bluuebunny/crossref_metadata_2025_split huggingface dataset:
Long‐term prognostic value of a normal dipyridamole thallium‐201 perfusion scan
Authors: Gal Rami A. , Gunasekera Joseph , Massardo Teresa , Shalev Yoseph , Port Steven C. 
Published: February 2009

AbstractIn a 4‐year period, 84 patients who were referred for a dipyridamole thallium‐201 stress test to rule out significant coronary artery disease had normal scans. A dipyridamole study was recommended instead of exercise because of arthritis, severe obesity, peripheral vascular disease, pulmonary disease, other chronic illnesses, or combinations of these problems. All patients had three‐view (i.e., anterior, shallow left anterior oblique, and steep left anterior oblique) planar thallium‐201 imaging 10 minutes and 3.5 hours after administration of 0.6 mg/kg of intravenous dipyridamole. The patients were followed for 42±13 (range 1–58) months to document the cardiac event rate. Of the 84 patients with normal results, 14 died during the follow‐up period from noncardiac causes. Three other patients died 29–51 months after the test due to an acute myocardial infarction, a probable acute myocardial infarction, and sudden cardiac death, respectively. Of the survivors, 5 suffered an acute myocardial infarction 28–50 months after the dipyridamole thallium scan and 1 had coronary artery bypass grafting due to increasing angina pectoris 58 months after the scan (overall cardiac event rate of 0.4% per year). Of the remaining 61 patients, 39 (64%) were asymptomatic, 20 (33%) had the same symptoms they had at the time of testing without significant deterioration, while 2 patients (3%) had deterioration of their chest pains but no cardiac complication. Thus, in this group of patients, a normal dipyridamole thallium‐201 perfusion scan predicted a good cardiovascular outcome for at least 24 months following the test.
Development and progression of aortic valve stenosis: Atherosclerosis risk factors—a causal relationship? a clinical morphologic study
Authors: Mohler Emile R. , Nichols R. , Harvey W. P. , Sheridan M. J. , Waller B. F. , Waller Bruce F. 
Published: February 2009

AbstractHospital records of 120 patients undergoing aortic valve replacement were retrospectively reviewed for risk factors associated with early aortic valve replacement. Patients were separated into four groups (rheumatic, congenital bicuspid, degenerative, and miscellaneous) based upon the morphologic etiology of aortic stenosis. Multiple regression analysis was performed using age at surgery as the dependent variable. Independent variables for the study were race, gender, systemic hypertension, total triglyceride level, total serum cholesterol level, tobacco smoking history, diabetes mellitus, and angiographic coronary artery disease. In the rheumatic valve group only race showed a statistically significant risk effect whereas in the congenital bicuspid valve group race, gender, and triglycerides were statistically correlated with age at surgery. In the degenerative valve group gender and smoking were found to be statistically significant risk factors. The establishment of aortic stenosis risk factors might be an indication for clinical trials of risk factor modification in patients with aortic stenosis.
Electromechanical concordance in alternans during sustained tachycardias
Authors: Tai Yau‐Ting , Lau Chu‐Pak , Chow Wing‐Hing , Leung Wing‐Hung 
Published: February 2009

AbstractElectrical alternans and mechanical alternans are intriguing phenomena that have been reported to occur during tachycardias. Their precise pathophysiologic mechanism and in particular their interrelation have not been well defined. This report documents an unusual electromechanical concordance in alternans during sustained supraventricular tachycardia and ventricular tachycardia in two patients, raising interesting possibilities on the underlying mechanism of the concordant phenomena. The findings highlight the principle of excitation‐contraction coupling of the heart.
Limited clinical utility of endomyocardial biopsy in patients presenting with ventricular tachycardia without apparent structural heart disease
Authors: Oakes David F. , Manolis Antonis S. , Mark III N. A. Estes 
Published: February 2009

