bluuebunny/crossref_metadata_2025 huggingface dataset:
Termination of pacemaker‐mediated tachycardia by adenosine
Authors: Conti Jamie B. , Curtis Anne B. , Hill James A. , Raymenants Erwin R.
Published: February 2009

A 30‐year‐old woman was referred for follow‐up right‐ and left‐heart catheterization 4 years after cardiac transplantation. She had an implanted epicardial pacemaker for bradycardia; this was programmed to the DDD mode. At the time of her catheterization, as a pigtail catheter was pulled back across the aortic valve, runs of premature ventricular complexes occurred and tachycardia with ventricular pacing spikes and ventricular capture was initiated at a rate of 126 beats/min. Adenosine 6 mg was given intravenously through a femoral venous sheath and within 20 s the tachycardia broke. The tachycardia was consistent with pacemaker‐mediated tachycardia (PMT), a circus movement tachycardia occurring when ventricular pacing causes retrograde atrial depolarization followed by triggering of ventricular pacing. With reprogramming of the pacemaker to an AV delay of 160 ms and a postventricular atrial refractory period of 300 ms, no further episodes of PMT have occurred. This case illustrates that intravenous adenosine can effectively terminate PMT by causing ventriculoatrial block, thus interrupting the reentrant circuit by eliminating retrograde atrial activation.
High frequency qrs electrocardiography in the detection of reperfusion following thrombolytic therapy
Authors: Aversano Thomas , Rudikoff Bari , Washington Antonio , Traill Saskia , Coombs Vicki , Raqueno Judith
Published: February 2009

The hypothesis that an increase in the amplitude (root‐mean‐square voltage) of the high frequency (150‐250 Hz) components of the QRS complex occurs with successful reperfusion following thrombolytic therapy in acute myocardial infarction (AMI) and fails to occur when thrombolysis fails was tested. Clinical markers for successful or failed reperfusion following thrombolytic therapy for AMI are notoriously insensitive. The amplitude of the high‐frequency components of the QRS complex decreases during ischemia and returns to normal with resolution of ischemia, but neither the variability in measurement of these potentials nor their patterns of change during the course of AMI have been described. In 32 control subjects, the average coefficient of variation for the amplitude of the highfrequency QRS complex was 10% or 0.3 uV. Based on these data, for the acute infarction population a significant change in this measurement was therefore defined as a change in amplitude > 20% or 0.6 uV on two consecutive recordings. In 30 patients with AMI treated with a thrombolytic agent, either cardiac catheterization, serial serum myoglobin, or complete resolution of ST‐segment elevation were used to define successful or failed reperfusion. High‐frequency QRS electrocardiograms were obtained at the start of treatment with a thrombolytic agent and for 3 h thereafter using a signal‐averaging technique and digital filtering. Standard 12‐lead electrocardiograms were obtained at the same time. In patients who reperfused successfully, the high‐frequency QRS amplitude increased significantly (1.2 ± 0.9 uV above its nadir at 83 ± 36 min after initiation of thrombolytic therapy) in 23 of 25 patients. In contrast, the highfrequency QRS amplitude did not change or declined in all five patients who failed to reperfuse (‐0.4 ± 0.4 uV, p < 0.05 compared with successful reperfusion). Traditional clinical markers such as resolution of chest pain and ST‐segment elevation failed to distinguish successful and failed reperfusion. High‐frequency QRS electrocardiography is a rapid, reliable bedside technique for discriminating between successful and failed reperfusion in patients treated with thrombolytic agents for AMI.
A case of trichosporon beigelii endocarditis 8 years after aortic valve replacement
Authors: Sidarous Michael G. , O'Reilly Michael V. , Cherubim Charles E.
Published: February 2009

We report a case of Trichosporon beigelii endocarditis in a 77‐year‐old diabetic man who presented with an embolic stroke 8 years ago after a porcine aortic valve replacement. He was treated successfully with amphotericin, rifampin, and replacement of the original porcine valve; however, he died suddenly 8 months later from unknown causes. Blood cultures 2 months prior to death were negative. The first manifestation of the endocarditis was a left hemiparesis followed some days later by a splenic infarction. Transthoracic echocardiography failed to demonstrate the aortic vegetation, which was clearly visualized subsequently by transesophageal echocardiography. The literature on Trichosporon beigelii endocarditis is reviewed.
Idiopathic dilated cardiomyopathy
Authors: Hackel Andrea J. , Wagner Galen , Hackel Donald B.
Published: February 2009

A 43‐year‐old man had a 9‐year history of congestive heart failure manifested by an enlarged heart and symptoms of shortness of breath and chest discomfort. Heart failure had been preceded by a “viral illness” and he had been a heavy alcohol user until that time. Autopsy showed congestion and edema characteristic of heart failure and cardiomegaly with biventricular dilatation. Either viral or alcoholic disease, or both, could have been the cause of the cardiac problems.
The osborn wave of hypothermeia in normothermic patients
Authors: Patel Archana , Getsos John P. , Moussa Ghias , Damato Anthony N,
Published: February 2009

The Osborn wave (also referred to as “the J wave,” “the J deflection,” or “the camel's hump”) is a distinctive deflection occurring at the QRS‐ST junction of approximately 80% of hypothermic patients (core body temperature ≤95°F). Generally, the amplitude and duration of Osborn waves are inversely related to core temperature. We report on eight normothermic patients whose 12‐lead electrocardiograms demonstrated QRS‐ST junction notches similar to those seen in hypothermia. These data support the concept that the Osborn wave is not pathognomonic of hypothermia.
Response to upright exercise after cardiac transplantation
Authors: Martin Timothy W. , Gaucher Jay , Pupa Lawrence E. , Seaworth John F.
Published: February 2009

