Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nisoldipine is an orally administered calcium entry blocking drug structurally related to nifedipine. In limited clinical trials it has been shown to be effective and relatively well tolerated in the treatment of patients with chronic stable angina pectoris and mild to moderate essential hypertension. As for all dihydropyridine-calcium antagonists, its major properties include potent peripheral and coronary vasodilation and improvement in myocardial oxygen supply relative to demand. These actions occur without depression of cardiac conduction or left ventricular function. Short term clinical trials have shown nisoldipine to produce both symptomatic and objective improvements in patients with chronic angina of effort and have suggested a benefit in vasospastic angina. A small number of comparative trials indicate that nisoldipine is equally as effective as nifedipine. In addition, in combination with beta-adrenoceptor blockade nisoldipine appears to offer additional benefit compared with beta-blockade alone and is well tolerated. In patients with mild to moderate essential hypertension nisoldipine monotherapy, in 1 or 2 daily doses, has maintained blood pressure control and has also been a useful addition to diuretics and beta-adrenoceptor blocking drugs in patients with poorly controlled disease. Side effects appear to be dose related, generally mild and transient, and are primarily those resulting from potent peripheral vasodilation - headache, flushing and pretibial or ankle oedema. Although studies to date are promising, there are no published long term studies (greater than 1 year) of nisoldipine in comparison with other calcium entry blockers and other drugs currently in clinical use for the treatment of angina pectoris or hypertension. Until such studies are completed the exact place of nisoldipine in the treatment of these diseases remains to be established.
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PMID:Nisoldipine. A preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in the treatment of angina pectoris, hypertension and related cardiovascular disorders. 306 58

A study was made of exercise tolerance and indices of central hemodynamics in 151 patients with "isolated" angina and its combination with cardialgia, arterial hypertension and postinfarctional cardiosclerosis. Daily attacks of angina of effort (III functional class) were noted in all the patients. In patients with "isolated" angina and angina in postinfarctional cardiosclerosis exercise tolerance was the lowest. It was the highest in angina combined with cardialgia. The lowest indices of cardiac output were observed in patients with "isolated" angina and angina in postinfarctional cardiosclerosis. The best effect of nitrate therapy was obtained in patients with typical angina.
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PMID:[Clinico-functional characteristics of stenocardia and the effectiveness of its treatment with nitrong and erinit]. 309 Jul 30

An epidemiologic study of rural residents in 4 districts of Novosibirsk Province demonstrated different incidence of arterial hypertension (AH) and angina of effort, related to the consumption of water of different quality. The prevalence of AH (33.2 +/- 1.7%) and angina of effort (21.2 +/- 1.5%) was the highest in the area with soft high-mineral water and the lowest (3.7 +/- 0.7% and 1.2 +/- 0.5%, respectively) in the area with hard low-mineral water. The prevalence of AH and angina of effort is inversely related to water hardness and calcium and magnesium levels, and directly related to water mineralization and sodium level, i.e. soft and high-mineral waters are associated with an adverse cardiovascular effect.
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PMID:[The prevalence of arterial hypertension and stenocardia of effort among the rural population living in geochemically contrasted regions of the Novosibirsk Province]. 319 51

Sotalol is a beta-adrenoceptor blocking agent devoid of intrinsic sympathomimetic activity, membrane stabilising actions and cardioselectivity. It lengthens repolarisation and the effective refractory period in all cardiac tissues independently of its antiadrenergic properties. Combining Class II and Class III antiarrhythmic properties, sotalol can be given either intravenously or orally and its pharmacokinetic properties permit long dosing (once or twice daily) intervals. Controlled and uncontrolled studies have established the efficacy of sotalol in mild-to-moderate essential hypertension and in angina of effort. Sotalol reduces anginal frequency and glyceryl trinitrate (nitroglycerin) consumption and increases exercise capacity during treadmill stress tests. In addition, although there is evidence that the drug reduces reinfarction rate in survivors of acute infarction, the data for reduction in sudden death rates in these patients are not as compelling as for other beta-blockers. However, comparative and additional long term studies are required before an accurate assessment of the use of sotalol in these disorders can be made. When used in the treatment of mild-to-moderate hypertension sotalol is more effective than placebo and comparable to other beta-blockers in reducing elevated blood pressures. In addition, a synergistic antihypertensive response is achieved when sotalol is combined with hydrochlorothiazide. Still, additional well-controlled comparative studies are required before the value of sotalol relative to other drug treatment regimens in the management of hypertension can be made. In preliminary studies sotalol appeared effective in most forms of supraventricular tachyarrhythmias with its effects being similar to those of other beta-blockers. However, preliminary data indicate that sotalol is likely to be more effective than than conventional beta-blockers in converting atrial flutter and fibrillation to sinus rhythm and maintaining stability post-conversion. Sotalol also appears to be a promising agent in the control of ventricular arrhythmias. In suppressing premature ventricular contractions it is at least as effective as procainamide. In ventricular tachycardia and fibrillation, intravenous sotalol (1.5 mg/kg), prevents reinduction by programmed electrical stimulation in 40 to 50% of cases if double stimuli are used. Both prevention of reinducible arrhythmia and the suppression of spontaneous arrhythmias on Holter recordings are predictive of a long term favourable clinical outcome. In patients with reduced ejection fractions, sotalol depresses ventricular function less than conventional beta-blockers.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Sotalol. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic use. 331 21

