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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mitochondrial calcium uptake, but not binding, like microsomal calcium uptake in failing human hearts, was less than the control values for dog, rabbit, and hamster hearts. Decrease in mitochondrial calcium binding and uptake was observed in genetically myopathic hamsters (BIO 14.6) at early, moderate, and late stages of congestive heart failure. Inhibitors of mitochondrial calcium transport, Dicumarol, dinitrophenol, and sodium azide, were found to produce a rapid fall in contractility of the isolated rat heart. Inability of rat hearts to generate contractile force on perfusion with Na+- or K+-free medium was associated with an increase in mitochondrial calcium uptake. A dramatic increase in mitochondrial calcium uptake was observed on perfusing rat hearts with control medium after CA++-free medium. No change in mitochondrial calcium uptake was noted in acute ischemic dog myocardium or hypoxic rat heart in which contractile force was severely depressed. Both mitochondrial calcium transport and contractility were decreased on perfusing rat hearts with substrate-free medium; however, the change in calcium uptake was secondary to the fall in contractile force. Decrease in pH, ATP:ADP ratio, ATP6AMP ratio, and K+:Na+ ratio were found to reduce the dog heart mitochondrial calcium uptake. It is likely that various factors such as pH, ATP:ADP ration, ATP:AMP ratio, and K+ :Na+ ration, in addition to damage in mitochondrial structure, play an important role in inhibiting mitochondrial calcium transport in failing hearts. The results also suggest that alterations in mitochondrial calcium transport are dependent upon the degree and type of heart failure.
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PMID:Role of mitochondrial calcium transport in failing heart. 5 79

Twenty-three patients with recurrent ventricular tachycardia or ventricular fibrillation, or both, were treated with aprindine, a new antiarrhythmic agent. It was found that: (1) no patient had a recurrence of ventricular fibrillation after aprindine therapy was begun, except as a terminal event subsequent to the development of acute myocardial infarction and cardiogenic shock or refractory congestive heart failure; (2) 6 patients experienced ventricular tachycardia after the loading dose, but with continued aprindine therapy the ventricular tachycardia was suppressed in 3 of these 6 patients, and a fourth patient was asymptomatic during brief paroxysms of ventricular tachycardia; (3) in 2 patients, aprindine was ineffective and was discontinued; (4) electrical cardioversion was not required in any patient receiving aprindine; (5) premature ventricular extrasystoles were decreased in 18 of the 23 patients treated with aprindine; (6) aprindine was discontinued in 1 patient because of intolerable side effects, although ventricular arrhythmias were suppressed in this patient; and (7) 5 patients died from acute myocardial infarction or severe heart failure while receiving aprindine.
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PMID:Treatment of recurrent ventricular tachycardia and fibrillation with aprindine. 6

Digitalis and diuretics constitute conventional therapy of congestive heart failure, but systemic vasodilators offer an innovative approach in acute and chronic heart failure of decreasing increased left ventricular systolic wall tension (ventricular afterload) by reducing aortic impedance and/or by reducing cardiac venous return. Thus, vasodilators increase cardiac output (CO) by diminishing peripheral vascular resistance (PVR) and/or decrease increased left ventricular end-diastolic pressure (LVEDP) (ventricular preload) by diminishing venous tone. Concomitantly, there is reduction of myocardial oxygen demand, thereby reliably reducing angina pectoris in coronary disease, and potentially limiting infarct size and ischemia provided systemic arterial pressure remains normal. The vasodilators produce disparate modifications of cardiac function depending upon their differing alterations of preload versus impedance: nitrates principally cause venodilation (decrease LVEDP); nitroprusside, phentolamine and prazosin produce balanced arterial and venous dilation (decrease LVEDP and increase CO) provided left ventricular filling pressure is maintained at the upper limit of normal; whereas hydralazine predominantly effects arteriolar dilation (increases CO). With depressed CO plus highly increased LVEDP and increased PVR, nitrates also induce some increase of CO by reducing PVR. Combined nitroprusside and dopamine synergistically enhance CO and decrease LVEDP. Mechanical counterpulsation aids nitroprusside in acute myocardial infarction. The 30-minute venodilator action of sublingual nitroglycerin is extended for 4 to 6 hours by cutaneous nitroglycerin ointment, by sublingual and oral isosorbide dintrate, and by oral pentaerythritol tetranitrate and sustained-release nitroglycerin capsules. Ambulatory oral vasodilator therapy is provided by long-acting nitrates (relieve pulmonary congestion); hydralazine (improves fatigue); prazosin alone, combined nitrate-hydralazine combined prazosin-hydralazine (improve both dyspnea and fatigue).
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PMID:Afterload reduction and cardiac performance. Physiologic basis of systemic vasodilators as a new approach in treatment of congestive heart failure. 9 30

