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

208 hospitalized patients, nearly 80 years old, were investigated because of risk factors and complicating diseases. Hypertension (58.2%), typical myocardial infarctions (37.2%) and diabetes (45.2%) were twice often as in our comparable cases without stroke. Corresponding we found signs of left ventricular hypertrophy in more than 50% post mortem. The dimensions of heart failure by hypertension are visible in ECG indicating LVH with many dysrhythmias. Early mortality (40%) as survival time are dependent on the size of the stroke. Cardiovascular causes of death were found mainly. The differences to younger patients with brain infarction seem to be only of gradually nature and especially to refer to the more intensive damaged heart.
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PMID:[Survived brain infarction in old age - clinical and morphological findings. II. Risk factors (author's transl)]. 3 Mar 24

Hemodynamic effects of isoproterenol, dopamine, and epinephrine were studied before and after acute beta-adrenergic blockade in 16 open-chest, anesthetized mongrel dogs. Beta blockade was induced with 1 mg. per kilogram of intravenous propranolol. Cardiac output measurements were obtained by thermal dilution, and pressure recordings were obtained in the right ventricle, pulmonary artery, left atrium, left ventricle, and aorta. Derived parameters included stroke volume, pulmonary and systemic vascular resistances, and peak left ventricular dP/dt. In the presence of propranolol, epinephrine became a lethal drug in large doses and did not increase cardiac output in standard doses. Dopamine, in 25 to 50 mcg. per kilogram per minute doses, increased arterial pressure and systemic resistance; cardiac output was diminished compared with dopamine, 10 mcg. per kilogram per minute, prior to propranolol, as a result of increased resistance and decreased LV contractility. Isoproterenol, 0.6 to 0.9 mcg. per kilogram per minute, 15 to 20 times standard dosages, had moderately positive inotropic effects and increased cardiac output. Left ventricular systolic pressure with isoproterenol after propranolol was reduced when compared with effects of smaller doses prior to propranolol. These observations suggest that none of the catecholamines studied would be optimal for circulatory support in heart failure in the presence of propranolol. The present results define a pharmacologic basis for design of appropriate drug combinations for circulatory support in beta-blocked animals.
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PMID:Pharmacologic antagonism of beta-adrenergic blockade in dogs. I. Hemodynamic effects of isoproterenol, dopamine, and epinephrine in acute propranolol administration. 3 98

The heart of the old hemiplegic patient is examined as follows: 1. The preapoplectic situation of the heart which often induces in a conclusive manner the beginning of a stroke, 2. the occurrence of heart troubles with the stroke itself and 3. the influence of rehabilitation measures and the heart function. Preexistent heart troubles are very frequent (in ca. 80%). Thereby the hypertension with a left ventricular hypertrophy and later with heart failure play an important role. The stroke itself especially in subarachnoidal bleedings can cause severe electrocardiographic anomalies. The telemetric controlled heart shows specially while rehabilitation more extrasystoles and alterations of repolarisation but usually do not impair the rehabilitation. With a systematic rehabilitation (training) the heart is most favourably influenced.
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PMID:[The heart of the old hemiplegic patient (author's transl)]. 3 57

The haemodynamic effects of the carboxylic ionophore monensin have been examined in cats anaesthetized with sodium pentobarbitone. Marked increases in left ventricular dP/dtmax (and dP/dt at fixed isovolumic pressures) and slight increases in cardiac output and stroke volume occurred, indicating increased myocardial contractility. Heart rate was unchanged but systemic arterial pressure was substantially increased. Satisfactory increases in contractility and arterial pressure were obtained when monensin was infused intravenously in a total dose of 0.25 mg kg-1 over 10 min. Larger doses, especially if rapidly injected, resulted in very marked increases in myocardial contractility leading eventually to cardiac failure. The haemodynamic effects of monensin were markedly reduced during shock induced by E. coli endotoxin and there was unfortunately no evidence to suggest that this extremely potent compound might be potentially beneficial in this form of profound cardiovascular shock.
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PMID:Haemodynamic effects of the carboxylic ionophore monensin when administered before and during shock induced by E. coli endotoxin. 4 Oct 57

A case of an acutely beginning histologically proved panarteritis is described which was initiated by hepatitis B caused by blood transfusions. After one year of steroid therapy the arteritis was no longer seen histologically, Australia-antigen became negative. Terminally the patient developed an apoplexy, renewed gastric bleeding, septicemia with obstructive jaundice, nose bleeding, increasing renal insufficiency, and cardiac failure. The Australia-antigen reappeared in the serum. It could be assumed that the panarteritis had progressed. Immune complexes of Australia-antigen and corresponding antibodies which are deposited in the vascular wall and cause an inflammatory reaction, are being held responsible for the panateritis. They were proved serologically and by immunofluorescence in the vascular wall. In cases of panarteritis of unknown origin Australia-antigen can be found in a high percentage, as was demonstrated by a second case.
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PMID:[Hepatitis-B-surface antigen and panarteritis (author's transl)]. 4 44

