bluuebunny/crossref_metadata_2025 huggingface dataset:
Early hemodynamic effects at rest with acute and chronic isosorbide dinitrate treatment in patients with ischemic heart disease
Authors: Jørgensen Lars H. , Thaulow Erik , Refsum Harald E.
Published: February 2009

Asymmetric dosage regimens are used to circumvent development of nitrate tolerance and are believed to restore totally the hemodynamic responsiveness to an acute dosage of nitrates. This study assessed invasively the hemodynamics during supine rest before and for 50 min after peroral 30 mg isosorbide dinitrate (ISDN) in 16 patients with stable ischemic heart disease; 8 previously untreated patients (NT group) and 8 patients treated asymmetrically b.i.d. with 30 mg ISDN for 14 days prior to the invasive investigation (T group). Before initiation of treatment, both groups had identical mean arterial pressure (MAP) and heart rate (HR). On the day of invasive investigation, before intake of ISDN, MAP was higher in the T group but unchanged in the NT group. After the intake of ISDN, right atrial pressure (RAP), mean pulmonary arterial pressure, and pulmonary arterial wedge pressure declined markedly within 10 to 15 min in both groups, while MAP showed a more protracted decline, reaching a new level only after 25 to 30 min. In the NT group, HR accelerated markedly and remained elevated throughout the observation period, whereas in the T group HR showed no significant alteration after ISDN intake. At the end of the observation period, the cardiac index (CI) was definitely reduced in the NT group, but remained unchanged in the T group, while the systemic vascular resistance index was unchanged in the former and was clearly reduced in the latter. It is concluded that the fall in MAP in the NT group was solely due to a fall in CI, and that the decline in RAP and venous return in the NT group induced neurohumoral reflexes leading to a rise in HR and prevention of arterial dilation, whereas in the T group, already influenced by chronic treatment, such acute counterregulatory responses were markedly attenuated or absent.
Advanced cardiac life support: Update on recent guidelines and a look at the future
Authors: Tucker Kelly J. , Larson James L. , Idris Ahamed , Curtis Anne B.
Published: February 2009

The objectives of this article are to provide an update of the American Heart Association (AHA) 1992 National Conference guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care and to review the investigation and development of new methods of CPR which may be considered in future recommendations. Despite an organized approach to sudden cardiac arrest, survival in patients receiving CPR is in the range of 5–15%. The new AHA guidelines recommend standard manual CPR performed at a rate of 80–100 compressions/min and organized algorithms of advanced cardiac life support. These guidelines stress widespread community training and rapid response in the following sequence: (1) recognition of early warning signs, (2) activation of the emergency medical system (EMS), (3) basic CPR, (4) early defibrillation, (5) intubation, and (6) intravenous medication. Several new recommendations pertain specifically to in‐hospital care and are, therefore, particularly relevant to physician management of cardiac arrest. The best predictor of survival in patients requiring circulatory support after cardiac arrest is attainable coronary and cerebral perfusion. Unfortunately, the minimal levels of end‐organ perfusion required to sustain life are often difficult or impossible to achieve with standard manual cardiopulmonary resuscitation and several new techniques have therefore been introduced. The most promising of these techniques are (1) interposed abdominal compression, (2) pneumatic vest, and (3) active compression‐decompression resuscitation. Each of these techniques offers unique advantages when compared with standard manual cardiopulmonary resuscitation. The 1992 National Conference recommendations provide a rational framework for the resuscitation of cardiac arrest victims. New methods of cardiopulmonary resuscitation are now available and investigation into these methods continues. In the future, these modalities may be incorporated in newer guidelines and be available on a widespread basis to supplement our current approach to cardiac arrest.
Left ventricular outflow tract pulmonary artery fistula in endocarditis
Authors: Mizock Barry A. , Nachman Sami A. , Varquez Mir
Published: February 2009

Patients with infective endocarditis are at risk for the development of a fistulous communication between chambers or great vessels of the heart. The presence of a continuous murmur may suggest the diagnosis. The first case of aortic valve endocarditis complicated by the development of a fistulous communication between the left ventricular outflow tract and the pulmonary artery is reported. Transesophageal Doppler echocardiography did not detect the defect preoperatively. However, pulmonary artery catheterization revealed very high mixed venous oxygen saturation which supported the presence of a left‐to‐right shunt.
Antiphospholipid antibodies in heart transplant recipients
Authors: Mcintyre John A. , Waoenknecht Dawn R. , Page Faulk W.
Published: February 2009

