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

The interaction between cedilanid-D and metoprolol, a selective beta receptor blocking agent, on exercise tolerance and systolic intervals was studied in 15 patients with angina pectoris. The patients had been treated with metoprolol for several months in a dose of 50 mg, three times daily (one patient received 25 mg three times daily). Each patient participated in two studies separated by at least 1 week. After arriving at the laboratory each received 50 mg of metoprolol orally; thereafter, either cedilanid-D or placebo was infused intravenously in a double-blind study performed in randomized order. When the effect of the drugs was maximal, the systolic intervals and the heart volume were recorded at rest, and the exercise tolerance was tested with a bicycle ergometer. The mean maximal value of plasma concentrations of metoprolol assessed during the study was about 50 ng/ml but the variation among subjects was great (20 to 187 ng/ml). After administration of cedilanid-D there was a shortening of the pre-ejection period and left ventricular ejection time compared with results after placebo; the reduction was similar to that found after administration of cedilanid-D without beta blocking drugs. The total heart volume decreased by an average of 55 ml, but the individual variation was great. The patients' average work capacity, expressed as total work, was not altered by cedilanid-D when compared with results after placebo. No relation was found between initial heart size and the effect of cedilanid-D on capacity for physical work. It therefore appears that there is no indication for the routine use of digitalis during beta blocking therapy in patients with angina pectoris who do not have cardiac failure.
Am J Cardiol 1976 Mar 31
PMID:Effects of cedilanid-D in combination with metoprolol on exercise tolerance and systolic time intervals in angina pectoris. 0 61

Systemic hemodynamic changes and noradrenaline concentrations in coronary sinus blood were studied at rest and during work before and after acute beta-receptor blockade. Patients with congestive cardiomyopathy were compared to patients with primary valvular diseases and to healthy subjects. Noradrenaline concentrations were higher in coronary sinus blood than in arterial blood and increased after beta blockade and during work. Noradrenaline concentrations were more increased in patients with more pronounced myocardial failure and did not seem to separate patients with congestive cardiomyopathy from those with valvular disease. Patients with congestive cardiomyopathy showed a good hemodynamic tolerance toward acute beta blockade.
Clin Cardiol 1979 Dec
PMID:Effects of work and acute beta-receptor blockade on myocardial noradrenaline release in congestive cardiomyopathy. 4 91

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.
Am J Cardiol 1977 May 26
PMID:Treatment of recurrent ventricular tachycardia and fibrillation with aprindine. 6

In 9 patients with various forms of heart rhythms and rates, all of whom had a temporary pacemaker electrode inserted, several single premature ventricular contractions (PVC) with various coupling intervals (CI) were induced. The relative systolic area of the carotid pulse curve in the postextrasystolic beat was used as an indicator of the degree of postextrasystolic potentiation (PESP). A close correlation between PESP and CI was found only in sinus rhythm patients (r = -0.85). The patients with junctional and ventricular rhythms had no PESP regardless of CI or the degree of heart failure. Compensatory pause (CP) in these patients surprisingly related (r = 0.95) to heart rate, slower rates having a shorter relative CP.
Bibl Cardiol 1979
PMID:The relation of heart rhythm to postextrasystolic potentiation. 9 14

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.
Clin Cardiol 1978 Aug
PMID:Non-parenteral combined afterload and preload reduction therapy in congestive heart failure. 11 91

The purpose of the present study was to investigate the effect of the dose of nitroglycerin (NTG) on myocardial ischemic injury. In 20 closed chest dogs the anterior descending branch of the left coronary artery was occluded by inflating a balloon in its lumen. Compared with the untreated control group the sigma ST elevation was significantly lower when NTG was applied at a rate of 0.02 mg/min, but significantly higher when NTG was administered at a rate of 0.10 mg/min. In 12 patients with acute myocardial infarction NTG was infused at a rate of 3 mg in the first hour (0.05 mg/min) and 6 mg in the second hour (0.1 mg/min). Sigma ST elevation and sigma ST depression decreased during the lower infusion rate (p less than 0.001). When the rate of NTG infusion was raised to 6 mg/hr, the improvement in ST segment deviation was partially reversed. This effect, particularly evident in patients not in heart failure, was associated with a significant rise in heart rate (p less than 0.05) and a fall in diastolic arterial pressure (p less than 0.025). Patients with left ventricular failure were less sensitive to higher doses of NTG than those without failure. Thus, the effect of NTG on myocardial ischemic injury depends on the NTG dose and on the functional state of the injured left ventricle.
Clin Cardiol 1979 Apr
PMID:Nitroglycerin in acute myocardial infarction. X. Effect of small and large doses of nitroglycerin on sigma ST segment deviation -- experimental and clinical results. 12 66

