UMLS:C0002962 - FACTA Search

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Query: UMLS:C0002962 (angina)
21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antianginal efficacy of niludipine (Bay a 7167), a new calcium antagonistic drug, was investigated in 51 patients with ischemic heart disease. 16 patients were diagnosed as effort angina and 31 patients had both angina at rest and on effort. Six anginal patients had myocardial infarction. One patient was diagnosed as a variant form of angina and 3 others as unstable angina. 11 patients had essential hypertension. 49 completed the study and 2 dropped out. Niludipine (60 mg to 80 mg every 24 h) significantly reduced the mean weekly rate of angina attacks from 6.5 to 2.2 (p less than 0.001). Marked reductions of nitroglycerin requirement were also noted (p less than 0.001). In 71% of the patients complete control of anginal attacks was achieved, and in over 77% the frequency of angina was reduced by at least 50%. Niludipine was at 93.8% effective in patients with ischemic heart disease. It decreased significantly both systolic and diastolic blood pressure in angina patients with essential hypertension, but there were no significant changes of blood pressure in normotensive anginal patients. The agent was tolerated very well and there were no side effects. These findings suggest that niludipine is a highly effective drug for the treatment of both ischemic heart disease and essential hypertension.
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PMID:Clinical effectiveness of niludipine in patients with ischemic heart disease. 680 15

Eight patients taking metoprolol (300 mg/day) for essential hypertension were studied after abrupt withdrawal and placebo replacement of the drug. A 52% average rebound increase in cardiac chronotropic sensitivity to isoproterenol and 15% rebound rise in resting heart rate occurred in all patients between 2 to 8 days after metoprolol withdrawal (P less than 0.05). Holter monitoring showed no associated arrhythmia. A transient increase in blood pressure occurred in one patient and withdrawal-like symptoms were noted in three patients. There were no meaningful changes in plasma norepinephrine, epinephrine, thyroxine, or triiodothyronine. Seven of the eight patients were again studied serially after the same metoprolol dosing, during a prolonged low-dose withdrawal schedule (50 mg/day for 10 days) and during placebo. Prolonged low dose before complete metoprolol withdrawal decreased but did not completely prevent the changes observed after abrupt withdrawal. The observed rebound of cardiac beta-adrenergic sensitivity may have application to the mechanism and prevention of the beta-blocker syndrome in patients with angina.
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PMID:Metoprolol withdrawal phenomena: mechanism and prevention. 705 9

Carvedilol is a beta-adrenoceptor antagonist which also causes peripheral vasodilation primarily via alpha 1-adrenergic blockade. Carvedilol produces its antihypertensive effect partly by reducing total peripheral resistance by blocking alpha 1-adrenoceptors and by preventing beta-adrenoceptor-mediated compensatory mechanisms. This combined action avoids many of the unwanted effects associated with traditional beta-blocker or vasodilator therapy. In clinical trials published to date, most of which enrolled small numbers of patients, the antihypertensive efficacy of carvedilol administered once daily was similar to that of atenolol, labetalol, pindolol, propranolol, metoprolol, nitrendipine (in elderly patients), slow release nifedipine or captopril in patients with mild-to-moderate essential hypertension. Combined therapy with carvedilol 25 mg and hydrochlorothiazide 25 mg, nicardipine 60 mg or slow release nifedipine 20 mg has an additive antihypertensive effect. Carvedilol and atenolol at similar doses were equally effective at reducing blood pressure in patients who had previously not responded adequately to hydrochlorothiazide monotherapy. As a result of its multiple mechanisms of action, carvedilol is suited for the management of specific groups of hypertensive patients, such as those with renal impairment. In patients with non-insulin-dependent or insulin-dependent diabetes mellitus carvedilol does not appear to affect glucose tolerance or carbohydrate metabolism. Initial studies have demonstrated that carvedilol and slow release nifedipine have similar efficacy in patients with stable angina pectoris and there is evidence that carvedilol has a beneficial haemodynamic effect in patients with congestive heart failure (NYHA class II or III) secondary to ischaemic heart disease. A postmarketing surveillance study has shown that carvedilol is generally well tolerated with only 7% (164/2226) of patients (83% of the total number received 25mg daily for 12 weeks) withdrawing from treatment because of adverse events. Vertigo, headache, bronchospasm, fatigue and skin reactions were the most common events causing withdrawal. Thus, clinical experience to date suggests that carvedilol is likely to be a valuable addition to the options currently available for treating patients with mild-to-moderate essential hypertension, and may offer particular benefit in specific populations of hypertensive patients.
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PMID:Carvedilol. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy. 768 74