Antiphospholipid antibodies (aPA) are found in patients with systemic lupus erythematosus, aPA syndrome, myocardial infarction, and stroke. The presence of aPA may predict recurrent events in certain victims of heart attack and stroke. Blood samples from 105 cardiac transplant recipients (81 men. 24 women) were tested by enzyme‐linked immunosorbent assay (ELISA) for the presence of IgG, IgM, and IgA aPA to phosphatidylserine (PS), cardiolipin (CL), and phosphatidylethanolamine (PE). Patients' ages ranged from 17 to 70 years (mean 51 years). Collection times ranged from Day 1 to 9 years post transplant (mean 36 months). All patients received triple immunosuppressive therapy. We report our aPA ELISA results in multiples of the normal median (MoM) of the OD405 values calculated for 252 healthy individuals. A positive MoM is greater than the MoM that encompasses 95% of the controls; for example, above 3 MoM is considered positive for IgG anti‐CL, IgA anti‐PS, and CL. Above 4 MoM is positive for IgG anti‐PS and PE and IgM anti‐PS and CL. Thirty‐nine patients had IgG anti‐PS (range 4.1–14.8 MoM), 63 had IgG anti‐CL (3.1–9.4 MoM), 7 had IgM anti‐PS (4.1–12.1 MoM), 1 had IgM anti‐CL (14 MoM), 47 had IgA anti‐PS (3.1–13.1 MoM), and 58 had IgA anti‐CL (3.1–11.5 MoM). In our patient population, the incidence of IgG and/or IgA aPA was significantly higher (p < 0.001) than IgM. Few patients showed specificity for either PS, CL, or PE, and many were positive with more than one antibody iso‐type. Because aPA were elevated in these patients, we investigated pretransplant serum samples which were available from 79 of the 105 recipients, and found aPA in 52 of 79 (66%) patients before transplantation. Longitudinal studies were done in three patients: two had increasing IgA aPA, beginning on Days 13 and 26 post transplant, whereas the third patient showed an increased aPA on Day 8 but a decrease on Day 23. Studies are in progress to determine whether a correlation exists between the presence of aPA, immunocytochemical (biopsy) findings, and clinical outcome.
The power spectral analysis of heart rate variability in athletes during dynamic exercise—Part I
Authors: Shin Kunsoo , Minamitani Haruyuki , Onishi Shohei , Yamazaki Hajime , Lee Myoungho
Published: February 2009

In this study, the effects of long‐term physical training on autonomic function in athletes and the response of the autonomic nervous system to dynamic exercise were investigated in nonathletes and athletes with power spectral analysis of heart rate variability (HRV). This study was performed on 13 healthy subjects (5 athletes and 8 nonathletes). Eleclrocardiographic (ECG) signals were continuously recorded during (1) 15 min of rest in a sitting position on a bicycle ergometer, (2) the dynamic exercise test to the point of exhaustion, and (3) a 15 min postexercise period. After the recorded ECG signals were sampled at 500 samples/s, the instantaneous HRV signal was constructed from the detected R peaks and then resampled at 4 Hz in order to obtain an evenly spaced time series applicable to power spectral analysis. After linear trends were removed by the robust locally weighted regression algorithm, the power spectrum of HRV was estimated for contiguous records of 512 samples by Burg's maximum entropy method. HRV was quantified by determining the spectral area (power) in two frequency bands, low‐frequency power (LF power: 0.05–0.15 Hz) and high‐frequency power (HF power: 0.15–0.8 Hz), and their ratio. The comparison between athletes and nonathletes was performed in terms of the above‐mentioned parameters. Although both groups showed similar trends in heart rate (HR) at all stages of protocols, HR in athletes was significantly lower than that in nonathletes during rest and postexercise. In athletes and nonathletes, LF and HF powers gradually decreased with exercise. As recovery progressed, they continued to increase gradually, but remained below resting level. During rest and postexercise, HF power in athletes was significantly (p < 0.05) higher than that in non‐athletes. Also, the recovery of HR and HF power during early recovery (POI) was more rapid in athletes than in nonathletes. Both groups showed an attenuation of LF and HF powers during dynamic exercise. It is likely that, in athletes, the lower HR during rest and the more rapid recovery of HR postexercise was due to a high level of HF power, indicating that vagal activity was enhanced by the adaptive changes in neural regulation produced by long‐term physical training.
Peripheral vascular complications following coronary interventional procedures
Authors: Nasser Tony K. , Mohler Emile R. , Wilensky Robert L. , Hathaway David R.
Published: February 2009

We report the incidence, diagnosis, prevention, and treatment of peripheral vascular complications following coronary interventional procedures as reviewed in the English‐language literature. Peripheral vascular complications include hematomas, pseudoaneurysms, arteriovenous fistulae, acute arterial occlusions, cholesterol emboli, and infections that occur with an overall incidence of 1.5–9%. Major predictors of such complications following coronary interventional procedures include advanced age, repeat percutaneous transluminal coronary angioplasty, female gender, and peripheral vascular disease. Minor predictors include level of anticoagulation, use of thrombolytic agents, elevated creatinine levels, low platelet counts, longer periods of anticoagulation, and use of increased sheath size. Ultrasound‐guided compression repair of pseudoaneurysms and arteriovenous fistulae are discussed, as are newer methods of treatment such as hemostatic puncture closure devices. Anticipation and early recognition of possible peripheral vascular complications in conjunction with careful attention to the optimal activated clotting time for sheath removal following coronary interventional procedures may translate into fewer vascular complications as well as into shorter and less costly hospital stays.
Inotropic therapy for the failing myocardium
Authors: Shipley Joshua B. , Hess Michael L.
Published: February 2009

Congestive heart failure (CHF) is a common clinical entity with diverse causes. Patients may present with acute decompensation or have a more indolent course, with diminishing exercise tolerance and increasing dyspnea. The management of this clinical entity traditionally has focused on restricting fluid intake, decreasing dietary sodium, decreasing afterload with vasodilatory agents, and supporting the failing myocardium with agents which produce a positive inotropic response. In the acutely decompensated patient, short‐term therapy with positive inotropics is clearly beneficial. The role of long‐term inotropic therapy for chronic CHF remains less clear. A number of clinical trials have recently evaluated the effects of long‐term therapy on morbidity and mortality, with disappointing results. For a number of the newer, nonglycocide oral positive inotropics, at doses of drug which produce measurable hemodynamic improvement, increased mortality in treatment groups has been unacceptably high. Ironically, patients with worse left ventricular dysfunction show the most clinical improvement, but have the highest increased mortality. However, as with digoxin, there is some evidence that employing lower doses of drug that do not produce measurable improvement in hemodynamic parameters may result in both improved clinical state and decreased mortality. This review discusses the role of both oral and intravenous inotropic agents, discusses the difficulty in translating short‐term hemodynamic improvement into long‐term clinical benefit, and presents a rationale for the use of lower‐dose inotropic therapy to improve long‐term clinical outcome.
Comparison of the efficacy of simvastatin and standard fibrate therapy in the treatment of primary hypercholesterolemia and combined hyperlipidemia
Authors: Bruckert E. , De Gennes J. L. , Malbecq W. , Baigts F.
Published: February 2009

