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

In this study, observation of the effects of verapamil on pulmonary arterial pressure and on treating right heart failure were done in 15 patients with chronic cor pulmonale complicated with heart failure using monitoring of hemodynamic changes by right cardiac catheter. The results showed that verapamil had remarkable effect on pulmonary arterial pressure. With no significant effect on systemic blood pressure, verapamil decreases right ventricular systolic pressure by 1.3 kPa (9.6 mmHg), pulmonary arterial systolic pressure by 1.5 kPa (11 mmHg) and mean pulmonary arterial pressure by 1.1 kPa (8.5 mmHg). Verapamil is clinically useful by decreasing cardiac afterload, improving cardiac function, treating right heart failure and relieving bronchial spasm.
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PMID:[Effects of verapamil on pulmonary arterial pressure in patients with cor pulmonale complicated by heart failure]. 263 53

The influence of long-term verapamil administration on the consequences of Trypanosoma cruzi infection in mice was studied with regard to animal mortality, morbidity, myocardial pathologic features and myocardial beta-adrenergic adenylate cyclase activity. Verapamil administration dramatically decreased the mortality rate from 60% to 6% during the 70 day period of infection. Three clinical stages of infection were evident. In the acute stage (17 days after infection with maximal parasitemia), verapamil treatment not only decreased the incidence of myocardial disease (fibrosis and inflammation), but also protected myocardial beta-adrenergic adenylate cyclase activity. In addition, there was no increase in total body weight, which was regarded as an index of right-sided heart failure. In the subacute stage (30 to 60 days after infection), administration of verapamil continued to decrease myocardial disease and preserve beta-adrenergic adenylate cyclase activity. In addition, verapamil ameliorated the morbidity and mortality associated with this stage of infection. The chronic stage of infection was characterized by a decrease in myocardial disease and in beta-adrenergic adenylate cyclase activity. Thus, independent of the state of infection, long-term verapamil treatment enhanced beta-adrenergic adenylate cyclase activity. In addition, verapamil ameliorated the morbidity associated with infection. Although the relation among these various effects of verapamil in the setting of T. cruzi infection remains to be determined, collectively the results suggested that verapamil administration attenuated the consequences of T. cruzi infection.
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PMID:Verapamil ameliorates clinical, pathologic and biochemical manifestations of experimental chagasic cardiomyopathy in mice. 267 Oct 96

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

Calcium channel blocking drugs are a chemically heterogenous group, so it might be expected that their effects on vascular smooth muscle, cardiac contractility, and conduction tissue may differ. However, the majority of adverse reactions are predictable from their pharmacological actions and may be conveniently grouped in the following categories: 1) vasodilatation, 2) negative inotropic effects, 3) conduction disturbances, 4) gastrointestinal effects, 5) metabolic effects, and 6) drug interactions. Vasodilatory symptoms, namely, dizziness, headaches, flushing sensation, and palpitation, are more likely with nifedipine. Peripheral edema is also common with nifedipine, but the mechanism is uncertain. For a given degree of vasodilation, the greatest negative inotropic effect is seen with verapamil first, diltiazem second, and nifedipine last. Calcium channel blocking drugs are contraindicated in hypertensive patients with second and third degree heart block, sick sinus syndrome, and severe heart failure. Verapamil and diltiazem have a significant effect on cardiac conduction, whereas nifedipine, in therapeutic doses, does not. Local gastrointestinal symptoms, such as nausea and constipation, are common with verapamil. None of the calcium channel blocking drugs have been reported to adversely affect lipid or protein metabolism. However, nifedipine, verapamil, and diltiazem in high doses may inhibit liberation of insulin. The significance of this finding needs to be explored further in hypertensive diabetics. Serum digoxin levels have been shown to increase after administration of verapamil and nifedipine, but there is no evidence that this change has any clinical relevance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Side effects of calcium channel blockers. 328 Apr 92