AbstractTo determine the cardiac pathology underlying ventricular tachyarrhythmias, endomyocardial biopsy was performed in 14 patients, 10 men and 4 women, with a mean age of 40 years (range 17–63) and no apparent structural heart disease, presenting with high‐density symptomatic nonsustained ventricular tachycardia (VT) (n = 4), sustained VT (n = 6), and ventricular fibrillation (n=4). The absence of coronary or valvular heart disease was documented by cardiac catheterization. The mean left ventricular ejection fraction was 56±10%. Noninvasive assessment of the ventricular arrhythmia was made in all patients with Holter monitoring and/or exercise testing, while invasive evaluation with programmed electrical stimulation was performed in 13 patients. Biopsy findings included subendocardial and interstitial fibrosis in 7 patients, and monocytes containing periodic acid Schiff (PAS) positive vacuoles in 1 patient; biopsy was normal in 6 patients. There was no relationship between the presence or absence of pathologic abnormalities on biopsy and left ventricular ejection fraction, presenting or induced arrhythmias, or prognosis. Pathologic evidence supporting a specific treatable diagnosis was not present in any biopsy. Drugs to suppress spontaneous (3 patients) or induced (8 patients) VT were instituted, while 2 patients were not treated. In 1 patient who was resuscitated from out‐of‐hospital cardiac arrest an automatic defibrillator was implanted. In 24.6 months of mean follow‐up there was 1 nonfatal arrhythmia recurrence, 1 noncardiac death, and 1 sudden death in a patient with fibrosis on biopsy, an ejection fraction of 45%, and both inducible and spontaneous sustained VT suppressed with an antiarrhythmic agent. We conclude that endomyocardial biopsy in patients presenting with VT and no coronary or valvular heart disease can be normal, rarely demonstrates a specific treatable diagnosis, and thus has limited clinical utility.
An evaluation of the safety of the β‐modulator cicloprolol in chronic heart failure
Authors: Cocco G. , Alfiero R. , Pouleur H. 
Published: February 2009

AbstractThe new β‐adrenoceptor partial agonist cicloprolol acts as a β‐agonist at normal levels and as a β‐antagonist at high levels of adrenergic discharge. Treatment with cicloprolol should protect the heart against excessive stimulation, while providing a baseline level of sympathetic drive. The clinical interest of such a profile is, however, not yet established in heart failure. Accordingly this study examined the safety of oral cicloprolol, a step necessary before undertaking efficacy comparison with other compounds recently proposed to treat heart failure. Twenty‐five patients were studied. Cicloprolol was given once a day for 2 weeks in a crossover double‐blind placebo‐controlled design. Follow‐ups were obtained at baseline and at the end of each period. At baseline all patients had clear evidence of heart failure. Cicloprolol did not affect resting heart rate and blood pressure, but it reduced significantly peak exercise heart rate and peak rate‐pressure product. The effect was especially significant in patients with sinus rhythm. The drug did not induce bradycardia or arrhythmias. Resting and exercise ejection rate were not affected. Cicloprolol improved the quality of life and the work capacity of 5 of 12 patients with congestive failure due to ischemic etiology. Side effects were few and similar with placebo and cicloprolol. Thus, short‐term administration of cicloprolol is safe in moderate heart failure.
Paradoxical effect of long‐term treatment of nifedipine on total ischemic load in patients with stable angina pectoris
Authors: Radice Maria , Giudici Vittorio , Albertini Alberto , Mannarini Alberto 
Published: February 2009

AbstractIn 50 patients with stable effort angina the effect of three drugs, metoprolol, nifedipine, and diltiazem was assessed by analyzing exercise stress test response and ambulatory ECG recordings. Both metoprolol and diltiazem caused a significant increase in time to ischemic threshold during exercise and a significant decrease of maximum ST‐segment depression (during exercise and ambulatory ECG monitoring) and in the average number of daily ischemic episodes. Only metoprolol significantly reduced heart rate and rate–pressure product at the ischemic threshold during exercise. In the group of patients treated with nifedipine no significant improvement was observed in exercise tolerance or in number of ischemic episodes/24 h. Moreover, the subset of nonresponders in the two methods was larger than in the other two groups. In some of these patients a clearcut worsening of total ischemic load was observed, despite the control of symptoms. This adverse effect might be attributed to the different consequences of the vasodilatory effect of nifedipine on blood flow through stenosed vessels.
Is hypomagnesemia arrhythmogenic?
Authors: Millane Teri A. , Ward David E. , Camm A. John 
Published: February 2009