7 consecutive patients with congestive heart failure refractory to standard therapy were treated with nitroglycerin ointment (GTNO). The pulmonary wedge pressure decreased from a control value of 30+/-1 to 15+/-1 mm Hg (mean +/-SEM), and the arteriovenous oxygen difference narrowed from 6.8+/-0.5 to 5.5+/-0.3 ml%, after GTNO therapy. The heart rate decreased in 5 patients and the systolic blood pressure was either unchanged or decreased slightly. A reduction in the echocardiographic end diastolic dimension was noted in all patients. The transmyocardial gradient (systemic artery diastolic pressure - pulmonary artery wedge pressure) increased in all except 1 subject. The double product decreased in 5 of the 7 patients. Hemodynamic improvement was maintained for 4.5-7 h. All patients were symptomatically improved on chronic GTNO treatment. Our results indicate that GTNO is a useful agent in the management of heart failure which is unresponsive to standard therapy.
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PMID:Use of nitroglycerin ointment in congestive heart failure. Results of acute and chronic therapy. 10 Feb 19

The case of a 50 year old male with the Fiessinger-Leroy-Reiter syndrome, ankylosing spondylitis and generalised pustular psoriasis is reported. This condition wax complicated by non-obstructive cardiomyopathy, congestive cardiac failure and first-degree atrioventricular block, the site of which was localised by electrophysiological studies (nodal block with an infrahisian conduction defect). After failure of several therapeutic regimes, a spectacular improvement was obtained with Methotrexate associated with a diuretic; the signs of heart failure regressed and the cardiomyopathy stablised. A parallel improvement was seen in the skin, cardiac and articular lesions and has been maintained with an 18 months follow-up. Left ventricular performance was studied by echocardiography. The mechanism of the beneficial effect of Methotrexate is unclear; this therapeutic trial is to be extended to include other cases of primary cardiomyopathy without obstruction.
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PMID:[Fiessinger-Leroy-Reiter syndrome with non-obstructive cardiomyopathy treated with methotrexate]. 11 79

Two young Black female patients with pulmonary valve stenosis and intact ventricular septa are presented in protracted congestive cardiac failure with severe tricuspid insufficiency and, in one, atrial fibrillation. Right ventricular systolic dysfunction was manifested by peak systolic pressures below systemic level, raised end-diastolic pressures and low cardiac output, but without right-to-left shunt. These findings are in strong contrast to those found in most patients with pulmonary stenosis of long standing, where persistent impairment of right ventricular function is diastolic with a high end-diastolic pressure and reversal of an interatrial shunt which result from poor right ventricular compliance. Evidence of left ventricular dysfunction was also present in both cases. Protracted heart failure in these patients is believed to have been the result of coincidental cardiomyopathy in a racial group highly predisposed to this disorder. A diagnostic appreciation of this phenomenon is important in the evaluation of heart disease in the Black, since cardiomyopathy may modify or even mask the features of the underlying disorder.
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PMID:Pulmonary stenosis and impaired myocardial function. 12 85