There is little information on the hemodynamic response to upright exercise in patients who have undergone cardiac transplantation. We compared the hemodynamic and metabolic response to upright bicycle exercise in 11 patients with heart transplants and 12 controls. Patients performed two tests—a steady‐state test with a right heart catheter and a maximal incremental test. During steady‐state exercise at 20% of their predicted maximum workload, patients with heart transplants had a higher (mean ± SD, p < 0.05) heart rate (108 ± 11 vs. % ± 15 beats/min), mean systemic blood pressure (116 ± 17 vs. 101 ± 11 mmHg), mean pulmonary artery pressure (29 ± 9 vs. 22 ± 3 mmHg), mean pulmonary wedge pressure (14 ± 6 vs. 9 ± 2), pulmonary (302 ± 101 vs. 220 ± 50 d‐sec‐cm−5 ‐ m2) and systemic (2049 ± 531 vs. 1459 ± 520) resistance indices, and lactate concentration (3.4 ± 1.7 vs. 1.7 ± 0.4 mmol/1), and a lower stroke index (39 ± 8 vs. 50 ± 8 ml/m2) compared with controls. Cardiac index, right atrial pressure, and mixed venous oxygen saturation were similar. During the maximal exercise test, patients with heart transplants achieved a significantly lower percentage of predicted maximum heart rate (77 ± 13 vs. 91 ± 8%), workload (70 ±25 vs. 102 ± 23%), oxygen consumption (63 ± 11 vs. 108 ± 19%), and ventilation (67 ± 18 vs. 89 ± 15%) compared with controls. Heart transplant patients also had a lower blood pressure and anaerobic threshold. We conclude that heart transplant patients have an altered hemodynamic and metabolic response to upright bicycle exercise.
The differential diagnosis on the electrocardiogram between ventricular tachycardia and preexcited tachycardia
Authors: Steurer Günter , Gürsoy Sinan , Frey Berhaerd , Simonis Frank , Andries Eric , Brugada Pedro , Kuck Karl
Published: February 2009

The 12‐lead surface electrocardiogram is a simple and useful tool for the differential diagnosis of regular wide QRS complex tachycardia. However, criteria do not as yet exist to discriminate between ventricular tachycardia and supraventricular tachycardia with anterograde conduction over an accessory pathway (preexcited tachycardia). Therefore, we designed a new stepwise approach with three criteria for the electrocardiographic differential diagnosis between ventricular tachycardia and preexcited tachycardia and prospectively studied 267 regular tachycardias with electrophysiologically proven mechanism and a wide QRS complex (≥ 0.12 s): 149 consecutive ventricular tachycardias and 118 consecutive preexcited regular tachycardias. Underlying heart disease was old myocardial infarction in 133 of 149 (89%) ventricular tachycardias. The patients presenting with preexcited tachycardia had no additional structural heart disease. Atrial fibrillation with preexcited QRS complex was not included. The criteria favoring ventricular tachycardia were: (1) presence of predominantly negative QRS complexes in the precordial leads V4 to V6, (2) presence of a QR complex in one or more of the precordial leads V2 to V6, and (3) AV relation different from 1:1 (more QRS complexes than P waves). The final sensitivity and specificity of these three consecutive steps to diagnose ventricular tachycardia were 0.75 and 1.00, respectively. This new stepwise approach is sensitive and highly specific for the differential diagnosis between ventricular tachycardia in coronary artery disease and preexcited regular tachycardia.
Stress‐induced arrhythmic disease of the heart‐Part I
Authors: Meerson Felix Z.
Published: February 2009

This review deals with the following principal concepts: (1) Heart injuries in single severe stress episodes manifested primarily in disturbances of membrane lipid bilayer, sarcolemmal Na, K‐pump, and sarcoplasmic Ca‐pump with concurrent limited disturbances of the heart energy supply, namely, of the creatine kinase and glycolysis systems. These disturbances cause small focal myocardial lesions and reduce cardiac electrical stability: the fibrillation threshold falls and ectopic activity increases. in repeated stress, this damage, localized mainly in the richly innervated conduction system, accumulates to cause even more pronounced disturbances of electrical stability and severe arrhythmias. (2) Severe stress and beta‐adrenergic effects on the heart regularly result in coronary vasodilation and increased coronary blood flow. However, the entire primary complex of stress‐induced injuries and disturbances of the heart's electrical stability occurs despite the increased coronary blood flow. Thus, beta‐adrenergic stress‐induced injuries may indeed develop as primary stress damage to cardiomyocytes without any relation to ischemia. (3) The main factor determining high vulnerability or, on the contrary, resistance of the heart to stress is the state of stress‐limiting systems, namely, the opioidergic, GABAergic, cholinergic, adenosinergic, and other systems. Activation of these systems by adaptation to repeated stress or other factors prevents serious injuries to the heart in severe stress. Conversely, genetically determined or acquired dysfunction of these systems predisposes to severe arrhythmias and sudden death. Thus, in stress‐induced arrhythmic disease as well as in ischemic heart disease, the main pathogenetic links are outside the heart, but they differ from those observed in ischemia. (4) The clinical picture of stress‐induced arrhythmic disease, that is, alterations in electrocardiogram, coronarogram, and patient responses to stress, physical loads, and tranquilizers differ, as do pathologic alterations in the heart. These differences are summarized at the end of this review.
Pathology of mitral valve stenosis and pure mitral regurgitation—Part II
Authors: Waller Bruce F. , Howard Jane , Fess Stephen
Published: February 2009