Five multicenter, randomized, double‐blind, placebo‐controlled studies were conducted in France to compare the efficacy and safety of once‐daily simvastatin treatment (10–40 mg/day) with conventional therapy with gemfibrozil 900 mg/day, ciprofibrate 100 mg/day, bezafibrate 400 mg/day, and fenofibrate 300 or 400 mg/day in a total of 800 patients with hypercholesterolemia. Simvastatin was associated with statistically significantly greater (p ≪ 0.01) mean percent reductions in plasma low‐density lipoprotein (LDL) cholesterol compared with each of the five fibrate regimens, even when administered at its recommended starting dose of 10 mg/day. Furthermore, approximately 90% of patients treated once daily with simvastatin experienced an at least 20% decrease in plasma LDL cholesterol compared with only 36 to 68% of patients treated with the individual fibrate agents (p ≪ 0.05). The effectiveness of simvastatin in reducing LDL cholesterol did not differ as a function of the baseline plasma concentrations of total cholesterol or triglycerides. In contrast, the effectiveness of fibrate therapy in lowering plasma LDL cholesterol levels was significantly diminished (p ≪ 0.05) among patients with triglyceride concentrations > 1.7 mmol/1. Plasma highdensity lipoprotein (HDL) cholesterol levels were increased by approximately 10% after treatment with simvastatin or the fibrates. Although fibrate therapy was more effective overall in lowering plasma triglyceride levels, the effectiveness of simvastatin in reducing plasma triglyceride levels was generally 2‐ to 4‐fold greater in patients with hypercholesterolemia associated with triglyceride levels ≫ 2.3 mmol/1 than in those with hypercholesterolemia associated with triglyceride levels < 2.3 mmol/1. The results of these studies confirm the superiority of simvastatin to standard fibrate therapy in reducing plasma levels of total and LDL cholesterol. They further indicate that once‐daily treatment with simvastatin is effective in patients with isolated hypercholesterolemia or hypercholesterolemia associated with elevated triglyceride levels.
Plasma concentrations and coronary vasodilation after sublingual and intracoronary administration of isosorbide dinitrate
Authors: Hoshio Akira , Shirota Kinya , Sasaki Norihito , Doi Tetsuya , Sawada Yoshihiro , Fukuki Masaharu , Miyakoda Hiroyuki , Kotake Hiroshi , Mashiba Hiroto
Published: February 2009

To investigate the relationship between plasma levels and coronary vasodilation after administration of isosorbide dinitrate (ISDN), the plasma concentration and diarneters of six segments of the left coronary artery were measured before and after sublingual (SL) ISDN (5 mg) and left intracoronary (IC) administration of ISDN (3 mg) in 12 patients. After SL‐ISDN, the systolic aortic pressure decreased with no significant concomitant changes in heart rate or diastolic aortic pressure. After IC‐ISDN, all hemodynamic parameters showed significant changes, and these were greater after IC‐ISDN than those after SL‐ISDN. The individual mean vasodilation of six segments induced by SL‐ and IC‐ISDN, were 23± 9 and 35± 11% (p<0.01), respectively. Before SL‐ISDN, ISDN was not detected in plasma. After SL‐ and IC‐ISDN, however, the plasma values of the ISDN were 36.1± 53.3 and 101.5± 90.0 ng/ml (p<0.01), respectively. Thus, both coronary vasodilative responses and plasma ISDN levels after IC‐ISDN were significantly greater than those after SL‐ISDN. However, neither the individual mean coronary vasodilation nor the hemodynamic changes correlated significantly with plasma ISDN levels. Consequently, with administration of the same dose, the coronary vasodilative response to ISDN did not correlate with plasma levels. Furthermore, IC‐ISDN dilates coronary arteries more effectively than SL‐ISDN.
Treatment of silent ischemia in unstable angina: A randomized comparison of sustained‐release verapamil versus metoprolol
Authors: Singh Narendra , Mironov Dmitry , Goodman Shaun , Morgan Christopher D. , Langer Anatoly
Published: February 2009

Silent ischemia is a frequent finding in patients with unstable angina and portends a poor prognosis. We compared the efficacy of sustained‐release (SR) verapamil and metoprolol in reducing silent ischemia in patients with unstable angina and assessed whether detection of silent ischemia was related to unfavorable outcomes in the contemporary setting of concurrent therapy with heparin and aspirin. Holter monitoring (leads a VF, V2, V5) for the first 72 h was used to assess the frequency and duration of ST‐shift episodes. There were 37 patients in the verapamil‐SR group and 40 patients in the metoprolol group, with both groups having similar baseline characteristics. There were more episodes of angina in the verapamil‐SR group (29 vs. 12, p = 0.05). There was no difference between the two groups in the frequency (51 vs. 49 episodes, p = 0.9) or duration (23± 48 vs. 18± 50 min, p = 0.6) of ST‐shift episodes. There were 20 unfavorable in‐hospital outcomes distributed equally between the two groups (p = 0.9). Patients with unfavorable outcomes had ST shift more often (50 vs. 28%, p = 0.07) and for a longer duration (40± 69 vs. 13± 38 min, p = 0.03). Patients with ST shift > 60 min had a 60% probability of unfavorable outcome compared with 33% for ST shift of 1–59 min duration and 20% for no ST shift (p = 0.04). We conclude that metoprolol appears to reduce symptoms better than verapamil‐SR, but no difference in silent ischemia or unfavorable outcomes was seen. Silent ischemia remains a common occurrence in these patients despite heparin and aspirin therapy and its detection continues to have prognostic value.
Cardiovascular effects of dobutamine stress testing in healthy women
Authors: Blomstrand Peter , Thulesius Olav , Wranne Bengt
Published: February 2009

