[Acute coronary syndrome].
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Biomedical subjects
Publications and source records attributed to N A Mazur.
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In a randomized controlled trial 329 postmyocardial infarction patients with high-grade ventricular extrasystoles were divided into 3 groups. Group 1 of 112 patients received calcium antagonists (verapamil, nifedipine, verapamil+nifedipine), group 2 of 100 patients received propranolol hydrochloride, group 3 consisted of 117 controls. The aim of the study was to elucidate the effect of the above drugs on sudden death and repeated nonfatal infarction risk. The mean follow-up duration made up 16 +/- 0.9, 16.8 +/- 1.1, 20.8 +/- 1.0 months for groups 1,2 and 3, respectively. 35 patients of the treatment groups turned out inappreciable because of early discontinuation of chemotherapy. Overall lethality for the groups 1, 2 and 3 reached 0.9%, 4% and 12% of patients, respectively. Most of lethal outcomes in the controls were sudden. Repeated nonfatal myocardial infarction arose less frequently in groups 1 and 2, but the difference was insignificant.
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A short treatment course (2-3 weeks) of calcium antagonist isoptin-retard has been tried in 20 patients with stable essential hypertension stage II-III. The treatment achieved: clinical response in the majority of the patients in the presence of minor prolongation of the atrioventricular conduction, a clear tendency to reduction of systolic, mean arterial and resting diastolic pressures. Stroke volume increased both at rest and under loading, peripheral resistance of the vessels diminished, maximum filling rate for the left ventricle increased, its peak was reached more rapidly, hemodynamic contribution of the first third diastole to left ventricular filling rose against less contribution of the left atrial systole. Thus, it is shown that isoptin-retard in a mean dose 420 mg/day demonstrates hypotensive activity and beneficial hemodynamic effects without pronounced increase in atrial-ventricular conduction in hypertensive subjects with the disease stage II-III.
Calcium antagonist dilren in a short course was given to 11 hypertensive subjects (AH stage II). A clinical response in the majority of the patients was associated with a decline in systolic, mean arterial and resting diastolic pressure (by 8.1, 7.8 and 11.5%, respectively). In orthostasis and under isometric loading dynamic values of arterial pressure tended to lowering, especially diastolic (by 6.7 and 8.3%, respectively). Reduced pressure resulted from a significant reduction in the total peripheral resistance (by 19.8% at rest, in orthostasis by 10%, in isometric load by 26.1%). Minute blood volume increased because of a rise in stroke output. Dilren is recommended in a standard dose 300 mg/day in mild hypertension and in an individual dose 600 mg/day in moderate disease.
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Technetium-99m pertechnetate equilibrium ventriculography was used to evaluate the effects of captopril in a single dose of 50 mg on the changes in ST segment depression during the identical bicycle ergometer exercise, as well as on systemic and regional hemodynamic parameters in 10 patients (mean age 52 years) with Functional Classes II-III exercise-induced angina pectoris. During exercise performed 45 and 90 minutes after captopril, ST segment depression decreased by 30 +/- 0 (p less than 0.05), and 32 +/- 10% (p less than 0.02), respectively as compared to baseline ST segment displacement. Following 90 minutes after the drug administration, end-systolic volume reduced both at rest and during exercise, resting stroke volume increased from 71 +/- 4 to 76 +/- 4 ml (p less than 0.01), whereas exercise stroke volume rose from 69 +/- 3 to 74 +/- 3 ml (p less than 0.03); with the drug, ejection fraction showed a 5% increase (p less than 0.02) at rest and a 4% increase (p less than 0.02) on exercise. Thus, captopril had a beneficial effect on the hemodynamics and reduced myocardial ischemia in patients with exercise induced angina.