This two‐part article examines the histologic and morphologic basis for stenotic and purely regurgitant mitral valves. in Part I, conditions producing mitral valve stenosis were reviewed. in over 99% of stenotic mitral valves, the etiology is rheumatic disease. Other rare causes of mitral stenosis include congenitally malformed valves, active infective endocarditis, massive annular calcium, and metabolic or enzymatic abnormalities. in Part II, conditions producing pure mitral regurgitation are discussed. in contrast to the few causes of mitral stenosis, the causes of pure (no element of stenosis) mitral regurgitation are multiple. Some of the conditions producing pure regurgitation include floppy mitral valves, infective endocarditis, papillary muscle dysfunction, rheumatic disease, and ruptured chordae tendineae.
Prognosis, severity of symptoms, and aspects of well‐being among patients in whom myocardial infarction was ruled out
Authors: Karlson Bjöurn W. , Wiklund Ingela , Bengtson Ann , Herlitz Johan
Published: February 2009

In a high proportion of patients hospitalized due to suspected acute myocardial infarction (AMI) the diagnosis cannot be confirmed. The majority of these patients have ischemic heart disease and are at risk for subsequent cardiac events. The aim of this study was to describe the severity of symptoms and various aspects of well‐being 1 year after hospitalization due to suspected AMI in surviving patients in whom the diagnosis was not confirmed, and to relate the observations to those found among survivors of a confirmed AMI. All patients admitted to Sahlgrenska Hospital, Göteborg, due to suspected AMI and who were alive after 1 year were asked to answer a questionnaire including questions regarding cardiovascular, psychiatric, and psychological symptoms. Patients in whom AMI was not confirmed reported more cardiovascular symptoms, for example, chest pain (p <0.001), dyspnea (p <0.01), palpitations (p <0.001), and fatigue (p <0.01) when compared with patients who suffered confirmed AMI. The majority of psychosomatic and psychological parameters evaluated were also more frequently reported by these patients and their quality of life seems to be worse compared with survivors of AMI.
Congenital heart disease and pregnancy
Authors: Perloff Joseph K.
Published: February 2009

In Europe and North America, a dramatic fall in the incidence of rheumatic fever and rheumatic heart disease has coincided with advances in medical and surgical management of congenital heart disease and has resulted in a shift in the relative incidence of these two categories of cardiac disorders in women of child‐bearing age. This review deals with pregnancy and congenital heart disease—unoperated and operated. Central to this topic is the intricate interplay between maternal circulatory and respiratory physiology and maternal congenital heart disease, and the effects of this interplay upon the fetus which is exposed to risks that threaten its intrauterine viability and to risks that subsequently express themselves as developmental defects or transmitted congenital malformations of the heart or circulation.
Neuroendocrine activation in relation to left ventricular function in chronic severe congestive heart failure: A subgroup analysis from the cooperative north scandinavian enalapril survival study (CONSENSUS)
Authors: Eriksson S. V. , Eneroth P. , Kjekshus J. , Offstad J. , Swedberg K.
Published: February 2009

Left ventricular (LV) function and plasma levels of cardiovascular hormones were examined in patients with severe chronic congestive heart failure (CHF), randomized to placebo or enalapril, in addition to conventional therapy. M‐mode echocardiography and plasma hormone concentrations were available at baseline and after 6 weeks of treatment. There was a significant relationship between LV systolic function and levels of angiotensin‐II and norepinephrine. Enalapril increased LV fractional shortening (FS%) (13.3±5.6 to 15.4±5.8, p<0.05) and decreased the systolic time interval index (0.58±0.14 to 0.48 ± 0.15, p < 0.05) concurrent with a significant decrease in angiotensin‐converting enzyme activity and in aldosterone, angiotensin‐II, and norepinephrine concentrations after 6 weeks. No changes were found in the placebo group. However, there was no direct relationship between the amount of change in neurohormones and improvement in LV function after 6 weeks.

These findings indicate that in patients with severe chronic CHF, severe LV systolic dysfunction is associated with high plasma levels of angiotensin‐II and norepinephrine, which can be favorably modified by enalapril. This may be of importance for prolonging life in severe heart failure. The lack of relationship between changes in individual hormones and systolic function suggests complex dynamic interaction. It is, therefore, not sufficient to predict changes in LV function by measuring changes in only one hormone.
Artificial intelligence versus logistic regression statistical modelling to predict cardiac complications after noncardiac surgery
Authors: Lette Jean , Colletti Bruce W. , Cerino Michel , Mcnamara Daniel , Eybalin Marie‐Claire , Levasseur André , Natnel Stanley
Published: February 2009

The traditional approach to developing models predictive of cardiac events has been to perform logistic regression (LR) analysis on a variety of potential predictors. An alternative is to use an artificial intelligence system called a neural network (NN) which simulates biological intelligence. To evaluate the potential applicability of the latter method, we compared the ability of LR and NN techniques to predict cardiac events after noncardiac surgery. A total of 200 patients (training group) underwent cardiac risk assessment before major noncardiac surgery using 17 clinical parameters and 7 quantitative indices based on dipyridamole‐thallium imaging. There were 21 postoperative myocardial infarctions and/or cardiac deaths. Data from the training group were used to develop two predictive models: one based on backward stepwise LR multivariate statistical analysis and the other one using a neural network. Both models were then validated on a second group of 160 consecutive patients also referred for preoperative risk stratification (validation group). The NN consisted of 14 input, 29 hidden, and 1 output neurons and used a back‐propagation algorithm (learning rate 0.2, training tolerance 0.5, sigmoid transfer function). The sensitivity, specificity, positive and negative predictive accuracies for the prediction of postoperative events in the validation group of 160 patients were, respectively, 67% (6/9), 82% (124/151), 18% (6/33), and 98% (124/127) for LR, and 67% (6/9), 96% (145/151), 50% (6/12), and 98% (145/148) for the NN, with a difference in specificity which attained statistical significance (p < 0.01). Artificial intelligence may provide a useful alternative to conventional LR statistical analysis for the purpose of preoperative cardiac risk assessment.
Regression of left ventricular hypertrophy with long‐term treatment of nifedipine in systemic hypertension
Authors: Yamakado Tetsu , Teramura Shinobu , Oonishi Takahiro , Maeda Mitsugu , Nakano Takeshi
Published: February 2009