Dobutamine echocardiography is frequently used for detection of coronary artery disease. The circulatory response in patients is known to some extent, but studies in normals are lacking. Hypotensive response during the test is a common side effect, the cause of which is unclear. The aim of this study was, therefore, to investigate the hemodynamic response to dobutamine in women without cardiovascular disease and interfering medications. Eleven healthy women, age 53–71 years, were investigated with Doppler echocardiography and venous occlusion plethysmography during intravenous infusion of increasing doses of dobutamine according to a standardized protocol. An average peak dose of 22 ± 7.5 μMu kg‐1min‐1was administered. Cardiac output increased by 93%, heart rate by 68%, and stroke volume by 15%, while peripheral vascular resistance decreased by approximately 50%. Systolic blood pressure remained unchanged and diastolic blood pressure decreased by 21%. One subject demonstrated a decreased systolic blood pressure exceeding 10 mmHg. Outflow obstruction from the left ventricle was seen in two subjects, one of whom had a slight decrease of 10 mmHg in systolic blood pressure. Subjects > 65 years demonstrated a less pronounced increase in heart rate, cardiac output, and decrease in peripheral vascular resistance compared with those < 65 years.
Intracardiac thrombi: Frequency, location, etiology, and complications: A morphologic review—Part IV
Authors: Waller Bruce F. , Grider Larry , Rohr Todd M. , Mclaughlin Todd , Taliercio Charles P. , Fetters Julie
Published: February 2009

Intracardiac thrombus may develop as a consequence of multiple underlying cardiac disorders. Valvular heart disease, in particular, rheumatic mitral stenosis is frequently associated with intracardiac thrombus. Pant IV of this 5‐part article on intracardiac thrombus focuses on the frequency and consequences of thrombus in valvular heart disease.
The role of prolonged thrombolytic infusions and transesophageal echocardiography in thrombosed prosthetic heart valves: Case Report and review of the literature
Authors: Puleo John A. , Fontanet Hector L. , Schocken Douglas D.
Published: February 2009

Thrombolytic therapy for prosthetic heart valve thrombosis has recently been receiving increased attention and is now frequently used an alternative to high‐risk surgery. A case is presented describing a novel thrombolytic therapy regimen with emphasis on the role of transesophageal echocardiography in diagnosis and management. A complete review of the literature is presented.
Invtracardiac thrombi: Frequency, location, etiology, and complications: A morphologvic review—Part V
Authors: Waller Bruce F. , Rohr Todd M. , Mclaughlin Todd , Grider Larry , Taliercio Charles P. , Fetters Julie
Published: February 2009

Intracardiac thrombus may develop as a consequence of multiple underlying cardiac disorders. Other systemic disorders may predispose formation of thrombus within the heart, or the heart may be the site of emboli in transitthrombus originating elsewhere and traveling through the heart to the pulmonary or arterial circulation. Part V of this five‐port series on intracardiac thrombus will focus on “migrating thrombi,” miscellaneous systemic conditions associated with intracardiac thrombi, and echocardiographic detection of intracardiac thrombus.
Dobutamine‐induced transmural myocardial ischemia in a patient with mild coronary lesions
Authors: Kardaras Fotis G. , Bonou Maria S. , Kardara Dimitra F. , Kranidis Athanasios I. , Sioras Elias P. , Anthopoulos Lambros P.
Published: February 2009

A 70‐year‐old man was admitted for evaluation of retrosternal pain at rest. During infusion of dobutamine (25 μg/kg/min) the patient developed angina, ST‐segment elevation in the inferior leads, and echocardiographic hypokinesia in the inferior‐basal myocardial wall. Coronary angiography revealed insignificant (20‐30%) stenosis of the right coronary artery and a normal remaining tree. This case suggests that dobutamine may induce transmural myocardial ischemia in patients with mild coronary lesions, probably by producing occlusive coronary spasm on a substrate of arterial endothelial dysfunction.
Resolution of an aortic mobile mass with anticoagulation without evidence of arterial embolism
Authors: Pasierski T. , Jasek S. , Firek B. , Przbylski A. , Szwed H. , Sadowski Z.
Published: February 2009

The prognostic significance of aortic mobile debris detected by transesophageal echocardiography (TEE) in patients without history of embolism has not been established. A mobile aortic arch mass was found by TEE in a 59‐year‐old man with coronary artery disease, and with rheumatic mitral valve disease, and with no embolic symptoms. The patient was anticoagulated for 6 weeks and the mass was no longer seen on repeated TEE. He had no embolic symptoms during 9 months of follow‐up. Different therapeutic approaches to mobile aortic debris are discussed and anticoagulant treatment of asymptomatic cases is advocated.
Manifestation of severe coronary heart disease after anabolic drug abuse
Authors: Mewis C. , Spyridopoulos I. , Kühlkamp V. , Seipel L.
Published: February 2009