Calcium-channel blockers have been successfully used in the treatment of angina of effort and systemic hypertension. Many patients present with concomitant angina pectoris and hypertension. Controlled clinical trials demonstrate that the calcium-channel blockers are safe and effective as monotherapy in the treatment of these patients, and that their use compares favorably with that of propranolol. The effectiveness of these agents in hypertension appears to be primarily due to their ability to induce systemic vasodilation. Calcium-channel blockers have several therapeutic effects in angina pectoris. Beneficial actions on the major determinants of oxygen consumption, i.e. heart rate, blood pressure and contractility, are generally seen. The potent coronary vasodilating actions of these agents allow for increased coronary blood flow. Improvements in ventricular compliance, regression of left ventricular hypertrophy and cardioprotection appear to be additional effects of the calcium-channel blockers; their contribution to the drugs' overall therapeutic efficacy is presently being evaluated. Calcium-channel blockers are a welcome addition to drug regimens available for the management of patients with coexisting angina pectoris and hypertension.
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PMID:Calcium-channel blockers for combined angina pectoris and systemic hypertension. 351 13

The purpose of this study was to delineate the clinical, ECG, and angiographic features of a large series of consecutive patients with angina at rest. Transient ST segment elevation during pain was observed in 219 patients (group I), while 220 patients showed ST segment depression during pain (group II). Group II patients were found to have higher incidence of hypertension (p less than 0.001), prior myocardial infarction (p less than 0.0005), history of exertional angina (p less than 0.0005), and a progressive aggravation of symptoms before hospitalization (p less than 0.0005), while group I patients had a prevalence of recent onset angina (p less than 0.05) and more frequently developed severe ventricular arrhythmias during pain (p less than 0.0005). Furthermore, a larger number of patients showing ST segment depression during chest pain had multivessel disease (p less than 0.0005), left main involvement (p less than 0.005), and lower values of left ventricular ejection fraction (p less than 0.001) than patients with ST segment elevation during pain. Survival curves of medically treated patients showed a significantly better long-term prognosis in patients of group I (p less than 0.01). The direction of the ST segment shift during anginal attacks at rest may therefore allow a classification of patients included into the broad spectrum of unstable angina. This distinction should be taken into consideration in studies aimed at evaluating long-term prognosis or the results of medical and surgical therapy.
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PMID:Clinical and angiographic findings in angina at rest. 394 60

Diltiazem and propranolol alone and in combination as antianginal agents were compared with placebo in 12 patients with stable exertional angina at Stanford University Medical Center. The patients performed symptom-limited, multi-stage upright bicycle ergometric exercise while undergoing radionuclide angiographic studies every two weeks while being treated with 90 mg of diltiazem four times daily, 60 mg of propranolol four times daily, a combination of 90 mg of diltiazem and 60 mg of propranolol four times daily, and placebo. Diltiazem, propranolol and a combination all significantly increased exercise duration compared to placebo (526 +/- 149, 525 +/- 115, and 549 +/- 129 vs 430 +/- 132 sec.). Although rate pressure product and heart rate decreased with diltiazem therapy at submaximal workloads, these values were unchanged at peak exercise in contrast to propranolol or the combination of propranolol or diltiazem. Diltiazem decreased the sub-maximal and maximal degree of exercise-induced ST segment depression by over 50% compared to placebo (P less than 0.01 vs placebo). Diltiazem resulted in a higher exercise left ventricular ejection fraction compared to placebo, propranolol or the combination of diltiazem or propranolol (all less than P less than 0.05). Sinus bradycardia or orthostatic hypertension occurred in four patients on the high-dose combination therapy and required dose reduction. We concluded that high-dose diltiazem, appeared to be even more effective than moderate-dose propranolol or the combination of diltiazem and propranolol in improving exercise tolerance, electrocardiographic evidence of myocardial ischaemia and left ventricular function in patients with stable effort angina due to occlusive coronary artery disease.
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PMID:Diltiazem and propranolol, alone and in combination, on exercise performance and left ventricular function in patients with stable effort angina: a double-blind, randomized, and placebo-controlled study. 406 Nov 5

