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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitroglycerin reduces elevated left ventricular filling and pulmonary arterial pressures in resting patients with rheumatic valve disease and reduces symptoms when given over long periods to patients with primary myocardial disease. To determine whether nitroglycerin may prove effective therapeutically in ambulatory patients with heart valve disease, its effects on hemodynamics and exercise capacity were studied in 11 severely symptomatic adults who were already receiving optimal treatment with digitalis and diuretic agents. Seven had predominant mitral valve disease, one had predominant aortic insufficiency and three had equally severe mitral and aortic valve disease. Maximal exercise capacity was assessed with graded treadmill exercise after placebo and after nitroglycerin (0.5 mg sublingually) administered in random sequence to each patient. Exercise capacity (exercise time to limiting fatigue or dyspnea) increased from a mean of 8.3 minutes after placebo to 9.8 minutes after nitroglycerin (P less than 0.005). Eight patients were studied hemodynamically during further intense treadmill exercise. Pulmonary arterial pressure was significantly lower (P less than 0.05) after nitroglycerin than after placebo (mean 44 versus 56 mm Hg), but cardiac output was greater after nitroglycerin (5.0 versus 4.6 liters/min, P less than 0.005). Thus, nitroglycerin appears to increase exericse tolerance and improve the hemodynamic response to exercise in patients with heart valve disease and may be valuable in the long-term pharmacologic therapy of such patients.
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PMID:Nitroglycerin-induced improvement in exercise tolerance and hemodynamics in patients with chronic rheumatic heart valve disease. 41 13

In order to determine their exercise tolerance, 20 patients with artificial ventricular demand pacemakers below the age of seventy were studied by bicycle ergometry. Only 30% of the patients showed a normal exercise tolerance according to the criteria by Kaltenbach, while 70% stopped the test prematurely because of leg fatigue, dyspnoe or chest pain. In terms of their exercise tolerance, there was no difference between patients who developed normal sinus rhythm or rapid atrial fibrillation during the exercise and those who remained at the fixed pacemaker rate throughout the test. It is concluded, therefore, that the exercise tolerance of pacemaker-patients is not only limited by the fixed heart rate but mainly by the underlying heart disease (coronary heart disease, cardiomyopathy, hypertensive heart disease etc.) and the general physical condition of the patients. In an age-matched control group of 20 patients 50% showed a normal exercise tolerance and the duration of exercise in this group was only slightly longer (21%) than in the pacemaker-group.
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PMID:[Exercise tolerance of patients with artificial cardiac pacemakers (author's transl)]. 54 95

45 patients with an age of 3--15.5 yr are reported. Only 9 of them showed symptoms (palpitations, dyspnea, fatigue). The murmur was often uncharacteristic, only 42% had a click. ECG changes could be found in 60%. The associated cardiac lesions and the angiographic findings are represented. Correlating to an angiocardiographically LVOTO we found in 13 patients (28.9%) the echocardiographic signs of an ASH with a septum/LV posterior wall quotient of 1.45 +/- 0.15. We conclude, that myocardial disease is one pathogenetic factor in the MVPS.
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PMID:Clinical and angio- and echocardiographic findings in 45 children with mitral valve prolapse syndrome. 64 79

Mitral valve prolapse is a condition that is being recognized with increased frequency. It is not known whether its incidence is increasing, or whether we are better able to diagnose it today. In the idiopathic or familial variety, the mitral valve pathology is almost always that of myxomatous degeneration. Some authors have suggested the presence of a cardiomyopathy because of significant left ventricular dysfunction in many cases. Idiopathic prolapse occurs predominantly in females, often at a young age, and may be associated with chest pain, dyspnea, fatigue, presyncope, syncope, and/or sudden death. The clinical findings are variable and typically consist of a nonejection click and/or late systolic murmur, heard best at the cardiac apex. Diagnosis can be confirmed by echocardiography and/or ventricular cineangiography, the latter permitting accurate recognition of the anatomy of the prolapsed leaflets. The complications of infective endocarditis, severe mitral insufficiency, and life-threatening ventricular arrhythmias represent the major problems of management. It is important to distinguish the idiopathic form of mitral valve prolapse from that due to coronary artery disease and to realize that mitral valve prolapse may occur in Marfan's syndrome, Turner's syndrome, or in association with secundum atrial septal defect or ruptured chordae tendineae. Typical clicks and/or murmurs have also been described in patients with a history of rheumatic fever and in hypertrophic cardiomyopathy. Although much descriptive knowledge has accumulated over the past 15 years, many unanswered questions remain regarding the idiopathic type of prolapse. What is the nature and cause(s) of myxomatous degeneration? What is the relation of the valve pathology to the left ventricular dysfunction? What is the relation of both of these factors to disabling chest pain, electrocardiographic changes, and life-threatening arrhythmias? Hopefully, answers to these and other important questions regarding mitral valve prolapse will be forthcoming.
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PMID:Mitral valve prolapse. 77 95