Anabolic steroids are frequently abused, thus increasing the risk of cardiovascular disease, despite the known unfavorable influence on lipid profiles. We report on a young bodybuilder who presented with ventricular tachycardia as the first manifestation of severe underlying coronary heart disease. Coronary angiogram revealed severe stenotic lesions in the right coronary artery and the left descending coronary artery, and hypokinetic regions corresponded to posterolateral and anterior myocardial infarctions. This young patient had a history without any coronary risk factors, but with a 2‐year abuse of the anabolic steroid stanazolol. No report published so far has shown possible atherogenic consequences of long‐term abuse of stanazolol.
Retinal artery embolization: A rare presentation of calcific aortic stenosis
Authors: Reimers Carl D. , Berger Marvin , Williams Richard J. , Tranbaugh Robert F. , Jay Wisnicki H.
Published: February 2009

Retinal artery embolization is an unusual but serious complication of calcific aortic stenosis. However, it is rare for retinal embolization to be the presenting feature of aortic stenosis. This report describes a young patient who presented with an acute retinal artery occlusion secondary to calcific aortic valve disease, and discusses the rationale for early surgical intervention.
Postpericardiotomy syndrome and cardiac tamponade following transvenous pacemaker placement
Authors: Miller Gregory L. , Coccio Elizabeth B. , Sharma Satish C.
Published: February 2009

This is the first reported case of cardiac tamponade presumed to be caused by postpericardiotomy syndrome (PPS) following endocardial pacemaker placement. An 84‐year‐old woman developed fever and dyspnea 3 weeks after pacemaker placement. Physical examination revealed hypotension, tachycardia, and pulsus paradoxus. Auscultation revealed clear lungs and diminished heart sounds. The sedimentation rate was 60 mm/h. Echocardiography revealed a large pericardial effusion with signs of cardiac tamponade. Surgical drainage of the pericardial space resulted in complete resolution of symptoms. The pericardial fluid was culture‐ and cytologically negative. PPS is a common complication of cardiothoracic surgery and chest trauma. It rarely occurs after percutaneous procedures such as percutaneous transluminal coronary angioplasty and transvenous pacemaker placement. While usually having a benign, self‐limited course, PPS can cause a serious complication as illustrated in this case report.
An unusual case of cyanotic heart disease in a patient with patent foramen ovale and right ventricular hypertrophy
Authors: Will Peter M. , Serrian John L. , Dawson John T.
Published: February 2009

An unusual case of cyanosis and patent foramen ovale/atrial septal defect with right‐sided septal hypertrophy is presented. Mild right ventricular dysfunction led to predominant right‐to‐left shunting. The atrial defect was surgically closed. The patient is from a family with hypertrophic cardio‐myopathy;she is negative for the gene abnormality.
Nonatherosclerotic causes of coronary artery narrowing—Part II
Authors: Waller Bruce , Waller Bruce F. , Fry Edward T. A. , Hermiller James B. , Peters Thomas , Slack John D.
Published: February 2009

Part II of this three‐part article on nonatherosclerotic causes of coronary heart disease focuses on myocardial bridges, coronary artery aneurysms, emboli, coronary dissection, and spasm as causes of luminal narrowing.
Possible mechanisms of mitral regurgitation in dilated hearts: A study using transesophageal echocardiography
Authors: Oki Takashi , Fukuda Nobuo , Iuchi Arata , Tabata Tomotsugu , Yamada Hirotsugu , Fukuda Kazuyo , Manabe Kazuyo , Ito Susumu
Published: February 2009

Hypothesis: This study was undertaken to clarify the mechanisms of mitral regurgitation (MR) in dilated hearts.

Methods: in all, 68 patients with dilated heart and MR, including 26 patients with dilated cardiomyopathy (DCM), 24 with prior anterior myocardial infarction (A‐MI), and 18 with prior posteroinferior myocardial infarction (I‐MI), as well as 25 normal subjects were examined by transesophageal two‐dimensional and color Doppler echocardiography.

Results: The maximum area of the MR signal in the DCM group correlated positively with the anteroposterior diameter of the mitral annulus at late systole. Although the coaptation edge length of the anterior and posterior mitral leaflets appeared shorter in dilated hearts than in the hearts of controls, a significant difference did not exist. The length of the coaptation edge correlated negatively with the maximum area of the MR signal in all dilated hearts, and characteristic systolic displacement of the coaptation point of both mitral leaflets occurred. The MI groups demonstrated anterior and posterior displacement in the direction of the short axis of the left ventricle in the A‐MI and I‐MI groups, respectively. However, the DCM group demonstrated inferior displacement toward the long axis of the left ventricle; its magnitude correlated positively with the maximum area of the MR signal.