The effect of atenolol, a new cardioselective beta-adrenogenic blocking agent, was studied in 11 patients with angina of effort in a double-bind trial involving monitored exercise tolerance tests. The drug significantly reduced the heart rate, blood pressure and time-tension index. As a result, ST segment depression also diminished after treatment. Although working capacity, compared with controls, increased after atenolol, no difference was observed in this respect between the drug and placebo, suggesting the development of physiological tolerance to exercise. It is concluded that atenolol is useful in the prevention of angina pectoris, particularly in patients in whom there is associated arterial hypertension.
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PMID:Effect of atenolol in angina pectoris of effort. 449 21

On 169 occasions anticoagulant therapy for thromboembolic disease was stopped electively and patients were followed for 16 subsequent weeks. The records of those who remained well and those who suffered a relapse were compared in an attempt to identify factors that might affect liability to thromboembolic relapse. During the follow-up period there were 37 thromboembolic recurrences, an incidence of 22 per cent. None occurred among the patients in whom the original diagnosis of thromboembolic disease was discarded or when a predisposing cause had ceased to be present. There was an inverse relation between liability to relapse and degree of prothrombin time prolongation.NO SIGNIFICANT RELATION COULD BE SHOWN BETWEEN LIABILITY TO RELAPSE AND ANY OF THE FOLLOWING: sex and age; type and severity of the initiating thromboembolic episode; history of earlier thromboembolic disease or relapse after stopping earlier anticoagulant courses; presence of hypertension, hypercholesterolaemia, or diabetes mellitus; type of anticoagulant drug used, duration of therapy, and method of stopping treatment. Patients with overt occlusive arterial disease at more than one site had a significantly increased liability to relapse when compared with patients with symptomatic disease at a single site. In the group of 134 subjects receiving anticoagulant therapy for coronary arterial disease, occurrence of a thromboembolic episode during the course of treatment and the presence of angina of effort in the months before it was discontinued were both associated with a significant increase in liability to relapse. It is suggested that, ideally, anticoagulant therapy should be continued indefinitely in any patient whose pattern of disease thus increases the likelihood of a thromboembolic recurrence.
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PMID:Recurrence of thromboembolic disease after discontinuing anticoagulant therapy. A study of factors affecting incidence. 542 82

Calcium antagonists, of which the best known are verapamil, nifedipine and diltiazem, are a powerful group of cardioactive agents with a clinical spectrum of indications rather similar to those of beta-adrenoceptor blockade, including angina of effort, angina at rest, hypertension and supraventricular tachycardias (nifedipine is ineffective for the latter). In angina caused by coronary spasm, calcium antagonists are preferred to beta-blockade. Calcium antagonists have a basically different mode of action from beta-adrenoceptor blockade, although both ultimately act on the free cytoplasmic calcium ion concentration. Critical differences between the calcium antagonists are dependent on the individual properties of the calcium antagonists concerned. Different binding sites on the sarcolemma have been identified for nifedipine-like agents and verapamil, but with a different interaction with the nifedipine site. None of these sites might be relevant to the binding of calcium antagonists to the tissue of their therapeutic site of action (arterial smooth muscle for all; atrioventricular node for verapamil and diltiazem). As a group, calcium antagonists cause vascular dilation and do not cause bronchial constriction, in contrast to the beta-adrenoceptor blocking agents. In many patients, these diverse properties allow safe combination of calcium antagonists and beta-adrenoceptor blockers if due care is observed, especially in the case of nifedipine. The clinical differences between the effects of various calcium antagonists reflect: (i) the greater vasodilator capacity of nifedipine, so that at a given concentration the afterload effect dominates over possible effects on the nodal or myocardial tissue; (ii) the greater inhibition of vagal tone by nifedipine than by verapamil or diltiazem; and (iii) the greater inhibition of the atrioventricular node by verapamil and diltiazem. In angina of effort, calcium antagonists are now becoming the agents of first choice in some centers. Experimental use of calcium antagonists include the possible prevention of ventricular fibrillation, the inhibition of ischemic injury, the prevention of catecholamine mediated injury to the myocardium and decreased arterial calcinosis.
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PMID:Calcium ions, drug action and the heart--with special reference to calcium antagonist drugs. 615 Nov 99


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