The management of essential hypertension can no longer be directed toward an isolated reduction in arterial pressure. Optimal reduction in the risk factors associated with hypertension and cardiovascular disease hopefully will reduce coronary heart disease, angina, fatal and nonfatal myocardial infarction, left ventricular hypertrophy, congestive heart failure, and sudden death. Hypertension is a genetic and acquired syndrome that consists of dyslipidemia, insulin resistance and carbohydrate intolerance, central obesity, renal abnormalities, structural abnormalities of smooth muscle, and ion transport abnormalities (membranopathy). The selection of pharmacologic agents should improve the components of the hypertensive syndrome by utilizing the "subsets of hypertension approach" to treatment.
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PMID:The management of hypertension and associated risk factors for the prevention of long-term cardiac complications. 769 47

A 4-week course of dilren under clinical, bicycle exercise, ECG, echo-CG control and 24-hour monitoring of AP was given to 19 subjects with essential hypertension stage I-II and ischemic heart disease. A single dose of the drug (300 mg/day) diminished hypertension and angina pectoris in 79 and 63% of the patients, respectively. A 4-week dilren produced a 10-11% decrease in the total peripheral vascular resistance, prolonged P-Q interval by 0.01-0.02 sec without atrioventricular block in 26% of the patients, reduced AP measured according to Korotkov by 14.2/10.5 mm Hg (in awake patients by 12.8/8.4 mm Hg, in sleeping ones by 8.6/4.5 mm Hg without changes in 24-h AP curve). Side effects occurred in 5.3% of the cases and were overcome without discontinuation of the treatment.
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PMID:[The antihypertensive and antianginal activity of Dilren--a prolonged-action calcium antagonist]. 790 33

Beta-blockers with less cardiodepressive effect than traditional nonselective beta(1+2)-blocking agents could be useful in the treatment of hypertension, provided the reduction in blood pressure was satisfactory. Epanolol, a selective beta 1-receptor blocker with intrinsic sympathomimetic activity, induced a fall in intraarterial pressure of 8% at rest sitting and 11% during 100 W bicycle exercise after the first dose of 200 mg in 12 patients with essential hypertension. Heart rate, stroke index, and cardiac index initially fell by 14%, 11%, and 23%, respectively. The total peripheral resistance index increased by 21% after 2 hours, and then reverted towards the pretreatment level. After 10 months of epanolol treatment (mean 300 mg/day), the reduction in arterial pressure was 5% at rest and 10% during exercise. Cardiac index and heart rate were still reduced 14-21%, while total peripheral resistance was unchanged or slightly increased (2-10%). Twenty-four hour ambulatory blood pressure was higher on epanolol (300 mg/day) than on atenolol (150 mg/day) treatment (137/97 vs. 128/91 mmHg). Thus, the achieved blood pressure reduction induced by epanolol was moderate, while other characteristics of beta-receptor blockade, in particular, the reduction of heart rate and cardiac output, were maintained. This suggests that the compound may be useful for other cardiovascular disorders, e.g., angina pectoris in patients without hypertension or cardiac arrhythmia.
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PMID:Modest antihypertensive effect of epanolol, a beta 1-selective receptor blocker with beta 1 agonist activity: an acute and long-term hemodynamic study at rest and during exercise and double crossover comparison with atenolol on ambulatory blood pressure. 809 25

