The paper deals with the history of discovery of the auscultatory method for measuring blood pressure, made by N.S, Korotkoff, a surgeon of the Military Medical Academy; the Korotkoff’s method lias stood almost 100-year tests in medical science and medical practice and become the generally recognized world standard in measuring and assessing a blood pressure level in healthy individuals and patients with different diseases. N.S. Korotkoff has deserved the whole mankind's gratitude and a place of honor in the 20th century list of men of great intellect. It is regrettable that the name of the Russian genius has remained unknown for more than 50 years while the whole civilized mankind has widely applied his discover)' from day to day. For almost 40 years, the author has made a research to bridge a serious gap in the history of medicine and lo perpetuate the memory and fame of the Russian classical scholar of world medicine.

The paper presents data on the methodological and clinical aspects of self-monitoring of blood pressure by means of automatic measuring devices, the advantages and disadvantages of the method, indications for and contraindications to its use, plots of measurements, and standards for assessing their results. It also gives examples of clinical application of the diagnostic method.

The paper summarizes the data available in the literature on the epidemiology, pathogenesis, and treatment of metabolic cardiovascular syndrome in postmenopausal females. It presents the results of an open-labeled randomized study covering 4 I females with hypertensive disease (first-grade arterial hypertension), abdominal obesity, and menopausal syndrome. The patients received therapy with moxonidine. 0,4 mg/day, alone and in combination with hormonal replacement therapy (17β-estradiol and didrogesterone). Treatment with moxonidine alone and in combination with hormonal replacement therapy was demonstrated to promote blood pressure lowering and to improve some parameters of the blood lipid spectrum.

Risk stratification is very important In patients with unstable coronary artery disease, i.e. unstable angina or non-ST-elevation myocardial infarction. In patients with unstable coronary artery disease, there is a relation between the short- and long-term risk of death and blood levels of troponin T (a marker of myocardial damage) and N-terminal fragment of the BNP. We sought to evaluate the prognostic implications of cardiac neurohormonal activation as reflected by the plasma level of NT-proBNP in patients with non-ST-segment-elevation Ml and unstable angina. High levels of NT-pro BNP in patients with normal left ventricular ejection fraction may also indicate diastolic dysfunction which also can contribute to prognosis. Angiotensin-converting-enzyme inhibitors improve the outcome among patients with left ventricular dysfunction, whether or not they have heart failure. We assessed the role of an angiotensin-converting-enzyme inhibitor enalapril, and ACE inhibitor valsartan in patients with non-ST-segment-elevation with high level of NT-proBNP and high risk for cardiovascular events but who did not have left ventricular systolic dysfunction. Our findings show that in patients with unstable angina and non-ST-elevation myocardial infarction, high levels of NT-proBNP were accompanied by a greater risk of death at 6 months and added information to concentrations of troponin T, and other markers. Also, NT-proBNP was associated with the occurrence of subsequent hear! failure. In addition, enalapril, an angiotensin-converting-enzyme inhibitor, is beneficial in a broad range of patients with non-ST-segment-elevation without evidence of left ventricular systolic dysfunction or heart failure who are al high risk for cardiovascular events. Treat men l with enalapril reduced the rates of death and the occurrence Of subsequent heart failure. Valsartan and enalapril arc able to alleviate the pathological remodeling of LV and to improve its diastolic function.

Background. The effect of antihypertensive drugs on different cardiovascular events (CVE) in patients with coronary heart disease (CHD) and normal blood pressure (BP) remains unknown to the present day. Objective: to evaluate the effects ol amlodipine or enalapril versus placebo on the development of CVE in patients with CHD. Design, subjects, and methods: This is a double-blind, randomized, multicenter, 24-month (from April 1999 to April 2002) study evaluating the effect of amlodipine or enalapril versus placebo in 1991 patients with angiographically verified CHD (> 20 % stenosis at coronary angiography) and a diastolic BP of < 100 mm Hg. A substudy assessed the progression of atherosclerosis in 274 patients by intravascular ultrasound study (IVUSS). Therapy. The patients were randomly given amlodipine, 10 mg enalapril, 20 mg, or placebo, IVUSS was performed before and ai the end of the study. Assessment of basic outcomes. The main index of the efficacy of the drugs was the frequency CVE when amlodipine versus placebo was used. The other indices involved the comparison of amlodipine with enalapril and the latter with placebo. CVE included its related death, nonfatal myocardial infarction, resuscitated cardiac arrest, intervention for coronary revascularization, hospitalization for angina pectoris, congestive heart failure, fatal and nonfatal stroke or transient ischemic attack, and first diagnosed peripheral vascular disease. The prime objective of IVUSS was to estimate percentage changes in the volume of atherosclerotic plaques. Results. The mean BP was 129/78 mm Hg in the total sample BP increased by 0.7/0.6 mm Hg in the placebo group and by 4.8/2.5 and 4.9/2.4 mm Hg in the amlodipine and enalapril groups, respectively (p < 0.001 for both groups versus placebo). CVE developed in 151 (23,1 %) patients in the placebo group, in 110 (16.0 %) patients receiving amlodipine [risk ratio (RR) = 0.69; 95 % confidence interval (CI) 0.54-0.88; p = 0.003 and in 136 (20.2 %) patients treated with enalapril (BR = 0.85: 95 % CI 0.67-1.07; p = 0.16). The basic parameter that was a difference in the frequency of CVE in the enalapril and amlodipine groups was statistically insignificant (RR = 0.81; 95 % CI 0.63-1.04; p = 0,10). IVUSS revealed a tendency for a decrease in progressive atherosclerosis in the amlodipine group as compared with the placebo group (p= 0,12) with a significantly less progression in the subgroup of patients with a systolic BP higher than the mean BP (p = 0.02). Comparison with the baseline IVUSS values indicated a growth of plaques in the placebo group (p < 0.001), a tendency for progressive atherosclerosis in the enalapril group (p = 0.08). and no progression in the amlodipine group (p = 0,031 ). In the amlodipine group, the relation (r) of BP lowering to the progression of atherosclerosis was 0,19 (p = 0,07). Conclusion. The use of amlodipine in patients with CHD and progressive atherosclerosis caused a reduction in the frequency of CVE. Enalapril was observed to produce the similar, but less pronounced and statistically not so significant effect. IVUSS demonstrated a stunted progression of a vascular atherosclerotic lesion when amlodipine was administered.

Моте than 40 years ago it was suggested that endogenous digitalis-like Nа+/К+-ATPase inhibitors played an important role in the pathogenesis of salt-sensitive arterial hypertension. Since there has been much evidence for that digitalis-like factors form with the adaptive aim of causing natriuresis through Nа+/К+-ATPase inhibition in the renal tubules. However, the excessive production of these substances leads to the inhibition of Na+/K+-ATPase in vascular smooth muscle cells, which in turn enhances vasoconstriction. The mammalian endogenous digitalis-like Nа+/К+-ATPase inhibitors that belong to the classes of cardenolides (endogenous ouabain) and bufadienolides (marinobutfagenin) are described. In experimental salt-sensitive hypertension, endogenous ouabain that activates the renin-angiotensin system stimulates in the central nervous system the adrenal cortical production of marinobufagenin that is a natriuretic and a vasoconstrictor. The investigation of a role of endogenous digitalis-like hormones may open up fresh opportunities for pharmacological therapy arterial hypertension.