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The purpose of the study was to explore the dynamics of the concentration of atrial natriuretic hormone (ANH) in response to changes in arterial pressure including those induced by hypertonic crisis, 7-day hypotensive monotherapy with the drugs having different action mode, and the acute test with the basic hypotensive drugs. 75 patients suffering from arterial hypertension were entered into the study. Measurements of the concentration of ANH in blood plasma were performed by radioimmunoassay with the aid of the kits manufactured by the Amersham Company (Great Britain). The activity of renin and aldosterone was determined by radioimmunoassay according to the standard technique. A strong positive correlation was revealed between the concentration of ANH and the level of both systolic and diastolic AP. A significant rise of the concentration of ANH elicited by hypertonic crisis reflects the growth of the tension of the depressor mechanisms by which AP is regulated. The lack of significant changes in the level of ANH during the acute pharmacological tests and effective continuous treatment with the hypotensive drugs attests to the existence of the complex mechanisms that regulate ANH secretion, determined not only by the level of AP.
The efficacy of allapinin, ethacizine, ritmilen, kinilentin, obsidan and finoptin given alone and in different combinations was studied in 44 patients with paroxysmal atrial fibrillation provoked by transesophageal pacing. The use of the combinations of the drugs belonging to the first group as well of those of the first group combined with the drugs belonging to the 2nd-4th group permitted one to significantly enhance the treatment efficacy, to reduce drug doses in a lot of patients and, therefore, to minimize the rate of side effects. The data obtained promoted the choosing of the therapy algorithm to prevent paroxysms of atrial fibrillation. While designing the algorithm, account was taken of the rate of paroxysms and of the initial sinus rhythm as was of the results of estimating the comparative efficacy of the drugs under study.
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Vasodilators (verapamil, nifedipine, and prazosin) versus hypothiazide and clofelin were studied for their effects on resting and exercise blood levels of catecholamines in 58 patients with moderate arterial hypertension. Clofelin decreased norepinephrine levels, whereas hypothiazide increased it at rest and during exercise test. The most marked effect on norepinephrine levels was produced by nifedipine, then prazosin, particularly in patients with initially enhanced total peripheral vascular resistance. Verapamil failed to substantially affect norepinephrine levels. Due to the fact that the elevated levels of norepinephrine may have a negative action, it is suggested that antiadrenergic agents should be supplemented to a long-term therapy with nifedipine or prazosin.
The examination comprised 58 patients with essential hypertension and 17 with nephrogenic arterial hypertension. An analysis of the baseline levels of natural natriuretic factor in patients with essential and nephrogenic hypertension revealed no intergroup differences (55.3 +/- 3.0 and 45.7 +/- 5.2 ng/ml, respectively). The concentration of natural natriuretic factor was significantly higher in even patients with mild arterial hypertension than in healthy persons (28.4 +/- 4.7 and 17.4 +/- 2.9 ng/ml). There was a direct correlation between the level of natural natriuretic factor and blood pressure and left ventricular myocardial hypertrophy. There were higher positive correlations between the levels of natural natriuretic factor and those of hormones of the renin-angiotensin-aldosterone system and catecholamines in patients having a diastolic pressure of greater than 115 mm Hg. A significant increase in natural natriuretic factor levels (92.1 +/- 11.8 ng/ml) was found in the presence of hypertensive crisis.
The intracardiac hemodynamics was studied in 33 patients with exertional angina pectoris undergoing an acute drug test with verapamil (n-15) and nifedipine (n-18) by using radionuclide ventriculography both at rest and during exercise. All the patients were divided into 2 groups by the increase in exercise duration with the two drugs: 1) those who exhibited a marked antianginal effect and 2) those without it. At rest, the calcium antagonists enhanced ejection fraction in the two groups. Exercise ejection fraction also increased, but in a subgroup of patients who displayed no higher exercise tolerance with verapamil. Verapamil and nifedipine in Group 1 patients resulted in lower left ventricular end diastolic volume. It is suggested that the antianginal effect of calcium antagonists is to a certain degree associated with decreased afterload, as manifested by diminished left ventricular end systolic volume.