Sixty-four patient with acute transmural myocardial infarction had daily echocardiograms while in the coronary care unit. Patients with previous infarction were excluded. The electrocardiographic site of infarction was anterior wall in 28, inferior wall in 33 and both anterior and inferior wall in 3 patients. Echocardiograms satisfactory for interpretation were obtained in 92 percent of cases. Abnormal left ventricular wall motion corresponding to the electrocardiographic site of infarction was seen in the echocardiogram in 84 percent of cases. Exaggerated normal motion in noninfarcted areas was seen in 30 percent. The left ventricular internal dimension correlated with clinical heart failure (P less than 0.005) and was increased in 50 percent. Abnormal mitral valve closure, which reflects increased left ventricular end-diastolic pressure, was present in 33 percent. This finding did not correlate significantly with clinical heart failure. By combining the measurements of left ventricular internal dimension and mitral valve closure, it was possible to predict hospital mortality from the echocardiograms. The results indicate that echocardiography is a useful technique in the study and management of patients with acute myocardial infarction.
Am J Cardiol 1975 Jul
PMID:Echocardiography in acute myocardial infarction. 12 33

There are two types of compensatory hypertrophy of the heart. In valvular diseases, systemic hypertension and pulmonary arterial hypertension, the resultant hypertrophy compensates the increased load on the organ and is designated as hypertrophy due to overload. In ischemic disease, hereditary cardiomyopathies and myocarditis, the hypertrophy compensates for the functional insufficiency of the damaged myocardial tissue and is designated as hypertrophy due to damage. It is shown in this paper that increase in cardiac mass in both types of compensatory hypertrophy prevents acute cardiac insufficiency but at the same time is a non-balanced form of growth. As a result, in severe hypertrophy a disturbance of normal proportions at all levels of cardiac structural integration occurs. Disturbances of this type which gradually become causes of cardiac insufficiency are the main subject of this paper.
Basic Res Cardiol
PMID:Insufficiency of hypertrophied heart. 13 57

The human heart can exceed the critical heart weight of 500 g in the course of pathological structural adaptation. This abnormal growth is performed not only by an increase in size (hypertrophy) but also in number (hyperplasia) of cardiac muscle cells. Coronary insufficiency, dilatation and chronic heart failure are noted frequently in hearts above this critical heart weight. Chronic heart failure is not a direct consequence of local destruction and scar formation following coronary insufficiency. Unlike acute cardiac dilatation with failure, chronic dilatation is not associated with stretching or overstretching of cardiac muscle cells. Starling's law is not applicable for explaining heart failure in these chronic cases. Chronic dilatation is a structural dilatation (Gefugedilatation) produced by sliding displacements (slippage) of heart muscle cells leading to a decrease in the number of muscle layers in the ventricular wall. Chronic heart failure in man therefore is rather a physical consequence of structural dilatation which severely impairs the working conditions, the efficiency and the effectiveness of the heart muscle cells than an immediate result of coronary insufficiency of inflammation with local metabolic alterations, which, of course, additionally impair the quality of the myocardium and the conducting system.
Adv Cardiol 1976
PMID:Hypertrophy, hyperplasia and structural dilatation of the human heart. 13 71

The magnitude of ventricular hypertrophy in response to afterloading is determined by wall stress, with wall thickness increasing in proportion to ventricular load until systolic wall stress is normalized. With use of echocardiographic measurements of left ventricular end-systolic wall thickness (Ws) and cavity transverse dimension (Ds), the pressure constant k was calculated in 16 patients without left heart obstruction according to the formula k = P-Ds/Ws. The mean value for k was 225 +/- 6.7 (standard deviation) mm Hg. From this value, left ventricular pressure was estimated in 13 patients with aortic stenosis aged 4 to 17 years using the formula P = k-Ws/Ds. No subject had evidence of cardiac failure. Peak systolic aortic pressure difference (delta P) was calculated by subtracting cuff-measured brachial arterial peak systolic pressure from the estimated left ventricular pressure. Excellent correlation was obtained between the estimated delta P and that found at cardiac catheterization (r = 0.89). In two patients, echocardiographic data predicted significant obstruction in the presence of normal electrocardiographic, vectorcardiographic and vector lead tracings. Echocardiography offers a noninvasive method for estimating the severity of aortic stenosis, in the absence of myocardial failure; it appears to be more sensitive than other currently employed techniques.
Am J Cardiol 1976 Nov 04
PMID:Echocardiographic assessment of the severity of aortic stenosis in children and adolescents. 13 84


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