This report details our total experience with documented chronic His bundle block in 24 patients. Ten patients had second-degree block (eight with 2:1 block and two with type-1 block), and 14 patients had complete heart block. There were 16 women (67 percent) and eight men (33 percent) with ages ranging from 17 to 87 years. Diagnoses were as follows: hypertensive cardiovascular disease, nine patients (38 percent); arteriosclerotic heart disease, six patients (25 percent); aortic valvular disease, three patients (13 percent); primary conduction disease, two patients (8 percent); primary myocardial disease, two patients (8 percent); congenital heart block, one patient (4 percent); and traumatic heart block, one patient (4 percent). Pacing was instituted in 20 patients because of the following; congestive heart failure, seven patients; syncope, seven patients; fatigue, four patients; and recurrent dizziness, two patients. Permanent pacing was indicated within ten days of initial diagnosis in 13 patients, from 20 to 80 days in four patients, and later than 100 days in three patients. An additional two asymptomatic patients were treated with prophylactic pacing.
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PMID:The clinical spectrum of chronic His bundle block. 100 Oct 51

A novel, simple, rapid and reproducible microassay is used for kinetic analysis of Ca-sequestration by homogenates of myocardium of turkeys with furazolidone-induced congestive cardiomyopathy. The assay monitors Ca in real-time using dual-emission ratiometric spectrofluorometry and the Ca-indicator dye indo-1. Using this assay and isolated SR studies we make several novel findings regarding the mechanism of SR failure in furazolidone cardiomyopathy. Qualitative differences in Ca-sequestration were not detected between groups. However, compared to controls the furazolidone treatment resulted in: 1) 50% depression in maximal activities (1.54 +/- 0.36 vs 0.73 +/- 0.12 microM/sec); 2) 2-fold increases in post-sequestration concentrations of ionized Ca (79 +/- 23 vs 141 +/- 13 nmol Ca/L homogenate); 3) 2-fold increases in Ca half-life (415 vs 790 msec); and 4) 25% increased passive Ca-binding capacity of homogenates. The Ca-ATPase specific activity of isolated sarcoplasmic reticulum was 60% increased in congestive cardiomyopathy (543 +/- 140 vs 873 +/- 108 nmol ATP hydrolyzed/min/mg membrane protein) although membrane yield was 20% decreased (0.79 +/- 0.09 vs 0.63 +/- 0.03 mg/g heart). The increased ATPase and decreased Ca-uptake activities in combination with the occurrence of 36% cardiac hypertrophy and 19% decreased body weights resulted in estimates of the relative energy cost to the animal for myocardial Ca transport being 5.5-fold increased with cardiomyopathy (20.5 vs 111 nmol ATP hydrolyzed per microM decrease of sarcoplasmic free Ca/kg body weight). These data indicate that congestive cardiomyopathy is associated with markedly increased permeability of sarcoplasmic reticulum to Ca and compensatorily increased Ca-ATPase activity. Accelerated energy consumption due to the increased energy cost of Ca transport and increased time of myocyte activation are predicted to predispose the myocardium to fatigue and irreversible failure.
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PMID:Myocardial Ca-sequestration failure and compensatory increase in Ca-ATPase with congestive cardiomyopathy: kinetic characterization by a homogenate microassay using real-time ratiometric indo-1 spectrofluorometry. 182 61