Today calcium antagonists (Ca-antagonists) are widely used agents in the management of various diseases of the circulatory system. More than 20 years ago the Ca-antagonists of the so-called 1st generation (Verapamil, Diltiazem, Nifedipine) were introduced for treatment of angina pectoris and later of essential hypertension. In the last decade an increasing number of agents structurally related to dihydropyridines were developed for the treatment of hypertension and/or coronary heart disease or cerebral disorders; the main target was to reduce side effects and to guarantee once or at least twice daily administration. Therefore the Ca-antagonists of the so-called 2nd generation (e.g. Amlodipine, Felodipine, Isradipine, Nitrendipine, Nicardipine, Nimodipine, Nisoldipine) tend to longer elimination-half-lives; Amlodipin is an exception with an elimination-half-life of 30 hours on the average. Apart from elimination rates, however, the biopharmaceutical and pharmacokinetic characteristics of all Ca-antagonists are similar: they are highly cleared drugs and are relatively highly protein bound. As they are subject to significant hepatic first-pass-metabolism old age and hepatic disease will increase their plasma-concentrations. Renal impairment affects little their pharmacokinetics since the fraction eliminated unchanged by the kidneys is small. For most agents, plasma-concentration-response relationships have been described. With exception of nicardipine a linear pharmacokinetic in all Ca-antagonists was demonstrated. Drugs and food affecting hepatic blood flow and drug metabolising capacity have predictable interaction potential. With regard to the acute pharmacodynamic effects the Ca-antagonists show similar qualitative effects, though there are quantitative differences. Orally administered dihydropyridine-derivatives induce acute hypotensive effects, whereas the other compounds show clinically relevant hypotensive effects only when administered chronically per os or less pronounced when given as intravenous infusion.
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PMID:[Principles of the pharmacokinetics and pharmacodynamics of calcium antagonists]. 813 31

The vascular endothelium is the site of formation of several powerful mediators. One of these is NO, a chemically unstable radical formed by enzymatic conversion of L-arginine in the presence of molecular oxygen. NO elicits relaxation of VSMC by activating cytosolic guanylate cyclase. NO also counteracts platelet adhesion and aggregation. The biological actions of NO make it a key substance in the endogenous defense against vascular occlusion and thrombosis. The basal formation of NO maintains a moderate but significant vasodilation in the systemic resistance vessels and counteracts platelet activity. When blood flow in conduit arteries is increased there is an augmented endothelial formation of NO, eliciting flow-dependent vasodilation. Beside this, several vasodilators (acetylcholine, bradykinin, histamine, substance P) operate by stimulating endothelial NO formation. On the other hand, drugs like nitroglycerin and papaverine operate independently of the vascular endothelium. Vasodilator mechanisms, physiological as well as pharmacological, may therefore be characterized as endothelium-dependent (i.e. NO-mediated), or endothelium-independent (i.e. not mediated by NO). Physiologically, mixed mechanisms occur. Failure of the vascular endothelium to elicit NO-mediated vasodilatation may be due to decreased formation, increased degradation, decreased sensitivity to the NO formed, or a mixture of these factors. Irrespective of the mechanism behind, this is referred to as endothelial dysfunction. Endothelial dysfunction occurs in several cardiovascular settings, like atherosclerosis, hypercholesterolaemia, diabetes, and essential hypertension. Endothelial dysfunction leads to an impaired tissue perfusion, increased local vascular resistance, decreased defense against thrombus formation, and possibly also decreased defense against hypertrophy of the VSMC in the vessel wall media. In patients with CHD, endothelial dysfunction leads to an impaired coronary flow response to physical and mental stress, and to promotion of platelet adherence and aggregability. Endothelial dysfunction is thereby a probable aggravating factor in the atherosclerotic process, adding a functional component on top of the structural lesions characterizing this disease. A particular form of endothelial dysfunction, limited to the arterial resistance vessels, may explain the symptoms and clinical characteristics of microvascular angina. In patients with essential hypertension, endothelial dysfunction prevails, adding a functional component to the structural factors also in this disease. Hitherto, the only therapeutic tools available to restore endothelial dysfunction appear to be restriction of the dietary intake of lipids, possibly reinforced with intake of antioxidants like fish oil and vitamin E. However, large clinical trials to confirm the efficacy of such therapy in reversing endothelial dysfunction have not been conducted. In the future, more directly acting therapeutic regimens, aimed at supporting or substituting the endogenous formation of NO, are likely to appear as well.
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PMID:Endothelial nitric oxide and cardiovascular disease. 815 Dec 63