AbstractAn understanding of the role of magnesium in cardiac conduction is complicated by the multiplicity of intracellular events coordinated by the magnesium ion. Several reports have cited magnesium deficiency as the cause of a variety of ventricular and supraventricular arrhythmias. On further inspection, the circumstances of each report strongly suggest the coexistence of significant potassium depletion; isolated hypomagnesemia as a cause of arrhythmia is not reported. This discussion brings together new data from basic science with that of clinical research to refute the suggestion that isolated hypomagnesemia is arrhythmogenic. However, there is sufficient evidence to indicate that hypomagnesemia will significantly exacerbate the proarrhythmic effect of hypokalemia, particularly if occurring in the presence of digoxin toxicity. Potassium and magnesium depletion are commonly concomitant, and simultaneous repletion of both ions in the presence of hypokalemia‐induced arrhythmia would be both logical and effective. The beneficial effects of intravenous magnesium in the acute control of ventricular tachyarrhythmia are concluded to occur as a result of a separate antiarrhythmic action, quite independent of underlying magnesium balance.
Very early acute myocardial infarct treated with streptokinase and balloon angioplasty
Authors: Hackel Donald B. , Wagner Galen 
Published: February 2009

AbstractA 57‐year‐old man developed anginalike chest pain for the first time but there was no objective evidence of an infarct (i.e., EKG and serum enzymes were normal). After 12 days the pain increased, but EKG and serum enzymes remained normal (“preinfarct,” crescendo, unstable, or accelerated angina). At this time a cardiac catheterization showed 90% occlusion of the left anterior descending (LAD) coronary artery. On the 17th day after the onset of pain, severe pain recurred together with an abnormal EKG and the patient was taken immediately to the laboratory where a total occlusion of the LAD was now found and he was treated with intracoronary streptokinase. The artery remained open for only a short time, and balloon angioplasty was performed. However, the patient died 12 hours after onset of the last episode of severe pain. A very early acute myocardial infarct was diagnosed at autopsy together with severe coronary atherosclerosis especially of the LAD which had disruption of atherosclerotic plaques and microscopic evidence of embolization.
Adenosine's effectiveness in long RP' re‐entrant tachycardia: Additional evidence of the decremental qualities of the retrograde limb
Authors: Wienecke Matthew M. , Case Christopher L. , Gillette Paul C. 
Published: February 2009

AbstractAdenosine's ability to terminate atrioventricular (AV) re‐entrant supraventricular tachycardia is well documented. Typically, termination occurs as a consequence of transient conduction block in the atrioventricular node, a tissue with decremental qualities. However, the atrioventricular node is not always the site of action when adenosine is used on the re‐entrant types of long RP′ tachycardias. These tachycardias are, in part, characterized by the decremental qualities of the retrograde limb of the tachycardia circuit, which, in turn, are typically exemplified by retrograde Wenckebach during ventricular (VVI) pacing during intracardiac electrophysiology studies. This case report involves adenosine's ability to block conduction in the retrograde limb of the permanent form of junctional reciprocating tachycardia to provide further evidence as to the AV “nodelike” decremental qualities of this limb.
Efficacy and safety of calcium channel blockers in hypertensive patients with concomitant left ventricular dysfunction
Authors: Parmley William W. 
Published: February 2009