We investigated the regression of left ventricular (LV) hypertrophy with long‐term treatment of nifedipine in patients with systemic hypertension. Echocardiograms of the LV were obtained in nine patients before and at a mean of 50 months (13‐105 months) after nifedipine monotherapy (30‐60 mg/day). Nifedipine significantly reduced both systolic and diastolic blood pressures (BP) by a mean of ‐46 mmHg and ‐21 mmHg, respectively. With systemic BP reduction, LV mass was significantly reduced by a mean of ‐ 15%, associated with a decrease in LV posterior wall thickness and end‐diastolic dimension. There was no significant change in LV fractional shortening. We conclude that nifedipine may cause regression of LV hypertrophy in systemic hypertension, and that reversal of the increase in LV mass could be maintained during long‐term nifedipine treatment.
Amyloid disease of the heart
Authors: Hackel Andrea J. , Wagner Galen S. , Reimer Keith , Hackel Donald B.
Published: February 2009

A 70‐year‐old woman with a history of hypertension had been well until 3 years before when she developed atrial fibrillation and subsequently congestive heart failure. The heart failure became worse and she had three fainting spells. Low voltage on electrocardiogram and global hypokinesis on echocardiography were suggestive of cardiac amyloidosis. The patient died suddenly of intractable ventricular fibrillation. Autopsy confirmed heavy infiltration of the myocardium by amyloid.
Clustered lipid droplets in the endomyocardial biopsies from a patient with neuroleptic malignant syndrome
Authors: Watanabe Kenichi , Inomata Takayuki , Miyakita Yasushi , Masani Fumiaki , Shibata Akira , Izumi Tohru
Published: February 2009

Neuroleptic malignant syndrome is caused by serious adverse effects of antipsychotic agents and occurs only rarely. Endomyocardial biopsies documented unique clustered lipid droplets in a Japanese man with this disease. After administration of haloperidol, he had symptoms of high fever, respiratory dysfunction, and cardiogenic shock, and subsequently suffered from multiple organ failure. Fortunately, he was completely cured with intensive therapy. in the convulsant stage, left ventricular endomyocardial biopsies were performed that yielded the interesting discovery of unique clustered lipid droplets among the myofibrils. It was suggested that although the pathomechanism of neuroleptic malignant syndrome is unknown, this disease may be characterized by a lipid metabolic disorder of the cardiac muscle cell.
Percutaneous transvenous mitral commissurotomy for restenosis after surgical mitral valvotomy
Authors: Bahl Vinay K. , Chandra Subhash , Talwar Kewal K. , Sharma Sanjiv , Kaul Upendra , Wasir Harbans S.
Published: February 2009

Percutaneous transvenous mitral commissurotomy (PTMC) was performed in 350 patients. Of these patients, 51 (15%) (30 women and 21 men, aged 32 ± 11 years) had restenosis 11 ± 4 years following surgical valvotomy. Forty (79%) patients were in New York Heart Association (NYHA) class III and 11 (21 %) were in class IV. PTMC resulted in an increase in mitral valve area from 0.82 ± 0.3 to 1.9 ± 0.2 cm2 (p < 0.001), an increase in cardiac index from 1.9 ± 0.4 to 2.8 ± 0.51/min/m2 (p < 0.001), and a decrease in mean transmitral gradients from 29 ± 4 to 6 ± 4 mmHg (p < 0.001). The results did not differ from those observed in 299 patients without prior surgical valvotomy. On univariate analysis, the subvalvular fibrosis, assessed angiographically, and the duration from prior surgery were not found to influence the overall outcome. At 24 weeks, 46 of 48 (96%) patients in whom clinical follow‐up was available, were found to be in NYHA class I and 2 (4%) patients were in class II. Thus, PTMC is a safe and effective procedure for patients with mitral restenosis following surgical valvotomy.
A clinical and in vitro study on the possible interaction of intravenous nitrates with heparin anticoagulation
Authors: Pye Maurice , Oldroyd Keith G. , Hutton Ian , Cobbe Stuart M. , Conkie James A.
Published: February 2009

It has been reported that intravenous nitrates inhibit the anticoagulant effect of heparin. This possible interactior has potentially serious implications for the management of patients with acute coronary ischemic syndromes. This possible interaction was assessed prospectively in a clinical and in an in vitro study involving 24 patients receiving both drugs for the management of unstable angina pectoris. There was a small in hibitory effect of intravenous glyceryl trinitrate or isosorbide dinitrate on the anticoagulant effect of heparin in 3 of 24 case in vivo, as assessed by activated partial thromboplastin time measurements. Nitrates or propylene glycol had no effect or heparin activity in vitro. It was concluded that there may be an inhibitory effect of nitrates on anticoagulation in a small miority of patients, but close attention to detail in monitoring heparin anticoagulation is far more important.
High cardiac output state in patients with multiple myeloma: Case report and review of the literature
Authors: Kosinski Daniel J. , Fraker Theodore D. , Grubb Blair P. , Roush Kenneth
Published: February 2009