Verapamil has been shown to be effective in reducing the frequency of episodes of ischemic pain in patients with unstable angina pectoris, and to be more effective than beta-adrenoceptor antagonists in such patients. However, in many patients ischemic symptoms persist despite verapamil therapy. In a group of 33 consecutive patients admitted to the Coronary Care Unit with unstable angina pectoris and treated with verapamil and nitroglycerin, we prospectively tested the hypothesis that plasma concentrations of verapamil were a direct determinant of resolution of ischemic symptoms over the initial 72-h period of admission. During this period, improvement or resolution of symptoms occurred in 23 of the 33 patients. With patients receiving 240 to 320 mg/day of verapamil, plasma verapamil concentrations varied between 8 and 487 ng/ml, rising significantly with increasing duration of therapy. Mean plasma verapamil concentrations were somewhat greater in patients who improved than in those with ongoing or worsening symptoms, but the differences were not statistically significant. Furthermore, no correlation was found between symptomatic status and plasma concentrations of norverapamil, the active metabolite of verapamil. In one patient cardiac failure worsened, possibly attributable to an elevated plasma verapamil concentration (336 ng/ml). We conclude that in this clinical setting there is little place for routine monitoring of plasma verapamil concentrations.
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PMID:Verapamil in unstable angina pectoris: failure to demonstrate a relationship between efficacy and plasma levels. 337 79

The relation between metabolic and functional derangement in various cardiomyopathies has not been well characterized. This information was specifically sought in a spontaneous cardiomyopathic model. Metabolic and hemodynamic parameters were obtained in glucose-perfused beating hearts of 180-200-day-old cardiomyopathic Syrian hamsters and age-matched healthy animals. This period in the cardiomyopathic hamster lifetime is intermediary between the necrotic phase and the appearance of heart failure. We used 31P nuclear magnetic resonance spectroscopy to analyze energy metabolites and intracellular pH. Cardiomyopathic hamsters had significantly higher mole fraction values for inorganic phosphate, lower phosphocreatine mole fraction as well as lower phosphocreatine/inorganic phosphate and adenosine triphosphate/inorganic phosphate ratios. Analysis of pH indicated the presence of regions of increased acidity within the heart of myopathic hamsters. Cardiomyopathic hamsters also had significantly lower left ventricular pressure, coronary flow, and myocardial oxygen consumption. Separate groups of normal and myopathic hamsters were given verapamil for 24 hours (one injection of 4 mg/kg s.c. followed by 1.2 g/l in drinking water). Verapamil-treated myopathic hamsters had evidence of markedly improved mitochondrial function when compared with untreated animals. Left ventricular pressure and coronary flow rose to normal levels. Replacing glucose by pyruvate in the perfusate of myopathic hamsters results in a marked increase in left ventricular pressure, coronary flow, and oxygen consumption with a moderate rise in phosphocreatine. Thus, 180-200-day-old cardiomyopathic hamster heart is characterized by evidence of decreased mitochondrial function, by areas of increased acidity within the heart, and by reduced left ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of the hereditary Syrian hamster cardiomyopathy by 31P nuclear magnetic resonance spectroscopy: improvement after acute verapamil therapy. 381 56