AbstractThe use of calcium channel blockers (CCBs) in the treatment of hypertension and concomitant left ventricular dysfunction is reviewed. Some CCBs, particularly second‐generation dihydropyridine agents such as felodipine, isradipine, nicardipine, nimodipine, and nitrendipine, have properties that enhance their usefulness in these patients. All CCBs have a similar mechanism of action. Differences in their selective action at various tissue sites determine which are most appropriate for patients with concomitant hypertension and left ventricular dysfunction. Most CCBs do not produce reflex stimulation of the heart or induce intravascular expansion. While all CCBs produce arteriolar dilation, all local beds and regional circulations in target organs are not affected equally. Most CCBs can decrease cardiac mass, and second‐generation CCBs tend to have little or no negative inotropic effects at therapeutic dosages. In addition, they increase blood flow and reduce myocardial oxygen requirements. Because of differences in functional and electrophsyiologic effects, specific CCBs may not be appropriate for all patients. Since second‐generation dihydropyridine CCBs lack clinically relevant negative inotropic effects, and have been shown to improve exercise tolerance and coronary artery perfusion, they are appropriate for hypertensive patients with left ventricular dysfunction, angina, and coronary heart disease. Second‐generation CCBs tend to lack cardiodepressant side effects and are less likely to react with digoxin than are first‐generation CCBs.
Cardiac free wall rupture in acute myocardial infarction: Ameliorative effect of coronary reperfusion
Authors: Nakamura Fumiaki , Nagano Masahiro , Higaki Jitsuo , Ogihara Toshio , Minamino Takazo , Higashino Yorihiko , Ito Hiroshi , Fujii Kenshi , Fujita Teruo 
Published: February 2009

AbstractTo investigate the pathophysiology of cardiac free wall rupture (cardiac rupture) following acute myocardial infarction (AMI), and to clarify whether reperfusion therapy prevents cardiac rupture, 1,329 cases of AMI (conventional therapy group: 807 cases and reperfusion therapy group: 533 cases) were studied retrospectively. The overall incidence of cardiac rupture was 2.3% (2.7% in the conventional therapy group vs. 1.7% in the reperfusion therapy group). Patients with cardiac rupture were divided into two subgroups according to the time interval from the onset of AMI to cardiac rupture (early rupture ≤72 h and late rupture ≥4 days). The indices of initial evolution of AMI was a significant risk of early cardiac rupture. The reperfusion therapy group showed significantly lower incidence of late rupture (0.4 vs. 1.5% in conventional therapy group; p<0.05). The incidence of cardiac rupture in the unsuccessful reperfusion therapy group was higher than that of the successful group (5.9% of 118 cases vs. 0.5% of 404 cases; p<0.05). It is concluded that the etiology of cardiac rupture following AMI cannot be explained by any single factor. Early rupture depends on the initial evolution of AMI, and early reperfusion and collateral flow prevent the late onset cardiac rapture.
Does cocaine cause coronary vasospasm in chronic cocaine abusers? a study of coronary and systemic hemodynamics
Authors: Majid Pirzada A. , Cheirif Jorge B. , Rokey Roxann , Sanders William E. , Patel Bharat , Zimmerman Janice L. , Philip Dellinger R. 
Published: February 2009

AbstractThe pathogenesis of acute myocardial ischemia or infarction following cocaine abuse is not known. Cocaine causes an increase in circulating catecholamines. Therefore alpha‐adrenergic mediated focal or generalized coronary artery spasm has been presumed to be the likely mechanism to induce ischemia. However, coronary vasospasm in chronic cocaine abusers has not been demonstrated angiographically. Moreover, it has been observed that patients commonly manifest ischemic changes hours up to a week after abusing cocaine. In order to evaluate direct effects of cocaine on coronary vasculature, 6 chronic cocaine abusers admitted with prolonged chest pain and electrocardiographic ST‐ and T‐wave changes were studied. Cocaine administered intravenously (maximum 32mg) produced subjective sensation of central nervous stimulation (the “high”) in all patients. However there was no significant change in coronary artery diameter (assessed by computer‐assisted quantitative technique), myocardial perfusion (assessed by contrast echocardiography) or left ventricular wall motion (assessed by two‐dimensional echocardiography) as compared with the baseline values. Coronary sinus flow (fhermodilution) showed an upward trend, a probable reflection of a significant increase in cardiac output (average 62%, p<0.007). Despite a significant elevation in heart rate (average 56%, p<0.007), mean systemic arterial pressure (average 12%, p<0.05) and rate‐pressure product (average 69%, p < 0.005), no symptomatic or acute electrocardiographic changes were observed. It is concluded that recreational doses of cocaine do not cause focal or generalized coronary vasospasm or reduced myocardial perfusion in patients who present with chest pain temporally related to cocaine. The results of this study are consistent with the hypothesis that cocaine‐induced activation of platelets may have an important role to play in producing myocardial ischemia by occlusion and spasm of diseased small coronary vessels; this was proven previously on biopsy and also in the initiation of acute coronary occlusion.
The effect of exercise‐induced myocardial ischemia on postischemic left ventricular diastolic filling
Authors: Stoddard Marcus F. , Johnstone John , Dillon Susan , Kupersmith Joel 
Published: February 2009