A high cardiac output state, with or without congestive heart failure, has recently been recognized in patients with multiple myeloma. This case report deals with a 62‐year old man with multiple myeloma refractory to treatment, a high cardiac output state, and life‐threatening pulmonary edema In addition, a brief review of the literature is presented.
Influence of the infarct site on the identification of patients with ventricular tachycardia after myocardial infarction based on the time‐domain and spectral turbulence analysis of the signal‐averaged electrocardiogram
Authors: Kulakowski Piotr , Hnatkova Katerina , Bashir Yaver , Heald Spencer C. , Staunton Anne , Malik Marek , Camm A. John
Published: February 2009

In a significant proportion of patients with sustained ventricular tachycardia (VT) following anterior myocardial infarction, the areas of slow conduction are activated early during cardiac depolarization. Therefore, they may not be detected by the standard time‐domain analysis of the signal‐averaged electrocardiogram (SAECG) which is limited to the terminal part of the QRS complex. Spectral turbulence analysis of the SAECG is a new frequency domain technique which examines the whole QRS complex and may improve identification of patients with sustained VT following anterior infarction. We compared the results of time‐domain and spectral turbulence analyses of the SAECG in 53 postinfarction patients with sustained VT and in 53 age‐, gender‐ and infarct site‐matched patients without VT. The receiver operator characteristic curves have shown that the time‐domain analysis resulted in better identification of patients with VT following inferior than following anterior infarction (e.g., at the sensitivity level of 90%, the corresponding values of specificity were 96 and 90%, respectively), whereas the spectral turbulence analysis performed better in the anterior site of infarction. When both time‐domain and spectral turbulence analyses were combined, the accuracy of the SAECG for identification of patients with VT following anterior infarction improved, reaching a specificity of 97% at the sensitivity level of 90%. In conclusion (1) spectral turbulence analysis of the SAECG results in better identification of patients with VT following anterior than following inferior infarction, and (2) the combination of time‐domain and spectral turbulence analyses of the SAECG may improve identification of patients with VT following anterior infarction.
Evaluation of QRST isointegral maps in detecting posterior myocardial infarction with and without conduction disturbance
Authors: Agetsuma Hirotaka , Suzuki Akira , Hiral Makoto , Sano Hiroaki , Tomita Yasushi , Ichihara Yoshio , Adachi Masayoshi , Takatsu Fumimaro , Hayashi Hiroshi
Published: February 2009

We investigated the usefulness of QRST isointegral maps (I‐maps) for detecting posterior myocardial infarction (MI) with and without conduction disturbance. The I‐maps were recorded during sinus rhythm and right ventricular (RV) pacing, which simulated left bundle‐branch block (LBBB) in 19 patients with and in 20 patients without MI. Data on 608 normal subjects were used as controls. The “‐2 SD area,” where the QRST integral value was less than the lower limit of the normal range, was assessed by ΣDM (sum of QRST integral values below the normal range). Posterior MI was diagnosed with a sensitivity of 84%, a specificity of 90%, and a diagnostic accuracy of 87%, assuming that MI was present if ΣDM exceeded 50 mVms. During simulated LBBB, when the criterion ΣDM more than 250 mVms was used, the sensitivity, specificity, and diagnostic accuracy were 79, 75, and 77%, respectively. Thus, I‐maps may be useful in detecting posterior MI in patients with and without an intraventricular conduction disturbance.
Emergency intracardiac defibrillation for refractory ventricular fibrillation
Authors: Haught W. Herbert , Conti Jamie B. , Tucker Kelly J. , Curtis Anne B.
Published: February 2009

Hemodynamically unstable ventricular arrhythmias induced during electrophysiologic testing almost always respond to prompt application of direct current transthoracic shocks. In rare cases, however, ventricular fibrillation may be refractory to conventional treatment. Recently, a technique of intracardiac defibrillation has been successfully used to resuscitate patients with ventricular fibrillation refractory to transthoracic defibrillation. We describe two patients with a history of myocardial infarction and left ventricular dysfunction who were admitted with symptomatic episodes of ventricular tachycardia. Both had inducible sustained monomorphic ventricular tachycardia. During a repeat electrophysiologic study in Patient No. 1 on procainamide and at the initial study in Patient No. 2, right ventricular burst pacing to terminate ventricular tachycardia resulted in ventricular fibrillation refractory to resuscitation efforts, including transthoracic defibrillation with 360 J. Emergency intracardiac defibrillation with 200 and 360 J, respectively, successfully converted both patients to sinus rhythm. Both patients were subsequently discharged from the hospital on amiodarone. These cases illustrate the life‐saving capabilities of intracardiac defibrillation.
Prevalence, characteristics, and risk stratification of electrocardiographic and symptomatic silence of myocardial ischemia despite scintigraphically evidenced ischemia in symptomatic patients presenting with severe coronary artery stenosis
Authors: Zehender Manfred , Kasper Wolfgang , Granzow Heike , Just Hanjörg , Krause Thomas , Moser E. , Olschewski Manfred
Published: February 2009

