Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of angiotensin converting enzyme inhibition on myocardial ischaemia was studied in 12 normotensive patients with chronic stable angina and exercise induced ST segment depression. The study was randomised, double blind, placebo controlled, and crossover with treatment periods of two weeks. Enalapril was used to inhibit angiotensin converting enzyme. Assessment was by angina diaries and maximum symptom limited treadmill exercise tests. The results for the whole group showed a significant reduction in systolic blood pressure at rest and at peak exercise. Mean total exercise duration was 466 s (95% confidence interval 406 to 525) when the patients were taking placebo and 509 s (436 to 583) when they were taking enalapril. Four patients prolonged their total exercise time (mean 450 to mean 591 s) by more than 20%. Two patients, however, developed ischaemia earlier on exercise and reduced their total exercise duration (mean 490 to mean 390 s). Although angiotensin converting enzyme inhibition tended to reduce myocardial ischaemia in the group as a whole, some patients improved while others deteriorated. Thus the effects of enalapril are variable and this may have important implications when enalapril is used to treat heart failure in patients with underlying severe ischaemic heart disease.
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PMID:The variable effects of angiotensin converting enzyme inhibition on myocardial ischaemia in chronic stable angina. 254 48

Coronary sinus blood flow, transmyocardial oxygen extraction, myocardial oxygen consumption, and transmyocardial lactate extraction were determined, along with systemic hemodynamics, in 34 patients with chronic stable angina without heart failure (group 1), in 66 patients with heart failure associated with coronary artery disease (group 2), and in 28 patients with heart failure caused by dilated cardiomyopathy without coronary artery disease (group 3). Compared with group 1 patients, in patients with heart failure in groups 2 and 3, resting coronary sinus blood flow was 30% and 24% higher, respectively (p less than 0.05), myocardial oxygen consumption was 25% higher (p less than 0.01), and coronary sinus oxygen content was 33% lower (p less than 0.01). The rate-pressure product was not different between the three groups. In eight patients with heart failure (five in group 2 and three in group 3), myocardial lactate production was observed without angina. Thus in patients with chronic heart failure resulting from either chronic coronary artery disease or dilated cardiomyopathy, resting coronary blood flow and myocardial oxygen consumption tend to increase probably because of an increase in myocardial oxygen requirements. Silent myocardial ischemia may also occur in both the presence and absence of coronary artery disease in patients with chronic heart failure. The abnormal coronary hemodynamics and myocardial metabolic function may play a role in causing progressive deterioration in cardiac function in dilated cardiomyopathy.
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PMID:Abnormal coronary hemodynamics and myocardial energetics in patients with chronic heart failure caused by ischemic heart disease and dilated cardiomyopathy. 335 9

Verapamil hydrochloride, a prototype calcium antagonist, is now marketed in the United States for the acute treatment of supraventricular tachyarrhythmias and for chronic management of vasospastic and chronic stable angina. It inhibits the slow inward channel in in the heart and blocks calcium influx in smooth muscle. Its intrinsic negative inotropic action, which is apparent in isolated tissues, is offset in vivo by peripheral vasodilation. It has a mild, noncompetitive sympathetic antagonist effect; its most important electrophysiologic action is a depression of AV nodal conduction, accounting for its effect in supraventricular tachyarrhythmias. Its hemodynamic actions are characterized by a complex interplay of changes in preload, afterload, contractility, heart rate, and coronary blood flow. It does not depress cardiac function, except in severe heart failure. The drug has a mild dilator action on coronary arteries and reverses ergonovine-induced vasoconstriction. Controlled trials have established its role in Prinzmetal's variant angina, unstable angina, and chronic stable angina. It has also been found to be effective in obstructive cardiomyopathies. The potential role of verapamil in such conditions as hypertension, cardioprotection, and Raynaud's phenomenon needs further evaluation; at present these indications have not been approved by the Food and Drug Administration. The most common side effects include constipation, skin rash, and dizziness; AV block, heart failure, and sinus arrest may occasionally be encountered, especially when ventricular function is compromised or conduction system disease is present.
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PMID:Verapamil hydrochloride: pharmacological properties and role in cardiovascular therapeutics. 676 30