The use of vasodilators represents a new approach in the treatment of heart failure. These drugs have the property of causing vasodilatation of either arterial or venous predominance or balanced between these two vascular beds. Arterio-dilators (phentolamine, hydralazine) increase stroke volume and cardiac output by decreasing ventricular afterload. Veno-dilators (nitroglycerine) have little effect on cardiac output but decrease ventricular filling pressure, thereby relieving pulmonary venous hypertension. Mixed vasodilators (Sodium nitroprussideate, trimetaphan) combine these two groups of properties in various degrees. The majority of these drugs can only be administered intravenously, with careful haemodynamic surveillance.
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PMID:[The treatment of congestive heart failure by using vasodilators. I. Physiological basis. Different vasodilators (author's transl)]. 9 22

In a study designed to investigate potential non-parenteral treatment for chronic heart failure, hydrallazine, 225 to 300 mg per day, was given orally to 9 patients. There was no significant change in heart rate or mean arterial pressure as cardiac output increased. Left ventricular stroke work increased significantly and pulmonary artery wedge pressure fell. Systemic and pulmonary vascular resistances fell. With the addition of 2 per cent glyceryl trinitrate paste, there was a further decline in mean pulmonary arterial and wedge pressures, without a significant change in heart rate, arterial pressures, cardiac output, or systemic or pulmonary vascular resistance. There were no untoward effects from either form of treatment. All patients reported relief of shortness of breath and other symptoms related to ventricular dysfunction. This study supports the suggestion that oral hydrallazine is effective in increasing cardiac output and decreasing pulmonary congestion. Furthermore, the addition of topical glyceryl trinitrate provides a greater reduction of pulmonary pressures, probably through its predominant venodilator action. In some selected patients with heart failure, oral hydrallazine and topical glyceryl trinitrate in combination produce beneficial clinical and haemodynamic effects, probably through afterload and preload reduction, respectively.
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PMID:Haemodynamic effects of hydrallazine and of hydrallazine plus glyceryl trinitrate paste in heart failure. 9 55

It has been shown that hydralazine is beneficial in chronic heart failure by virtue of its afterload reducing effect. Nitroglycerin paste results in venodilation and fall in left ventricular filling pressure (LVFP). Thirteen patients with chronic heart failure were given a combination of oral hydralazine and nitroglycerin paste. With oral hydralazine (75 to 100 mg every 8 h), left ventricular stroke work increased and LVFP slightly fell. Following addition of 2% nitroglycerin paste, an additional decline in mean pulmonary artery and LVFP was observed without significant changes in heart rate and arterial pressure. There were no untoward side effects from either therapy. Eight patients followed for three to eight months (mean five months) reported subjective improvement in shortness of breath and other symptoms related to ventricular dysfunction. This study shows that in certain patients with chronic heart failure, hydralazine and nitroglycerin paste combination produces salutary clinical effects on long term probably through afterload and preload reduction, respectively.
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PMID:Non-parenteral combined afterload and preload reduction therapy in congestive heart failure. 11 91

In acute and chronic left heart failure peripheral resistance is elevated due to increased sympathetic tone. This should compensate the decrease in stroke volume. In the diseased left ventricle however the augmentation of afterload leads to further reduction of stroke volume and to increase of heart size and myocardial oxygen consumption. This vitious cycle may be interrupted by vasodilators. Drugs like nitroglycerin, mainly acting on the venous system, reduce preload and thereby relieve symptoms of pulmonary congestion (backward failure). Phentholamin on the other hand primarily reduces afterload by an action on the resistance vessels and thereby increases cardiac output (forward failure). Nitroprusside has effects on both, the capacity and resistance vessels. So nigroglycerin is the remedy of choice in acute pulmonary edema. Nitroprusside in leftf heart failure in acute myocardial infarction and Phentolamin in acute left ventricular failure due to critical rise in blood pressure. For long term treatment of chronic left heart failure (coronary heart disease, cardiomyopathy, rheumatic heart disease) hydralazin or prazosin may be used as well as long acting nitrates.
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PMID:[Progress in the therapy of acute and chronic cardiac insufficiency by means of systemic vasodilators. Studies with prazosin and nitroglycerin]. 12 80

In almost all of the cases of cardiac hypertrophy due to sustained hypertension, left ventricular capacity is increased in proportion to increased left ventricular weight, even in the absence of manifest cardiac insufficiency. The condition is regarded as the general expression of cardiac response to pressure load, and the concept of "isomorphic hypertrophy" is proposed. Concentric hypertrophy of the current concept is observed only on rare special occasions, and its role in cardiac adaptation to pressure load is obscure. The increase in myocardial mass is sufficient to maintain the work done by a unit myocardial volume at a normal level. However, the calculation on pertinent models demonstrates that hypertrophied hearts of any type expel the normal stroke volume with smaller shortening of muscle fibers under larger stress, which is further elevated with the progress of cardiac contraction. Because the maximum force generated by muscle fibers declines with advancing cardiac contraction, hypertrophied hearts harbor a latent risk of mechanical insufficiency. Even under pressure load, ventricular dilation seems to precede the re-inforcement of ventricular wall in the development of cardiac hypertrophy. A common mechanism may be therefore assumed underlying the development and performance of all types of hypertrophied hearts, regardless of the difference in the character of physical loads.
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PMID:Quantitative analysis of cardiac hypertrophy due to pressure load in reference to the relations of blood pressure, left ventricular weight and left ventricular capacity. 13 18


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