AbstractTo determine whether exercise‐induced ischemia impairs left ventricular diastolic filling in the postischemic period in humans, 101 men (mean age 57±10 years) were studied before and 2 h after a symptom‐limited thallium‐201 tomographic treadmill with pulsed Doppler echocardiography of mitral valve inflow. In the postischemic period 2 h after exercise, diastolic filling was significantly impaired in the ischemia group (reversible thallium defect; n = 24) as reflected by a decrease in the peak early filling velocity (44.5±10.1 to 39.9±9.9 cm/s, p<0.01), peak early to atrial filling velocity ratio (0.91 ± 0.27 to 0.76 ± 0.25, p<0.001), and deceleration rate of early filling (281 ± 104 to 245±86 cm/s2, p<0.01). Similar alterations in the postischemic period occurred in the myocardial infarction‐ischemia group (partially reversible defect; n = 28) as seen by a decrease in the peak early filling velocity (47.6±11.6 to 41.8±12.0 cm/s, p<0.001), peak early to atrial filling velocity ratio (0.84±0.21 to 0.68±0.18, p<0.001), and early time–velocity integral (7.06±1.78 to 5.64±2.07 cm, p<0.001). In the control group (no defects; n=33) and myocardial infarction group (fixed defect; n = 16), diastolic filling was unchanged in the postexercise period. Heart rate and blood pressure were unchanged post‐exercise in all groups. Exercise‐induced ischemia impairs diastolic filling in the postischemic period in humans. This most likely reflects impairment of diastolic function, but alterations of loading conditions cannot be completely excluded. It is possible mat recurrent episodes may chronically depress diastolic function and contribute to morbidity in subjects with coronary artery disease. The mechanism of how exercise‐induced ischemia “stuns” or impairs diastolic filling remains unclear but requires further study.
Morphologic aspects of pericardial heart disease: Part II
Authors: Waller Bruce F. , Taliercio Charles P. , Howard Jane , Green Frank , Orr Charles M. , Slack John D. 
Published: February 2009

AbstractPericardial heart disease is a common entity at necropsy. Frequently, focal areas of fibrin deposits or parietal‐visceral pericardial adhesion are observed at necropsy without previous clinical evidence of pericardial dysfunction. Some of these instances are related to clinically silent acute or healed myocardial infarction but the vast majority of cases are incidental (idiopathic) findings. The purpose of this review is to summarize various morphologic responses of the pericardium and to provide an etiologic framework for these responses. Part II will review specific morphologic responses of pericardial layers to selected diseases.
The effect of treatment on survival in congestive heart failure
Authors: Pitt Bertram , Cohn Jay N. , Francis Gary S. , Kostis John B. , Packer Milton , Pfeffer Marc A. , Swedberg Karl , Yusuf Salim 
Published: February 2009

AbstractCongestive heart failure (CHF) is a disorder characterized by a variety of clinical, biochemical, electrophysiological, and hemodynamic abnormalities. During the past two decades, numerous drugs have been employed in the treatment of this complex syndrome, and many agents have been shown to improve symptoms and ventricular function in patients with CHF. Because CHF is associated with a high risk of death, treatment should be directed not only toward the relief of symptoms, but also toward a reduction in mortality. Many variables have been shown to be related to survival; taken individually, however, each is limited in its utility in predicting prognosis. In recent years, large‐scale studies with large sample sizes have directly assessed the effects of treatment on mortality in CHF. Results from these trials indicate that vasodilators and angiotensin‐converting enzyme (ACE) inhibitors may improve mortality in patients with symptoms of heart failure. Additional trials are now in progress to evaluate the effect of treatment on patients with asymptomatic left ventricular dysfunction.