The long-term efficacy of verapamil in a dose of 360 mg daily in patients with chronic stable angina pectoris was assessed by quantitated serial treadmill exercise tests. Twenty-eight patients were investigated with a placebo-controlled, double-blind, crossover protocol of 2 weeks each and afterward all patients were put on long-term therapy. Exercise tests were performed at the end of the placebo period and after 2, 4, 8, 16, 24 and 52 weeks of verapamil therapy. All 28 experienced angina during treadmill tests on placebo and the mean (+/- standard error of the mean) exercise time was 6.6 +/- 0.5 minutes. This increased to 9.2 +/- 0.8 minutes at 2 weeks and 50 11.2 +/- 0.8 minutes at 4 weeks. Fifteen and 20 of the 28 patients became angina-free during treadmill exercise at 2 and 4 weeks, respectively. The consumption of nitroglycerin showed a similar improvement. The improvement was maintained at 1 year of follow-up. The on-line computer-analyzed S-T segment changes showed a statistically significant improvement at all follow-up periods. Withdrawal of verapamil produced a return to pretreatment levels. The adverse effects noted were constipation in seven patients and reversible P-R interval prolongation in two. No heart failure occurred in any patient. These findings suggest that verapamil possesses a powerful and sustained antianginal action and, in a dose of 360 mg daily, merits a place as a primary therapeutic agent in the management of chronic stable angina.
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PMID:Long-term antianginal action of verapamil assessed with quantitated serial treadmill stress testing. 679 87

1. The efficacy of verapamil in a dose of 360 mg daily in patients with chronic stable angina pectoris was assessed by quantitative serial treadmill exercise tests and trinitrin consumption. Twenty-eight patients were investigated in a placebo-controlled, double-blind cross-over comparison of 2 weeks each, after which all were put on long-term verapamil treatment. Exercise tests were done at the end of the placebo period and after 2 and 4 weeks on verapamil. 2. On placebo, all twenty-eight patients developed angina during treadmill tests and the mean exercise time was 6.6 min (s.e.m. = 0.5 min). On verapamil, this increased to 9.2 min (s.e.m. = 0.8 min) at 2 weeks and to 11.2 (s.e.m. = 0.8 min) at 4 weeks, respectively. Trinitrin consumption showed a similar improvement. The double product and ST segment changes, analysed by on-line computer, showed a statistically significant improvement. The only side effects were constipation (in seven patients) and reversible PR-interval prolongation (in two patients). There was no clinical evidence of heart failure in any of the patients. 3. These findings suggest that verapamil has a powerful antianginal action and, in a dose of 360 mg daily, may have a place as a primary agent in the management of chronic stable angina.
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PMID:An objective comparison of verapamil and placebo in chronic stable angina. 681 Nov 77

Calcium channel blockers are used extensively in the treatment of the three major anginal syndromes. In the treatment of Prinzmetal's angina, their antivasospastic properties account for their therapeutic effectiveness. Calcium channel blockers are drugs of first choice in this syndrome. In chronic stable angina, calcium channel blockers may be used as monotherapy or in combination with beta-blockers and/or nitrates. In patients with unstable angina, reduction in the incidence of ischemic episodes produced by calcium channel blockers is well documented. Recent data suggest that calcium channel blockers should generally be used in combination with beta-blockers, nitrates and antithrombotic agents. Patients with ischemic heart disease often exhibit reduced ventricular function. All of the first generation calcium channel blockers exacerbate symptoms in patients with established heart failure and may precipitate heart failure, particularly when combined with beta-blockers. Second generation vascular-selective dihydropyridines have been introduced recently. Vascular selectivity determines the drug's degree of negative inotropic effect. Felodipine is one of the most vascular selective of the available dihydropyridines and has no negative inotropic effects at clinically administered doses. In a long term study, felodipine, 20 mg/day, abolished symptoms and chronic ischemic episodes in 81% of treated subjects with Prinzmetal's angina. In patients with stable angina, felodipine has been found to be effective either as monotherapy or in combination with beta-blockers. In patients with known or suspected ventricular dysfunction, vascular-selective dihydropyridines such as felodipine offer advantages over the nonselective calcium channel blockers, particularly in patients receiving beta-blockers.
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PMID:The evolving role of calcium channel blockers in the treatment of angina pectoris: focus on felodipine. 772 49

