training, the susceptible and resistant dogs exhibited similar responses to the beta(2)-AR antagonist: -12.1 +/- 5.7 and -16.2 +/- 6.4%, respectively. In contrast, ICI-118551 provoked even greater reductions in the isoproterenol response in the sedentary susceptible dogs: -62.3 +/- 4.6%. The beta(2)-AR agonist zinterol (1 microM) elicited significantly smaller increases in isotonic shortening in ventricular myocytes from susceptible dogs after training (n = 8, +7.2 +/- 4.8%) than in those from sedentary dogs (n = 7, +42.8 +/- 5.8%), a response similar to that of the resistant dogs: +3.0 +/- 1.4% (n = 6) and +3.2 +/- 1.8% (n = 5) for trained and sedentary, respectively. After training, VF could no longer be induced in the susceptible dogs, whereas four sedentary susceptible dogs died during the 10-wk control period and VF could still be induced in the remaining seven animals. Thus exercise training can restore cardiac beta-AR balance (by reducing beta(2)-AR responsiveness) and could, thereby, prevent VF. |
92 | Elimination of late potentials by quinidine in a patient with Brugada syndrome. | The beneficial effects of quinidine on ST-segment elevation, inducible ventricular tachyarrhythmias, and episodes of ventricular tachyarrhythmia have been reported in Brugada syndrome. This is the first report describing quinidine-induced elimination of the late potential, which is considered one of the parameters for an arrhythmic event, in a patient with Brugada syndrome. |
93 | The role of premature atrial contractions as the main triggers of postoperative atrial fibrillation. | To better understand the pathogenesis of postoperative atrial fibrillation (AF), the mode of onset of AF after coronary artery bypass grafting was analyzed with respect to the autonomic balance, the heart rate (HR), and the presence of arrhythmias preceding the onset of sustained AF.</AbstractText>Holter recordings of 24 hours, obtained from the first postoperative morning until clinically documented sustained AF, were analyzed in 29 untreated patients and in 13 patients treated with thoracic epidural anesthesia (TEA), who all developed AF after coronary artery bypass grafting. The presence of arrhythmias, the HR, and the autonomic balance, assessed by heart rate variability in the frequency domain, were analyzed at predefined time intervals within the 3-hour period before AF onset. Supraventricular premature beats (SPBs) and ventricular premature beats triggering the onset of AF were also evaluated.</AbstractText>An SPB triggering the onset of AF can be identified in 21 (72.4%) of 29 untreated patients and in 12 (100%) of 12 TEA-treated patients in whom the recordings permitted such an analysis. The heart rate variability components analyzed during 5-minute periods for 30 minutes before AF onset did not differ significantly from those at corresponding times at the first postoperative day in either patient group. The HR during the 8 beats immediately before AF onset was lower in TEA-treated than in untreated patients.</AbstractText>The finding of an SPB at the onset of postoperative AF in most of the patients and irrespective of changes in HR supports the hypothesis that postoperative AF is primarily triggered by latent focal atrial activity. The autonomic tone did not seem to be of major importance in the population studied.</AbstractText> |
94 | Predictive value of ventricular arrhythmia inducibility for subsequent ventricular tachycardia or ventricular fibrillation in Multicenter Automatic Defibrillator Implantation Trial (MADIT) II patients. | In the Multicenter Automatic Defibrillator Implantation Trial (MADIT) II, implantable cardioverter-defibrillator (ICD)-randomized patients underwent electrophysiologic testing. Both inducible and noninducible patients received an ICD. We correlated inducibility with the occurrence of subsequent ventricular tachycardia (VT) or ventricular fibrillation (VF). Intracardiac ICD electrograms for subsequent events were analyzed to categorize the spontaneous arrhythmia as VT or VF. The two-year Kaplan-Meier event rate for VT in inducible patients was 29.0% versus 19.3% in noninducible patients. However, ICD therapy for spontaneous VF was less common at two years in inducible patients (3.2%) than in noninducible patients (8.6%). In the MADIT II study, inducibility predicted an increased likelihood of VT but decreased VF.