Conclusion: A major cause of MR in dilated hearts is mitral malcoaptation due to displacement of the coaptation point of the mitral leaflets along the long or short axis of the left ventricle. This is caused by left ventricular enlargement and/or asynergy of the left ventricular wall, rather than by a decrease in mitral coaptation edge length due to mitral annular dilation.
Atrial Fibrillation in the Elderly
Authors: Reardon Michael , John Camm A.
Published: February 2009

The prevalence of atrial fibrillation is 11 % in persons older than 70 years and rises to 17% in those aged 84 years or more. One‐year mortality ranges from 0.2 to 16%, being highest in elderly patients, and is associated with a 4.8‐fold increased risk of stroke. Atrial fibrillation can be cardioverted to normal sinus rhythm electrically or pharmacologically and rapid ventricular rate can be controlled with drugs. While anticoagulation prevents embolic events in those with atrial fibrillation, the decision to anticoagulate should be based on an assessment of the risk/benefit ratio.
The role of magnesium therapy in acute myocardial infarction
Authors: Rabbani Llroy E. , Antman Elliott M.
Published: February 2009

Magnesium possesses numerous salutary effects for the treatment of acute myocardial infarction (AMI). It is a coronary vasodilator, calcium antagonist, afterload reducer, antiarrhythmic, and antiplatelet drug that modulates autonom‐ic function and limits reperfusion injury when administered early in infarction. Various clinical trials of magnesium therapy for AMI have proffered conflicting results as to the efficacy of magnesium therapy because of significant differences in the timing of magnesium administration. Additional clinical trials that focus on early administration of magnesium are warranted to delineate the role of magnesium therapy for AMI.
Refining the treatment of women with unstable angina—A randomized, double‐blind, comparative safety and efficacy evaluation of integrelin™ versus aspirin in the management of unstable angina
Authors: Goldschmidt‐Clermont Pascal J. , Schulman Steven P. , Chandra Nisha C. , Grigoryev Dmitriy , Dise Kirk R. , Sagar Manish , Fox Robert J. , Coleman Lindsay D. , Ouyang Pamela , Baughman Kenneth L. , Gerstenblith Gary , Bray Paul F. , Richardson Christine , Dorsey Frank C. , Du Mee Charles , Kitt Michael M. ,   on behalf of the Investigators of the Study
Published: February 2009

Background: Although women typically develop coronary artery disease several years after men, once they have symptomatic disease their thromboembolic complications are worse than in men. The mechanism mediating this gender difference in outcome after thromboembolic events is unknown. We previously studied platelet functions in siblings from patients with premature coronary artery disease. We observed that platelets from women are more responsive than their male counterparts. In particular, platelets from women stimulated ex vivo with various agonists bind more fibrinogen molecules than platelets from men.

Hypothesis: We hypothesized that in patients with acute coronary events, the control of platelet activity might require stronger antagonists in women than in men.

Methods: To test this hypothesis, we investigated retrospectively the results of a trial on Integrelin™ in unstable angina.

Results: We report that platelet aggregation and Holter‐de‐tected ischemic episodes are significantly reduced in women with unstable angina treated with the specific GPIIb‐IIIa inhibitor, Integrelin, compared with the standard platelet inhibitor aspirin. In contrast, both platelet aggregation and Holter‐detected ischemic events are well controlled in men with unstable angina treated with standard therapy including aspirin. Conclusion: Integrelin does provide protection in men, but, in contrast with women, not beyond what can be achieved with aspirin. Our data are consistent with the concept that the platelets from women require stronger and more specific inhibitors to limit their activity, and that platelets may play a more important role in women with acute coronary syndromes than in men. Most important, specific GPIIb‐IIIa inhibitors may represent a therapeutic option which provides as much suppression of ischemic events in women as they do in men with coronary artery disease.
Interference of cellular phones with implanted permanent pacemakers
Authors: Chen Wai‐Hong , Lau Chu‐Pak , Ho David Sai‐Wah , Lee Iris Siu‐Fong , Leung Sum‐Kin
Published: February 2009

Background and hypothesis: Occasional reports have suggested that cellular phones may interfere with permanent pacemakers. Our investigation sought to determine systematically the effects of commercially available cellular phones on the performances of different pacing modes and sensing lead configurations of permanent implanted pacemakers.

Methods: We conducted the study in 29 patients implanted with single‐ or dual‐chamber bipolar rate‐adaptive permanent pacemakers (a total of nine different models and six different sensors: minute ventilation, activity sensing using either accelerometer or piezoelectric crystal, QT and oxygen saturation sensing) from four different manufacturers. Three different cellular phones with analog or digital coding with maximum power from 0.6 to 2 W were used to assess the effect of pacemaker interference. Each cellular phone was positioned at (1) above the pacemaker pocket, (2) the ear level ipsilateral to the pacemaker pocket, and (3) the contralateral ear level. Surface electrocardiograms, intracardiac electrograms, and marker channels were recorded where possible during the following maneuvers at each position: (1) calls made by a stationary phone to a cellular phone, and (2) calls made from the cellular phone to a stationary phone. A total of eight different pacing modes [DDD(R), VDD(R), AAI(R) and VVI(R)] in both unipolar and bipolar sensing configurations was tested.

Results: Interference was demonstrated during cellular phone operation in 74 of 2,418 (3.1%) episodes in eight patients. Three types of interference were observed: inhibition of pacing output, rapid ventricular tracking in DDD(R) or VDD(R) mode, and asynchronous pacing. All were observed only with the cellular phone positioned above the pacemaker pocket. Interference occurred prior to and after the termination of the ringing tone of the cellular phone in 57% of cases. Cellular phones with either digital or analog technology could cause interference. Unipolar atrial lead was most susceptible to interference (relative frequency of interference: unipolar 1.8%, bipolar 0.4%, p<0.05;atrial 2.9%, ventricular 1 %, p <0.05). There was no sensor‐driven rate acceleration during all tests. In all patients, reprogramming of the sensitivity level successfully prevented cellular phone interference.