Elevated circulating insulin levels have been reported in ischaemic heart disease, and may be of aetiological importance. Previous studies have not considered the potential influence of heart failure or of previous myocardial infarction, as opposed to stable angina. We therefore measured the insulin response to a 75 g oral glucose tolerance test in five groups with normal glucose tolerance, comparing normal male controls to men with chronic stable angina, men with recent myocardial infarction (two groups, 3 weeks and 3 months post infarction), and men with chronic severe heart failure. Only patients with chronic heart failure had fasting hyperinsulinaemia, probably reflecting associated neuroendocrine abnormalities. Stimulated hyperinsulinaemia was present in all patient groups, but was less pronounced and of shorter duration in patients with angina. At 120 min, only patients with heart failure or previous myocardial infarction were hyperinsulinaemic. The degree of stimulated hyperinsulinaemia was not influenced by the presence of heart failure or by the length of time from infarction. Hyperinsulinaemia is associated with impaired peripheral muscle glucose uptake and metabolism, and might contribute to muscular fatigue on exertion in patients with previous myocardial infarction or heart failure.
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PMID:Hyperinsulinaemia in ischaemic heart disease: the importance of myocardial infarction and left ventricular function. 769 98

Hibernating myocardium refers to the presence of persistent myocardial and left ventricular dysfunction at rest due to reduced coronary blood flow that can be partially or completely restored to normal by myocardial revascularization. An increasing amount of data show it is most likely a downgrading of cardiac function so that blood flow and myocardial function are once again in a state of equilibrium. It has been demonstrated to occur in patients with unstable angina, chronic stable angina, acute myocardial infarction and in left ventricular dysfunction and/or congestive heart failure. Salvage of this viable myocardium by successful revascularization improves left ventricular dysfunction and probably also patient survival. Therefore, diagnosis of hibernating myocardium is important because it does not render left ventricular dysfunction a necessary contraindication to revascularization, nor does it leave the patient with chronic heart failure a candidate only for cardiac transplantation. Instead, these patients should have complete revascularization by coronary bypass surgery/percutaneous transluminal coronary angioplasty as soon as possible.
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PMID:The hibernating myocardium in ischaemia and congestive heart failure. 837 Mar 58

Carvedilol is a non-selective beta-adrenoceptor antagonist with vasodilating properties which has been shown to be effective in the management both of hypertension and of stable angina pectoris. In order to explore its wider efficacy in patients with manifest heart failure, a preliminary study was performed in patients with chronic stable angina pectoris accompanied by abnormal left ventricular wall motion, but without overt heart failure (mean ejection fraction < 40%). Six patients were given carvedilol 25 mg b.i.d. for 2 weeks followed by 50 mg b.i.d. for a further 2 weeks according to a single-blind placebo-controlled protocol. At the end of the 4 week period of treatment, in four patients left ventricular wall motion was improved, in two it was unchanged, and in none was there any deterioration; mean ejection fraction increased from 40 to 48%. These results prompted a further study in 17 patients with chronic ischaemic heart failure. The haemodynamic and clinical responses to intravenous carvedilol followed by the oral drug (50 mg b.i.d.) for 8 weeks were studied. There was an improvement in all haemodynamic variables, although postural hypotension necessitated withdrawing two patients, and clinical deterioration was evident in two others. The beneficial effects of carvedilol were considered to be related to the combined reduction in afterload and inhibition of neurohumeral activation. These results have been confirmed in placebo-controlled, double-blind studies.
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PMID:Vasodilating beta-blockers in heart failure. 852 82

The beta-blocking drugs are known to modify the course of hypertensive and atherosclerotic heart disease and significantly reduce the mortality and morbidity associated with these diseases. The place of vasodilating beta-blocking drugs, of which carvedilol is an example, has not been so clear, although they have obvious theoretical advantages. We performed a study on 12 hypertensive subjects using the technique of continuous ambulatory intra-arterial blood pressure recording which demonstrated that carvedilol (50 mg bid) achieved satisfactory blood pressure control throughout the full 24 h cycle. The addition, there was a marked reduction in left ventricular end-systolic and end-diastolic volumes with prolonged administration, suggesting a decrease in heart size, confirmed in other studies. A second study in patients with chronic stable angina and impaired left ventricular wall motion showed that carvedilol 25 mg bid not only improved exercise tolerance, but also reduced heart size, improved left ventricular ejection fraction, and abolished wall motion abnormalities. These results prompted a further study in 17 patients with chronic ischaemic heart failure. The haemodynamic and clinical responses to intravenous carvedilol followed by the oral drug 50 mgm b.i.d. for 8 weeks were studied. There was an improvement in all haemodynamic indices, although postural hypotension necessitated withdrawing two patients and clinical deterioration was evident in two others. The beneficial effects of carvedilol were considered to be related to the combined reduction in afterload and inhibition of neurohumeral activation. These results have been confirmed in placebo-controlled, double-blind studies from other workers.
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PMID:The preventative effects of vasodilating beta-blockers in cardiovascular disease. 873 69


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