</AbstractText>We correlated electrophysiologic inducibility with spontaneous ventricular tachycardia (VT) or ventricular fibrillation (VF) in the Multicenter Automatic Defibrillator Implantation Trial (MADIT) II.</AbstractText>In the MADIT II study, 593 (82%) of 720 implantable cardioverter-defibrillator (ICD) randomized patients underwent electrophysiologic testing. Patients received an ICD whether they were inducible or not.</AbstractText>A "standard" inducibility definition included sustained monomorphic or polymorphic VT induced with three or fewer extrastimuli or VF induced with two or fewer extrastimuli. We compared a narrow inducibility definition (only monomorphic VT) and a broad definition (standard definition plus VF with three extrastimuli). We used ICD-stored electrograms to categorize spontaneous VT or VF.</AbstractText>Inducible patients (standard definition) had a greater likelihood of experiencing ICD therapy for VT than noninducible patients (p = 0.023). Unexpectedly, ICD therapy for spontaneous VF was less common (p = 0.021) in inducible patients than in noninducible patients. The two-year Kaplan-Meier event rate for VT or VF was 29.4% for inducible patients and 25.5% for noninducible patients. Standard inducibility did not predict the combined end point of VT or VF (p = 0.280, by log-rank analysis). The narrow inducibility definition outperformed the standard definition, whereas the broad definition appeared inferior to the standard definition.</AbstractText>In the MADIT II study patients, inducibility was associated with an increased likelihood of VT. Noninducible MADIT II study subjects using this electrophysiologic protocol had a considerable VT event rate and a higher VF event rate than inducible patients. Induction of polymorphic VT or VF, even with double extrastimuli, appears less relevant than induction of monomorphic VT.</AbstractText> |
95 | Genomics and cardiac arrhythmias. | Sudden cardiac death in patients younger than 35 years of age is primarily due to genetic causes. Familial hypertrophic cardiomyopathy accounting for 30% to 40% is associated with structural heart disease while the Brugada syndrome and the long QT syndrome (LQTS) are associated with normal cardiac function. This is a review of the genetics of supraventricular and ventricular arrhythmias. Atrial fibrillation is mapped to nine chromosomal loci and four genes are identified. AMP-activated protein kinase is one gene responsible for Wolff-Parkinson-White syndrome. The LQTS and the Brugada syndromes are due to defects primarily in cardiac sodium and potassium ion channels. The role of single nucleotide polymorphisms in predisposing to arrhythmias in acquired disorders such as hypertrophy is discussed. |
96 | Analysis of the outcomes of cardiopulmonary resuscitation in an emergency department. | The aim of this study is to analyse the factors affecting emergency department (ED) cardiopulmonary resuscitation (CPR) outcome.</AbstractText>A standard CPR protocol was performed in all patients and certain pre and postresuscitation parameters including age, sex, initial arrest rhythm, primary underlying disease, initiation time of advanced cardiac life support, duration of return of spontaneous circulation were recorded. Patients were followed up to determine rates of successful CPR, survival and one-year survival.</AbstractText>From December 1999 to May 2001, 80 consecutive adult patients in whom a standard CPR was performed in the ED were prospectively included in the study. The overall rate for successful CPR, survival and one-year survival were found to be 58.8% (47/80), 15% (12/80) and 10% (8/80), respectively. Survival and one-year survival rates were better in patients with an initial arrest rhythm of ventricular fibrillation or pulseless ventricular tachycardia (VF/pVT) than both pulseless electrical activity (pEA) and asystole; survival and one-year survival rates were better in patients with a primary underlying disease of cardiac origin than non-cardiac origin. Acute myocardial infarction had the best prognosis among conditions causing arrest. Presence of sudden death was found to have a better survival and one-year survival rate.</AbstractText>Initial cardiac rhythm of VF/pVT, cardiac origin as the primary disease causing cardiopulmonary arrest and presence of sudden death were found to be good prognostic factors in CPR.</AbstractText> |