Symptoms of angina pectoris and transient ST‐segment depression are most commonly used to evidence acute myocardial ischemia during exercise testing. However, the diagnostic accuracy of either or both criteria in relation to clinical characteristics and the patient's exercise response has been a subject of controversy. The prevalence and severity of symptoms of angina pectoris and/or ST‐segment depression were studied prospectively in 147 consecutive patients with a history of daily angina pectoris, scintigraphic evidence of exercise‐induced myocardial ischemia, and coronary artery stenosis >75%. Logistic regression analysis was applied to determine absence of any or both criteria by the clinical characteristics or exercise response of the patient. During exercise testing, ST‐segment response failed to prove scintigraphically evidenced myocardial ischemia in 14/147 patients (10%) and 35/147 patients (24%) when ST‐segment depression ≥0.1 in either ≥1 or ≥2 ECG leads was chosen. Symptoms of angina pectoris were found to be absent in 69/147 patients (47%). Only 58 patients (40%) suffered from angina and met the ECG criterion at the time of scintigraphic myocardial ischemia. Absence of ST‐segment depression was best predicted by clinical variables such as large myocardial infarction (increase: 2.6 times, p = 0.007), number of stenoses ≥2 (2.0 times, p = 0.023), and presence of diabetes mellitus (4.3 times, p = 0.035). Painless myocardial ischemia was only determined by blood response to exercising. Thus, a double product > 23 increased the risk of painless myocardial ischemia by 1.5 times (p = 0.017). In multivariate analysis, only blood pressure response, infarction size, and the number of diseased vessels were found to be independent predictors of the absence of angina pectoris or ST‐segment depression during myocardial ischemia.
Prognostic significance of right ventricular dysfunction in patients with acute inferior myocardial infarction and right ventricular involvement
Authors: Serrano Carlos V. , Ant Ramires José Oanio F. , Ant César Lutz Oanio M. , Rati Miguel , Da Luz Protásio , Pileggi Fúlvio , Zweier Jay L.
Published: February 2009

Little is known about the influence of right ventricular (RV) dysfunction on prognosis of patients with acute inferior myocardial infarction (IMI) and RV involvement. Therefore, 99 consecutive patients (mean age 56.6 ± 3.4 years) with RV involvement during acute IMI were followed for a 12‐month period to clarify the influence of acute RV dysfunction on short‐ and long‐term survivals. Forty‐one patients with IMI evolved with severe arterial hypotension due to RV dysfunction, while 58 patients had no hemodynamic impairment due to RV involvement. Basal hemodynamic data (mean ± SD) for patients with RV dysfunction were blood pressure (BP) 92/59 ± 22/20 mmHg, systemic vascular resistance (SVR) 2314 ± 252 dynes·s·cm−5, and cardiac index (CI) 1.3 ± 0.31/min/m2. Patients without RV dysfunction demonstrated BP 113/74 ± 20/16 mmHg (p≤0.05), SVR 1324 ± 354 dynes·s·cm−5 (p≤0.01), and CI 2.6 ± 0.5 1/min/m2 (p≤0.05). Angiographic differences noted were that hemodynamically compromised patients showed lower RV ejection fractions (0.27 ± 0.08) than patients without hemodynamic disturbance [0.41 ± 0.11 (p≤0.05)]; however, left ventricular ejection fractions were 0.48 ± 0.10 and 0.52 ± 0.12, respectively. Short‐ and long‐term mortality rates were assessed during the follow‐up period. Patients with hemodynamic impairment due to RV infarction had a higher mortality rate for the first month and for 11 subsequent months post MI than patients without hemodynamic impairment, that is, 24.4 vs. 6.9 and 14.6 (p≤0.05) vs. 3.4% (p≤0.05), respectively. These data suggest that decreased RV ejection fraction possibly is linked with significantly reduced short‐ and long‐term survival in patients with RV involvement during acute IMI.
Effects of treatment with lovastatin and pravastatin on daytime cognitive performance
Authors: Gengo Fran , Cwudzinski Donna , Kinkel Peter , Block Gilbert , Stauffer Laura , Lines Chris
Published: February 2009

The HMG‐CoA reductase inhibitors lovastatin and pravastatin have both proven to be effective and well tolerated in the treatment of hypercholesterolemia. To evaluate whether lovastatin or pravastatin might affect daytime cognitive function, a double‐blind, placebo‐controlled, two‐period, incomplete block, crossover study was performed in 36 patients (24 per treatment) with primary hypercholesterolemia. Patients received placebo, Iovastatin (40 mg), or pravastatin (40 mg) for 4 weeks. Following a 1‐week washout period, patients were crossed over to either lovastatin, pravastatin, or placebo for an additional 4 weeks. Mental performance tests (digit symbol substitution, choice reaction time, auditory vigilance, selective reminding word recall, finger tapping), visual analogue rating scales, and the Profile of Mood States were administered before test drug administration and after 2 and 4 weeks of each treatment. After 4 weeks, no statistically significant differences between treatments in changes from baseline were observed on any parameter with the exception of digit symbol substitution, for which lovastatin and pravastatin were both significantly better than placebo but did not differ from each other. Low‐density lipoprotein cholesterol was reduced 38% by lovastatin and 30% by pravastatin. In summary, neither of these chemically distinct HMG‐CoA reductase inhibitors impaired daytime cognitive performance after 4 weeks of treatment in patients with primary hypercholesterolemia.
Transesophageal echocardiographically guided atrial transseptal catheterization in patients with normal‐sized atria: Incidence of complications
Authors: Hahn Kenneth , Gal Rami , Sarnoski Joseph , Kubota James , Schmidt Donald H. , Bajwa Tanvir K.
Published: February 2009