The primary goal in the treatment of essential hypertension is to reduce all end organ damage, not simply to reduce blood pressure. Hypertension is associated with an increased risk of cerebrovascular, cardiovascular and renal morbidity and mortality. Pharmacological therapy has reduced some, but not all, of these complications. In order to achieve maximal decrease in morbidity and mortality in hypertensive related diseases the overall impact of antihypertensive drug therapy on the pathogenesis of damage to each end organ must be considered. The pharmacological therapy of mild hypertension has reduced complications of most pressure related (arteriolar) damage such as cerebrovascular accidents, congestive heart failure, and some cases of chronic renal failure, but atherosclerotic complications, coronary heart disease, angina, myocardial infarction and sudden death have not been convincingly reduced. A more pathophysiologic and individualized approach to the treatment of hypertension is recommended in place of the traditional stepped care approach which has primarily emphasized diuretics and beta blockers as initial therapy. This new approach in the subsets of hypertension, which is based on eight parameters: (1) Pathophysiology; (2) Haemodynamics; (3) End organ damage; (4) Concomitant medical diseases and problems; (5) Demographics; (6) Adverse effects of drugs and quality of life; (7) Compliance with medication regimen; (8) Total health care costs: direct and indirect costs. Hypertension is not just a disorder of increased intraarterial pressure, but in fact, a syndrome of commonly associated genetic and/or acquired abnormalities including dyslipidaemia, insulin resistance, impaired glucose tolerance, central obesity, renal abnormalities, structural abnormalities of smooth muscle, and abnormal cellular cation transport or membranopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertension and coronary heart disease risk factor management. 819 21

The chemistry, pharmacology, pharmacokinetics, clinical uses, adverse effects, and dosage of felodipine and isradipine are reviewed. Felodipine and isradipine are new calcium-channel-blocking agents with FDA-approved labeling for use in the treatment of essential hypertension. Both agents are members of the dihydropyridine class of calcium antagonists, which also includes nifedipine and nicardipine. Like those agents, felodipine and isradipine affect blood pressure by producing peripheral vasodilation. Felodipine and isradipine undergo extensive first-pass metabolism; their bioavailabilities are approximately 15% and 17%, respectively. The drugs are highly protein bound but do not affect serum digoxin concentrations. Anticonvulsants may reduce the elimination half-life of felodipine. Felodipine and isradipine are effective antihypertensive agents when used alone or in combination with beta blockers or diuretics. Both agents have shown some benefit in the treatment of angina pectoris in limited studies. Clinical data do not support the use of either agent for the treatment of congestive heart failure or Raynaud's phenomenon. Felodipine and isradipine have similar adverse-effect profiles, and their adverse effects resemble those of other agents in the class. Common adverse effects are peripheral edema and increased heart rate. The initial dosage of isradipine for the treatment of hypertension is 2.5 mg twice daily. Felodipine should be started at a dosage of 5 mg once daily. Felodipine and isradipine are effective antihypertensive drugs but have not demonstrated clear advantages over other dihydropyridine calcium-channel blockers.
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PMID:Felodipine and isradipine: new calcium-channel-blocking agents for the treatment of hypertension. 845 78

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