97 | Predictors and outcome of cardiopulmonary resuscitation (CPR) calls in a large haemodialysis unit over a seven-year period. | Cardiac mortality is the leading cause of death in dialysis patients, with cardiac arrests being most frequent. Our purpose was to determine the epidemiology, predictors and outcomes of calls for cardiopulmonary resuscitation (CPR) occurring in our haemodialysis unit.</AbstractText>We reviewed retrospectively all calls for CPR occurring in our unit between August 1997 and December 2004 and compared data to a cohort of chronic haemodialysis patients from our unit. Dialysis sessions performed in the ICUs were not included.</AbstractText>A total of 38 calls occurred over 307,553 sessions, corresponding to an incidence of 0.012%. In a multivariate logistic regression model, statistically significant predictors to have a call for CPR were ischaemic heart disease (OR: 3.93; 95% CI: 1.70-9.07), heart failure (OR: 2.74; 95% CI: 1.12-6.74) and female gender (OR: 2.96; 95% CI: 1.37-6.43). Patients who had a call for CPR had a lower dialysis vintage than control patients (OR: 0.98; 95% CI: 0.965-0.996). Twenty of the 38 events presented on Mondays or Tuesdays (P = 0.012); 78% occurred during haemodialysis, vs 14 and 8% immediately after and immediately before dialysis but still on the unit, respectively. Of the 38 events, 24 were true cardiopulmonary arrests. Cardiac etiology was the most frequent (34%) and only 4 events were attributed to potassium disorders. One quarter of patients were dialyzed against a dialysate potassium concentration of 1 mmol/l or below. An arrhythmia was identified in 19 patients; a malignant ventricular fibrillation or ventricular tachycardia was most frequently found (32%), followed by severe bradycardia (26%). For the whole group, there were 6 deaths (16%) within 48 h; 30 patients (79%) were alive at 30 days and discharged from the hospital. Among the 24 cardiopulmonary arrests, there were 4 deaths (17%) within 48 h; 18 patients (75%) were alive at 30 days and discharged from the hospital. There was a trend for worse prognosis at 60 days when related to cardiopulmonary etiology (P = 0.054) and when a true cardiopulmonary arrest occurred (P = 0.134).</AbstractText>This study confirms that arrest codes occur more frequently on Mondays and Tuesdays in a haemodialysis unit. Survival after an arrest code appears to be better than in certain other circumstances, probably in part because of the presence of witness, physician and equipment, and vascular access being readily available.</AbstractText> |
98 | Plasma levels of NT-pro-BNP in patients with atrial fibrillation before and after electrical cardioversion. | Plasma levels of brain natriuretic peptide (BNP) have been examined in studies on patients with persistent atrial fibrillation, both before and after electrical cardioversion. Studied patients often showed a comorbidity with congestive heart failure, which complicates interpretation of measured BNP values as a natriuretic peptide. The aim of this study was to examine plasma levels of N-terminal fragment pro-brain natriuretic peptide (NT-pro-BNP), which is the more stable but inactive cleavage product of pro-BNP in patients with atrial fibrillation, but normal left ventricular ejection fraction, before and after electrical cardioversion.</AbstractText>NT-pro-BNP plasma levels of 34 consecutive patients were measured before, shortly after and 11 days after electrical cardioversion. All patients showed a normal ejection fraction after echocardiographic or laevocardiographic criteria.</AbstractText>At baseline, all patients showed elevated NT-pro-BNP compared to a healthy control group (1086 vs. 66.9 pg/ml, p<0.001). After a mean follow-up time of 11 days in patients with persistent restored sinusrhythm, NT-pro-BNP decreased from 1071 pg/ml at baseline to 300 pg/ml (p<0.001). In contrast, patients with recurrence of atrial fibrillation showed increased levels from 1570.5 pg/ml at baseline to 1991 pg/ml (p=0.13; n.s.). Recurrence of atrial fibrillation was independent from height of NT-pro-BNP levels at baseline (p=0.23).</AbstractText>Atrial fibrillation in patients with a normal left ventricular ejection fraction is associated with elevated NT-pro-BNP plasma levels, which decrease when a persistent sinus-rhythm can be restored by electrical cardioversion. On the other hand, NT-pro-BNP seems to increase (n.s.) when recurrence of atrial fibrillation occurs. Finally, NT-pro-BNP is no valid predictor for long-term success of sinus-rhythm restoration by electrical cardioversion.</AbstractText> |