Five patients were studied 5-13 months after dynamic cardiomyoplasty for refractory heart failure. In two, muscle flap stimulation caused a pronounced increase in cardiac index (mean 55%) and ejection fraction (mean 75%); no patient showed improvement in cardiac filling pressure. 2 years after surgery, one of the patients with haemodynamic improvement died from ventricular fibrillation, and histochemistry of the stimulated muscle flap revealed predominantly fatigue-resistant type I fibres, without evidence of fibrosis. In selected cases, dynamic cardiomyopathy could be of long-term benefit.
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PMID:Preliminary report: follow-up after dynamic cardiomyoplasty. 197 65

A case of right ventricular dilated cardiomyopathy which also involved the left ventricle was reported. On health screening, a 16-year old woman was pointed out to have multifocal PVC and cardiomegaly. Subsequently, she was admitted to our hospital because of general fatigue. CTR was enlarged to 54.9% on chest X-ray. ECG showed LBBB-type PVC, right axis deviation, low voltage and T wave changes. On UCG, RVdD was dilated to 40 mm and LVdD was 37 mm. There was no finding of abnormality of the tricuspid valve. On cardiac catheterization, there was no shunt disease. Intracardiac pressure was normal. The end-diastolic volume index (ml/m2) of RV and LV was 196.7 and 67.4, respectively. And ejection fraction (%) was 20 and 40. Ventriculography revealed diffuse dilatation of the right ventricle. And lowered contractility existed not only in the right ventricle but also in the anterior and apical segment of the left ventricle. T(1)201 myocardial perfusion imaging showed irregular perfusion defect of the left ventricle. Endomyocardial biopsy revealed marked hypertrophy, partial atrophy, disarrangement of myocyte and interstitial fibrosis of the right ventricle. This case was considered to be right ventricular dilated cardiomyopathy. It seemed to be an intermediate form of dilated cardiomyopathy since it also involved the left ventricle. It was an interesting case to illustrate the spectrum of expression of cardiomyopathy.
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PMID:[A case of right ventricular dilated cardiomyopathy, which involved left ventricle]. 228 24

This case report describes a patient with an uncommon type of mitral incompetence caused by a perivalvular communication between the left ventricle (LV) and the left atrium (LA) masked by a considerable fibrotic subvalvular aortic stenosis, endocarditis and congestive heart failure (CHF). A 64 year old farmer with a history of a systolic murmur since childhood complaining of increasing fatigue and dyspnoea, temperature over 39 degrees C, and signs of CHF was admitted and transferred to a cardiological unit. Invasive examination and continuing clinical deterioration caused urgent transfer for surgery under suspicion of a decompensated hypertrophic obstructive cardiomyopathy. Clinical investigation revealed a decompensated subvalvular aortic stenosis and a mild mitral insufficiency. At surgery the advanced fibrotic subvalvular stenosis was resected. After coming off bypass severe mitral insufficiency was detected by intraoperative analysis of the simultaneous intracavitary-pressure tracings. A midsystolic maximum of a high V-wave of the LA-pressure tracing was suggestive of an unusual reason of the mitral insufficiency. Reexploration indicated a perivalvular broad communication from the LA groove to the LV with an otherwise normal mitral valve. The communication was closed using buttressed mattress-sutures. This uncommon type of mitral incompetence via a perivalvular LA-LV communication was probably caused by endocarditis and an intramyocardial abscess in the LA-wall which subendocardially led to LV-LA communication.
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PMID:Uncommon type of mitral insufficiency caused by perivalvular communication between left ventricle and left atrium. 230 25

Two patients with similar symptoms referred for diagnosis and treatment of hepatic failure subsequently proved to have cardiomyopathy as the cause of their hepatic decompensation. Except for fatigue and edema, symptoms of congestive heart failure were absent and no history of dyspnea, orthopnea, or paroxysmal nocturnal dyspnea could be elicited. Hepatomegaly was present in both patients, but neck venous distension and hypotension were not apparent, and both patients were able to lie flat. The diagnosis of cardiomyopathy was made by echocardiogram showing global hypokinesis and low ejection fractions; right atrial pressures were markedly increased. Liver biopsies demonstrated centrilobular necrosis and congestion. Treatment for heart failure led to a prompt response in both patients with rapid return of all hepatic parameters toward normal. Paradoxically, our patients had striking evidence of hepatic failure and a notable absence of symptoms and signs of congestive heart failure. An awareness of this unique presentation may avoid prolonged evaluations in such critically ill patients.
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PMID:Cardiomyopathy unrecognized as a cause of hepatic failure. 236


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