The incidence of cardiac complications from atrial transseptal catheterization has never been quantified in patients with normal‐sized atria. Series defining the complication rate are derived from diseased hearts with structural changes that may alter the complication rate of the procedure. The generation of a standardized incidence of perforation in a population of structurally normal atria has important implications. A total of 46 atrial transseptal catheterizations guided by transesophageal echocardiography (TEE) for radiofrequency ablation of left‐sided accessory pathways was performed in 42 patients during a 3‐year period (1990–1993). Clinical and echocardiographic data were analyzed, with special attention given to TEE reports pre‐ and post‐transseptal catheterization. Only one complication occurred in the 46 procedures (2.2%): a perforation of the left atrium that led to pericardial effusion and cardiac tamponade. In a small series of patients with normal sized atria, we have demonstrated that TEE‐guided transseptal catheterization is a procedure with a low complication rate.
Effect of simvastatin on Lp(a) concentrations
Authors: Haffner Stevhn , Orchard Trevor , Stein Evan , Schmidt Donald , Labelle Patrice
Published: February 2009

The effect of HMG‐CoA reductase inhibitors on Lp(a) concentrations is controversial, with some studies showing an increase and others showing no effect on Lp(a) concentrations. Many of these studies have been limited by small sample size and the lack of a prospective design. We evaluated the effect of four treatments: (1) placebo, (2) simvastatin 10 mg PO QPM, (3) simvastatin 20 mg PO QAM, and (4) simvastatin 20 mg PO QPM on Lp(a) concentrations in a prospective, randomized, controlled clinical trial of 24 weeks in 343 subjects in 28 clinical sites in the United States. Simvastatin was not associated with a change in Lp(a) concentrations relative to placebo. These results were not affected by controlling for race, initial Lp(a) level, or urinary albumin excretion. Simvastatin significantly reduced low‐density lipoprotein (LDL) cholesterol levels (10 mg PO QPM: ‐ 27.6%; 20 mg PO QAM: ‐ 28.1%; and 20 mg PO QPM: ‐ 34.3%, all p<0.001). It was concluded that in a large, randomized, controlled trial, simvastatin does not affect Lp(a) levels but markedly lowers LDL cholesterol levels.
High‐density lipoprotein cholesterol level and smoking modify the prognosis of patients with coronary vasospasm
Authors: Miwa Kunihisa , Fujita Masatoshi , Miyagi Yuko , Inoue Hiroshi , Sasayama Shigetake
Published: February 2009

A cardiovascular event analysis was performed in a subset of 80 consecutive patients with vasospastic coronary artery disease. During the follow‐up period (30 ± 2 months, mean ± SD), 9 patients had vascular accidents, including acute myocardial infarction, unstable angina, and stroke (Group A), while the remaining 71 patients were eventfree (Group B). Serum total‐cholesterol, low‐density lipoprotein cholesterol, and triglyceride levels were not different between the two groups at the baseline as well as after follow‐up. However, the HDL‐C level at baseline was significantly lower in Group A (33.5 ± 2.6 mg/dl) than in Group B (41.9 ± 1.7 mg/dl, p < 0.05). The HDL‐C level increased significantly during the follow‐up in Group B (ΔHDL‐C: 6.2 ± 1.2 mg/dl, p < 0.01), but not in Group A (ΔHDL‐C: ‐ 3.2 ± 2.7 mg/dl). The HDL‐C level after follow‐up was significantly lower in Group A (30.3 ± 2.9 mg/dl) than in Group B (48.1 ± 1.5 mg/dl, p < 0.01). Current smokers at the end of the follow‐up period were more prevalent in Group A (67%) than in Group B (11%, p < 0.01). Cardiovascular accidents occurred more often in current smokers (6/14, 43%) at the end of the followup than in current nonsmokers, including quitters (3/66, 5%; p < 0.05). The HDL‐C level was increased significantly (ΔHDL: 6.2 ± 1.3 mg/dl, p < 0.01) in the latter patients, but not in the former (ΔHDL: –0.4 ± 2.9 mg/dl). Cardiovascular accidents were significantly (p < 0.01) more common in patients with lower (< 40 mg/dl) HDL‐C levels (7/23, 30%) than in those with higher HDL‐C levels (2/57, 4%) after followup, although this difference was not significant when patients were divided according to these levels at baseline. These results indicated that a low HDL‐C level after follow‐up is more predictive of subsequent cardiovascular events than at baseline. The increase in HDL‐C level attained by smoking cessation appears important for a favorable prognosis.
Torsade de pointes caused by high‐dose intravenous haloperidol in cardiac patients
Authors: Di Salvo Thomas G. , O'Gara Patrick T.
Published: February 2009

Intravenous haloperidol is the agent of choice for controlling severe agitated delirium in seriously ill cardiac patients in many institutions. Prior reports have proposed that high‐dose intravenous haloperidol may be without untoward effects in these patients. Recently, however, a few reports of significant QTc prolongation and torsade de pointes as complications of high‐dose intravenous haloperidol therapy have appeared. The present report describes three patients with definite haloperidol‐induced QTc prolongation and torsade. In each case, QTc prolongation preceded the arrhythmia and disappeared following the discontinuation of haloperidol. Neither electrolyte imbalance, therapy with other cardiac drugs, bradycardia, ischemia, left ventricular dysfunction, nor other known cause of torsade was present in these patients. It is hypothesized that QTc prolongation and torsade likely are idiosyncratic, unpredictable reactions to high‐dose haloperidol in select patients. Careful serial electrocardiographic monitoring and prompt discontinuation of the drug should suffice to prevent this relatively uncommon, life‐threatening complication of high‐dose intravenous haloperidol.
Update on the treatment of hypercholesterolemia, with a focus on hmg‐coa reductase inhibitors and combination regimens
Authors: Ginsberg Henry N.
Published: February 2009