Conclusions: Commercially available cellular phones can cause reversible interference to implanted single‐ or dual‐chamber permanent pacemakers. The effect is maximal with high atrial unipolar sensitivity, especially in single pass VDD(R) systems. Both digital and analog cellular phones can lead to interference. Pacemaker interference can occur prior to a warning sign (ringing tone) of the phone and may have significant implications in patient safety.
Severe right heart failure in a patient with grave's disease
Authors: Xenopoulos Nicholaos P. , Braden Gregory A. , Applegate Robert J.
Published: February 2009

This brief report presents a patient with isolated right heart failure and two rare underlying causes, hyperthy‐roidism and dysplastic tricuspid valve. Repair of the tricuspid valve and treatment of the hyperthyroidism were both essential for successful treatment of the right heart failure. Most important, recrudescence of hyperthyroidism in this patient was associated with reappearance of florid right heart failure. This report provides further information about a potential linkage of hyperthyroidism and severe right heart failure.
The iron hypothesis—Does iron cause atherosclerosis?
Authors: Meyers David G.
Published: February 2009

Women experience only 30–50% of the coronary heart disease (CHD) incidence and mortality of age‐matched men. Since oxidation of low‐density lipoprotein (LDL) cholesterol is important in atherosclerosis, and oxidation is catalyzed by iron, it has been hypothesized that the lower iron stores of women reduce their risk of CHD through lessened lipid peroxide. The biochemistry of oxidation is well described in the literature and involves iron as a catalyst in the formation of powerful free radicals which subsequently modify LDL cholesterol. Chelating iron with desferrioxamine stops oxidation. Iron is present in atherosclerotic gruel and this gruel stimulates lipid peroxidation. Serum deficient in iron has minimal oxidative capacity which increases with iron repletion. At least seven epidemiologic studies have found a positive association between CHD and various indicators of body iron. Conversely, 18 epidemiologic studies have found a negative or no association. While biochemically appealing, the iron hypothesis remains unproven.
QT interval change with age in an overtly healthy older population
Authors: Reardon Michael , Malik Marek
Published: February 2009

Background: Prolonged QT interval on the surface electrocardiogram (ECG) is known to be associated with arrhythmias, coronary heart disease, and sudden cardiac death. Increased QT dispersion has also been related to arrhythymias which are more frequent in the elderly.

Hypothesis: This study investigated the relationship between aging, QT interval, and QT dispersion.

Methods: Normal resting ECGs were recorded from 96 healthy subjects (73 women, age range 40‐102 years). No subject had symptoms or signs of heart disease and none was on medication affecting cardiac function. All had normal heart size on chest x‐ray and normal electrolytes. Using a digitizing board, the RR and QT intervals were measured on each lead of each ECG, excluding only the leads in which the T wave was not visible. Mean RR, mean QT interval, and heart rate‐adjusted QTc interval (standard Bazet's formula) were obtained from these measurements. Further, QT dispersion was calculated for each ECG as (1) the difference between the maximum and minimium QT interval, and (2) as the coefficient of variance of QT interval of all measurable leads.

Results: A significant correlation between aging and prolonged QTc was noted in the total population (r = 0.43, p <0.05), as well as in men (r = 0.4, p <0.05) and women (r = 0.23, p<0.05) separately. There was no association between QT dispersion and increasing age regardless of the method of calculation (r= ‐0.04, r= ‐0.08 respectively, both NS).

Conclusion: The rate‐adjusted QT interval is prolonged with increasing age and may contribute to the increased risk of ventricular arrhythmias and cardiac mortality in elderly patients.
Mechanism of left a trial enlargement related to ventricular diastolic impairment in hypertension
Authors: Matsuda Masako , Matsuda Yasuo
Published: February 2009

Background and hypothesis: Systemic hypertension is the leading cause of left ventricular (LV) hypertrophy. The present study aimed to investigate the mechanism of left atrial (LA) enlargement in patients with hypertensive heart disease during cardiac catheterization.

Methods: Data were obtained from eight control subjects and seven patients with hypertensive heart disease. Left atrial and LV pressures from catheter‐tip micromanometer, and LA and LV volumes from biplane cineangiograms were analyzed during the same cardiac cycle.

Results: Left atrial maximal volume were 93 ± 26 ml in patients with hypertensive heart disease and 63 ± 12 ml in control subjects (p<0.05). In patients with hypertensive heart disease, time constant of LV relaxation was significantly greater than that in controls (54 ± 18 vs. 31 ± 16 ms, respectively p<0.01). Left atrial maximal volume correlated with time constant of LV relaxation (r = 0.86, p<0.01). The ratio of LV filling volume before LA contraction to LV stroke volume in patients with hypertensive heart disease was significantly lower than that in control subjects (65 ± 13 vs. 76 ± 7%, respectively p<0.05). On the other hand, the ratio of LV filling volume during LA contraction to stroke volume in patients with hypertensive heart disease was significantly higher than that in controls (35 ± 13 vs. 24± 7%, respectively p<0.05). Left atrial volume before LA contraction in patients with hypertensive heart disease was significantly larger than that in controls (74 ± 22 vs. 47 ± 10 ml, respectively, p<0.01). During LA contraction, LA work was significantly increased in patients with hypertensive heart disease compared with that in controls (274 ± 101 vs. 94 ± 42 mmHg. ml, respectively p<0.001). Left atrial work showed significant correlation with LA volume before LA contraction (r = 0.75, p <0.01).