99 | [Protective effect of the pretreatment with Chuanxiong-phthalide A on the vascular endothelial cells impaired by the ischemia and reperfusion in isolated rats hearts]. | The aim of this study was to investigate the protective effect of Chuanxiong-pathalide A on the injury of endothelial cell induced by ischemia and reperfusion in isolated rat hearts.</AbstractText>The isolated rat hearts were perfused under constant pressure with Chuanxiong-pathalide A at the concentrations of 0.012 5 mg x mL(-1), 0.025 mg x mL(-1) and 0.05 mg x mL(-1) within 10 min followed by a 10-min washout period before the induction of a 30-min normothermic global ischemia and 60 min reperfusion.</AbstractText>Pretreatment with Chuanxiong-pathalide A produced a reduction in the incidence of reperfusion-induced ventricular fibrillation (VF) and ventricular tachycardia (VT). Pretreatment of the hearts with high dose of Chuanxiong-pathalide A (0.05 mg x mL(-1)) prior to the ischemia and reperfusion, reduced the incidence of reperfusion-induced VF and VT to 37.5% as compared with non-pretreated control group (P < 0.05). The duration of occurrence of VF and VT in the group pretreated with Chuanxiong-pathalide A at dosages of 0.012 5 mg x mL(-1), 0.025 mg x mL(-1) and 0.05 mg x mL(-1) were (7.50 +/- 1.61), (1.64 +/- 0.67) and (1.06 +/- 0.70) min respectively, which were significantly shorter than (23.51 +/- 3.99) min in non-pretreated control group; 0.05 mg x mL(-1) of Chuanxiong-pathalide A increased coronary flow in comparison with the control group. The content of SOD in the group pretreated with 0.05 mg x mL(-1) of Chuanxiong-pathalide A was (59.6 +/- 18.7) U x mg(-1), significant lower than (92.3 +/- 19.0) U x mg(-1) in the non-pretreated group. The contents of LDH and MDA were (2 378.0 +/- 196.3) U x g(-1) and (12.1 +/- 1.3) nmol x mg(-1) in the non-pretreated group, which were much higher than the values of (1 669.4 +/- 192.5) U x g(-1) and (6.9 +/- 0.8) nmol x mg(-1) in the group pretreated with Chuanxiong-pathalide A respectively. In addition, enzymeimmunoassays showed an decreased production of IL-1beta and the ratio of TXB2/6-Keto-PGF1alpha.</AbstractText>Our results show that chuanxiong-pathalide A pretreatment can protect the endothelial function from the injury caused by ischemia and reperfusion.</AbstractText> |
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Dataset Card
This dataset consists of abstracts from heart-related papers collected from PubMed. It can be used for pre-training a language model specialized in cardiology. The dataset was collected through the PubMed API, based on the names of heart-related journals and a glossary of cardiology terms.
Dataset
Data Sources
- Pubmed: PubMed is a database that provides abstracts of research papers related to life sciences, biomedical fields, health psychology, and health and welfare. Among these, we have collected abstracts of papers related to the heart.
Keywords Sources
- Scimago Journal & Country Rank : We used a list of cardiology-related journals provided by SJR as keywords for data collection.
- National Institutes of Health : We used a glossary provided by NIH as keywords for data collection.
- The Texas Heart Institute : We used a glossary provided by Texas Heart Institute as keywords for data collection.
- Aiken Physicians Alliance : We used a glossary provided by Aiken Physicians Alliance as keywords for data collection.
Dataset Field
| Field | Data Type | Description |
|---|---|---|
| title | string | The title of the paper. |
| abst | string | The abstract of the paper. |
Dataset Structure
DatasetDict({
train: Dataset({
features: ['title', 'abst'],
num_rows: 2600900
})
})
Use
from datasets import load_dataset
dataset = load_dataset("InMedData/Cardio_v1")
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