Numerous studies involving patients with hypercholesterolemia have demonstrated that reduction of lipid levels markedly reduces morbidity and mortality from cardiovascular disease. Diet alone may enable patients without established disease to attain target lipid levels, but pharmacotherapy generally is necessary for those with coronary artery disease. Choice of a suitable agent for monotherapy—a bile acid resin, niacin, or an HMG‐CoA reductase inhibitor—may be determined by patient phenotype. For resistant cases, therapy combining an HMG‐CoA reductase inhibitor with another agent generally is effective and well tolerated.
Constrictive pericarditis: Its history and current status
Authors: Fowler Noble O.
Published: February 2009

The diagnosis of constrictive pericarditis remains a challenge because it is often mimicked by restrictive cardiomyopathy. The last few years have seen numerous advances in our ability to differentiate between these two conditions which often have similar physical findings and hemodynamics. This review begins with a brief history of constrictive pericarditis; this is followed by an extensive discussion of newer etiologies, and then the classical clinical history and physical examination findings are described. Radiologic, electrocardiographic, and angiographic findings are discussed. The hemodynamics of constrictive pericarditis are reviewed. Recent results of echocardiographic and echo‐Doppler investigations are presented. Emphasis is placed upon the limitations of M‐mode echocardiography in the diagnosis of constrictive pericarditis. The value of echocardiographic Doppler studies of mitral and tricuspid flow velocity patterns, as well as of those in the pulmonary veins and hepatic veins, is described. Nuclear ventriculograms and angiocardiograms tend to show more rapid ventricular filling in constrictive pericarditis than in restrictive cardiomyopathy. Although only a small number of patients has been studied, these evaluations seem to have merit in separating restrictive cardiomyopathy from constrictive pericarditis. The role of computed tomography scanning and magnetic resonance imaging studies of pericardial thickness in confirming the presence of constrictive pericarditis is discussed. Abnormal pericardial thickening (> 3 mm) confirms the diagnosis of constrictive pericarditis, but only if the characteristic hemodynamic pattern is present. The usefulness of endomyocardial biopsy in recognizing specific varieties of restrictive cardiomyopathy is presented. The topic of occult constrictive pericardial disease is discussed briefly. A discussion of the timing of pericardial resection for the treatment of constrictive pericarditis ends the review.
Anatomical definition of aortic root abscesses by transesophageal echocardiography: Planning a surgical strategy using homograft valves
Authors: Brecker Stephen J. D. , Jin Xu Y. , Yacoub Magdi H.
Published: February 2009

Infective endocarditis of the native or a prosthetic aortic valve may be complicated by abscess cavity development in the aortic root, and successful treatment depends upon early diagnosis, clear anatomical definition preoperatively, and maintaining sterility of the second implant. Homograft valves offer many advantages in this setting. Timing of surgery and the choice of the particular technique depends on accurate characterization of the anatomical details of the abscess. Five cases of paravalvular aortic root abscess in the setting of prosthetic valve endocarditis are described. In each case the diagnosis was made with transesophageal echocardiography, and the information was used in planning the operative procedure of homograft valve replacement. This strategy is proposed as optimal management of this potentially lethal condition.
Electrolyte disturbances in chronic heart failure: Metabolic and clinical aspects
Authors: Dei Cas Livio , Metra Marco , Leier Carl V.
Published: February 2009

The pathophysiology of congestive heart failure (CHF) includes conditions (e.g., activation of the renin‐angiotensin‐aldosterone system) which, when combined with CHF therapies, make patients afflicted with this syndrome quite susceptible to electrolyte disturbances. The most commonly encountered are hyponatremia, hypokalemia, and hypomagnesemia. These derangements are of vast clinical importance; their development not only represents an immediate threat to the CHF patient (e.g., dysrhythmias secondary to hypokalemia), but are also indicative of underlying pathophysiologic events, an unfavorable clinical course, and occasionally an adverse therapeutic response. The optimal care of the CHF patient includes the recognition and management of these electrolyte disturbances.
Neuroendocrine changes in heart failure and their clinical relevance
Authors: Parmley William W.
Published: February 2009

The pathophysiology of heart failure is closely associated with neuroendocrine changes. Activation of these humoral systems apparently serves as a compensatory mechanism for the failing circulation. However, overshoot of such mechanisms may further depress cardiac function by increasing afterload, resulting in a vicious cycle of reflex neuroendocrine activation. Corollary decreases in renal function activate the renin‐angiotensin‐aldosterone system as well, which further contributes to the cycle of downward‐spiralling cardiac function. Many hormonal factors are increased in congestive heart failure. While some influences are vasodilatory, the net effect is marked vasoconstriction. The level of activation of these systems apparently corresponds to the severity of heart failure. Furthermore, elevated levels of these hormones, including norepinephrine, atrial natriuretic factor, plasma renin, and plasma arginine vasopressin, may play a more direct role in worsening heart failure. In fact, elevated catecholamine levels are directly related to prognosis. Catecholamines increase myocardial oxygen demand and are also arrhythmogenic. Oral catecholamines and phosphodiesterase inhibitors, which work by similar mechanisms, have yielded increased mortality rates in heart failure trials. In contrast, mortality rates are reduced in patients treated with angiotensin‐converting enzyme inhibitors. Thus, it is clear that neuroendocrine changes are not only a marker of the severity of heart failure, but also directly worsen it. Interventions that antagonize or diminish these neuroendocrine changes apparently benefit patients with heart failure.