Conclusion: Left ventricular diastolic filling was impaired in patients with hypertensive heart disease. Enlargement of left atrium might be attributed to the impairment of blood flow from left atrium to left ventricle due to the increased LV stiffness.
Biochemical markers of coagulation activation in mitral stenosis, atrial fibrillation, and cardiomyopathy
Authors: Ikeda Uichi , Yamamoto Keiji , Shimada Kazuyuki
Published: February 2009

Advances in the understanding of the biochemistry of the mechanism of hemostasis have led to the development of sensitive methods for determining levels of markers which reflect thrombin activity (thrombin‐antithrombin III complex, fibrinopeptide A, F1+2 fragment), active fibrinolysis (D‐dimer, plasmin‐α2‐plasmin inhibitor complex), and platelet activity (platelet factor 4, ß‐thromboglobulin) in vivo. Measurement of these markers may be useful in identifying patients with various cardiovascular disorders at high risk of thromboembolism.
Transesophageal pulsed doppler echocardiographic evaluation of left atrial systolic performance in hypertrophic cardiomyopathy: combinEd analysis of transmitral and pulmonary venous flow velocities
Authors: Oki Takashi , Íuchi Arata , Tabata Tomotsugu , Yamada Hirotsugu , Manabe Kazuyo , Kageji Yoshimi , Abe Miho , Ito Susumu , Fukuda Nobuo
Published: February 2009

Background: Hypertrophic cardiomyopathy (HC) is characterized by impaired left ventricular (LV) diastolic function due to an increase in LV wall thickness. The severity of this disease varies depending on the localization and extent of the hypertrophied myocardium and the presence and extent of myocardial disarray or fibrosis.

Hypothesis: The purpose of this study was to examine the background of hemodynamic abnormalities between the left atrium and the left ventricle during atrial systole in patients with HC using pulsed Doppler echocardiography.

Methods: Hemodynamic abnormalities between the left atrium and left ventricle during atrial systole were evaluated in patients with HC using transmitral flow (TMF) and pulmonary venous flow (PVF) velocities obtained by transesophageal pulsed Doppler echocardiography. The study population included 50 patients with HC, including 39 with asymmetric septal hypertrophy and 11 with apical hypertrophy, and showing fractional shortening of the left ventricle ≥ 30%. They were classified into three groups: (1) Group A (n = 11): the ratio of the late to early TMF velocity < 1, and peak atrial systolic PVF velocity (PVA) < 25 mm/s;(2) Group B (n = 13): their ratio < 1, and PVA ≥ 25 mm/s;and (3) Group C (n = 26): their ratio ≥ 1. The mean age of patients in Group A was lower than that in Groups B and C.

Results: Left atrial dimension in Group B was significantly greater than that in the other HC groups and the control group. Furthermore, left atrial volume changes during atrial systole in Group B were significantly smaller than those in the other HC groups and the control group. Peak atrial systolic PVF velocity in Group B was significantly higher than that in the control group and in Group C. The duration of the atrial systolic waves of the TMF and PVF in Group B was significantly shorter and longer, respectively, than that in Group A. Left ventricular end‐diastolic pressure (LVEDP) decreased in descending order with Group B > Group C > Group A. In all patients there was a significant positive correlation between the LVEDP and peak atrial systolic PVF velocity or the difference in duration between the atrial systolic waves of PVF and TMF. Plots of these values shifted toward the left and inferiorly in Group A, and toward the right and superiorly in Group B.

Conclusion: Peak velocity and duration of TMF and PVF during atrial systole by transesophageal pulsed Doppler echocardiography are useful indices of hemodynamic abnormalities between the left atrium and the left ventricle during atrial systole, particularly a forceful atrial contraction mismatched to the left atrial afterload and severity of LV diastolic dysfunction, in HC.
Creatine kinase isoforms as circulating markers of deterioration in idiopathic dilated cardiomyopathy
Authors: Hossein‐Nia Mojgan , Holt David W. , Mckenna William J. , Baig Kamran , Goldman Jonathan H , Keeling Philip J , Caforio Alida L.P.
Published: February 2009

Background: A proportion of patients with dilated cardiomyopathy (DCM) may have ongoing myocardial damage secondary to viral or immune mediated myocardial inflammation.

Hypothesis: The prognostic determinants identify patients with decreased survival but do not provide a measure of myocardial damage. To obtain an objective assessment of myocardial damage in DCM, we measured plasma levels of creatine kinase (CK), its isoenzymes (CK‐MM and CK‐MB), and separated the isoforms of CK‐MM and CK‐MB.

Methods: The cohort consisted of 77 consecutive patients (61 men, 16 women) with DCM (World Health Organization criteria), aged 49 ± 14 years (range 19–60). Patients had been symptomatic for 29 ± 38 months (range 0.5–200 months) with 48 in New York Heart Association class I/II and 29 in class III/IV at the time of diagnosis. During median follow‐up of 27 months from diagnosis (range 0.6–165), 50 patients remained clinically stable and 27 had deteriorated.

Results: A significantly higher proportion of patients with DCM had abnormal MB2/MB1 ratio compared with normal volunteers (11,14% vs. 1, 1%, p = 0.003). Patients who deteriorated had higher MB2/MB1 ratio, (1.22 ± 0.62 vs. 0.85 ± 0.56;p = 0.01), and more frequently had abnormal MB2/ MB1 ratio (8,30% vs. 3,6%;p=0.004) and CK and CK‐MM activities (5, 19% vs. 2, 4%;p = 0.03) than those who remained stable. Patients with DCM with high CK‐MB activity had 3.13‐fold increased odds of sudden death or need for cardiac transplantation (95% confidence interval 1.53–6.40, p = 0.008). Thus, CK measurements, in particular CK‐MB isoforms, are markers of myocardial damage in a subset of patients with DCM and could be useful in investigating the possibility of persistent myocardial damage in these patients.