To examine the relative potencies of verapamil, nifedipine and diltiazem on left ventricular (LV) function under ischemic conditions, 20 conscious closed-chest dogs that had partial occlusion of their circumflex coronary arteries were studied. Myocardial blood flow was measured by microspheres, LV function by radionuclide angiography. Drug effects were compared at doses causing equal decreases in mean arterial pressure (MAP) and in coronary vascular resistance of the nonischemic zone. Global ejection fraction (EF) and EF of the ischemic region were significantly decreased by verapamil (p less than 0.002) and increased by nifedipine (p less than 0.001); diltiazem caused no significant changes. Verapamil significantly increased peak diastolic filling rate (p less than 0.001); nifedipine also increased diastolic filling rate but only at doses that markedly decreased MAP and coronary vascular resistance. Diltiazem was not significantly different from placebo. For doses causing an equal decrease in MAP, verapamil decreased heart rate (p less than 0.001), and diltiazem and nifedipine increased heart rate (p less than 0.05). Myocardial ischemic zone flow remained unchanged during placebo, verapamil, diltiazem or nifedipine infusion. To study the influence of heart failure on the hemodynamic effects of the calcium-channel blocking agents, 6 foxhounds underwent total occlusions of the left anterior descending coronary artery, resulting in myocardial infarction, volume loading to increase left atrial pressure and partial occlusion of the circumflex coronary artery. Verapamil depressed global left ventricular ejection fraction and increased left atrial pressure to as high as 40 to 45 mm Hg. In contrast, nifedipine decreased left atrial pressure and increased global EF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative effects of calcium-channel blocking agents on left ventricular function during acute ischemia in dogs with and without congestive heart failure. 396 56

Symptoms range from mild palpitations to overt cardiac failure and cardiogenic shock, depending on the ventricular rate and the patient's underlying cardiac status. Drug therapy is the mainstay treatment. In atrial fibrillation, digoxin is used to control the ventricular response and therefore improve cardiac function. Verapamil may also be used for this purpose.
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PMID:Supraventricular tachyarrhythmias: atrial flutter and atrial fibrillation. 397 51

Verapamil in a 400 mg daily dose was used in 64 coronary patients with the unstable angina syndrome, their condition being assessed by means of coronarography (40) and the cold test (24). Anginal attacks subsided in more than 60% of the patients treated with verapamil alone or in combination with long-acting nitrates, and their treatment was continued on an out-patient basis. In 24 patients, the drug had no effect and was discontinued. Typically, all the three major coronary arteries were affected in these patients, and they were refractory to other antianginal drugs. Myocardial infarction developed during hospital stay in 7 (11%) patients. The cold test has no predictive value with respect to the efficiency of verapamil in these patients, as the rate of positive tests is rather low. The drug taken in a 400 mg dose is easily tolerated by patients over long periods of treatment (up to 1.5 pears), however, their circulatory status should be closely monitored because of a risk of heart failure and arterial hypotension.
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PMID:[Use of verapamil for treating patients with unstable stenocardia]. 402 Dec 96

We evaluated the effects of intravenous verapamil, a calcium antagonist, on hemodynamics and regional left ventricular (LV) performance in patients with acute myocardial infarction (AMI). Twenty patients having uncomplicated infarction or moderate heart failure were randomized to receive either verapamil or placebo and were studied a mean of 12 hours after onset of symptoms. Verapamil, 7.5 mg intravenously, acutely reduced systolic arterial pressure (p less than 0.0005), systemic vascular resistance, and LV stroke work (p less than 0.005) and rate-pressure product (p less than 0.05); the heart rate did not alter. The Frank-Starling relationship by Swan-Ganz catheter did not change for 1 hour. Segmental wall motion amplitudes were recorded from eight standardized segments around the left ventricle by a multidirectional M-mode echocardiographic technique. The systolic wall motion of the uninvolved LV segments and LV cavity size did not change after verapamil. Verapamil improved mechanical performance in the ischemic segments (p less than 0.005). Therefore, the overall regional contractile function of the left ventricle improved as well (by 11% to 13%, p less than 0.05). This echocardiographic improvement continued after the acute vasodilatory response of intravenous verapamil subsided and was preserved for 1 week, the patients having had oral verapamil, 240 mg daily. Chest pain was relieved in five of the six patients having ongoing slight pain before verapamil injection. No sequential hemodynamic or echocardiographic changes occurred in the placebo-treated patients. Thus, in patients with uncomplicated AMI, verapamil improve contractile function of the acutely ischemic LV segments by hemodynamic unloading and/or by direct myocardial effect, without manifest depression of the uninvolved myocardium.
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PMID:Effects of verapamil in patients with acute myocardial infarction: hemodynamics and function of normal and ischemic left ventricular myocardium. 669 58


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