There has been many studies on myocardial catecholamine (CA) in congestive heart failure and ishemias heart disease. However, it has been mainly studied pharmacologically and biochemically and has not been elucidated completely the local change of CA of the myocardium. CA in sympathetic nerves was first stained fluorescence histochemically by Falck-Hillarp in 1962, and many observations were made on its distribution and morphologically concentration of CA in tissue was also observed. Furthermore, the fluorescence histochemical simplified method (cryostat method) by Laties and Jacobowitz was published in 1967. This cryostat method produced the same good preparation instead of the freezed dried method of Falck-Hillarp and could be used semi-quantitatively for the determination of CA concentration in tissue. The author examined fluorescent-histochemically the distribution of CA in sympathetic nerve endings of the myocardium of animals (mouses, rabbits and dogs). After the administration of several agents and in some pathologic conditions, those were in the hypertrophied heart and impending heart failure, in myocardial infarction and A-V block. Furthermore, the change of CA in the myocardium was examined biochemically by von Euler method and its results were compared with the results of fluorescence-histo chemical method.
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PMID:[Catecholamine in the myocardium; a fluorescence histochemical study]. 12 82

A 63-year-old woman presented with progressive congestive heart failure and unexplained cardiomegaly. Diagnostic workup revealed large arteriovenous fistulae in the lower pole of the left kidney. A total left nephrectomy was performed and microscopic exam revealed renal cell carcinoma. Following surgery, the congestive heart failure cleared and the patient has been asymptomatic for one year. The pertinent findings of the 22 patients who have been reported previously in the literature with arteriovenous fistulae complicating renal cell carcinoma are reviewed. Thirty percent of the patients presented with cardiovascular complaints, and 60% had significant cardiovascular findings during the course of evaluation. An abdominal bruit was the most discriminating finding on physical exam, and it occurred in 72% of the reported cases. The diagnosis was unexpectedly established by surgery in 13%, and by angiography in 87% -- usually in the course of a workup for hypertension, abdominal pain, hematuria, or during search for an occult malignancy. An extensive evaluation is required for early diagnosis of this correctible cause of hypertension and heart failure.
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PMID:Arteriovenous fistulae secondary to renal cell carcinoma. Clinical and cardiovascular manifestations: report of a case. 12 58

Nine cases of the combination of coarctation of the aorta and mitral stenosis were evaluated over a seven-year period. Symptoms did not usually cause distress in infancy, but began subtly with pneumonia or cardiac failure at about 2 years of age. Important clues were differences in blood pressure between the arms and legs, paroxysmal dyspnea, congestive heart failure, right ventricular hypertrophy, and left atrial enlargement. Cardiac catheterization studies showed elevated right ventricular and main pulmonary artery wedge pressures. These features in patients with coarctation of the aorta should suggest associated mitral valve disease. The importance of demonstrating associated valvular lesions, particularly mitral stenosis, is emphasized. Two of our children had successful repair of the coarctation of the aorta and mitral stenosis simultaneously. In a third child, resection of the coarctation was followed in six years by mitral valve replacement.
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PMID:Associated coarctation of the aorta and mitral valve disease: nine cases with surgical correction of both lesions in three. 12 22

A study of 55 patients with heart disease suspected of being viral in origin was carried out a Medical College Hospital, Nagpur, over a period of 2 years. Virus studies as well as other routine tests were carried out on all patients. In 19 patients a virus aetiology of the heart disease was proved by isolation of one of the subtypes of Coxsackie B virus and/or on the basis of fourfold rise in neutralizing antibody titre in paired sera. Of these patients, 5 had acute myocarditis and 5 had acute myopericarditis; 3 had acute pericarditis; 3 had congestive cardiac failure of obscure aetiology; 2 had pleuropericarditis, and the remaining 1 developed post-partum heart failure with cardiogenic shock. All had electrocardiographic abnormalities. Thirteen had cardiomegaly; 1 had a right-sided pleural effusion and 2 had pericardial effusion. Virus could not be isolated from pericardial fluid or pleural fluid in these 3 patients. Follow-up studies up to 10 weeks from discharge revealed that 8 patients were clinically normal but 4 of these 8 had persisting ST-T wave changes, and in 4 the electrocardiogram had returned to normal. Of the remaining 11 patients, 3 had persistent chronic heart failure, 3 had vague symptoms of praecordial pain but no abnormal signs, and 5 patients were lost to follow-up.
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PMID:Heart disease caused by Coxsackie virus B infection. 12 98


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