[Changes of endotoxin concentration in blood serum in patients with uncomplicated acute myocardial Q-infarction].

The effectiveness of acute myocardial infarction (AMI) treatment does not correspond to high material costs for the study of its pathogenesis and development of new drugs. This circumstance gives the grounds to assume existence of nowadays unknown mechanisms of emergence and development of this disease. High probability of participation of endotoxin (ET) in the pathogenesis of AMI was theoretically proved by us for more than a quarter of the century ago, but it's clinical evidence to date is not found yet. As a result of the study a significant increase of endotoxin (ET) concentration in the blood serum of patients with AMI increasing from 1 to 14 day of the disease has been found. In women the concentration of ET was higher than in men. It allows to qualify the EA as a factor probably influencing the known difference in AMI tolerance in men and women. The source of ET were Bacteroides (most often--67.8% of patients), Klebsiella, Pseudomonas, Proteus, Escherichia coli. One or two bacteria more often took part in the development of EA. In 9.1% of patients the etiology of EA could not be verified, what indicates the presence of other sources of EA, not evaluated in this study. In 25% of patients with AMI serologic evidence of systemic candidiasis, caused by candida Albicans, has been found, what is able to enhance the biological effects of ET.

[Endotoxin aggression in pathogenesis of acute myocardial infarction and its origin].

Endotoxin aggression of intestinal origin occurs in 89% of patients with acute myocardial infarction and may be a factor of the induction and/or progression of the disease. Sources of the development of endotoxin aggression often are Escherichia coli, Bacteroicles, Klebsiella, Proteus and Pseudomonas.

[Apolipoprotein B100 as a risk factor of acute coronary syndrome and this risk factor effect on arterial hypertension in patients with ischemic heart disease].

AIM: To clarify correlations between an elevated concentration of apolipoprotein B100 (apoB) in blood plasma and risk of acute coronary syndrome (ACS); to study apoB level in hypertensive patients and its correlation with ischemic heart disease (IHD) risk in these patients. MATERIAL AND METHODS: Lipid serum spectrum (cholesterol, triglycerides (TG), lipoprotein a (Lpa) and apoB was studied in 456 patients with ACS by NYHA criteria, 119 patients with chronic IHD and 86 patients free of cardiovascular diseases (controls). All 575 patients with IHD were divided into those with and without hypertension (426 and 149 patients, respectively). RESULTS: Lpa was significantly higher in patients with ACS; apoB was higher in ACS and chronic IHD patients. ApoB was higher in IHD normotensive patients than in controls and higher in IHD hypertensive patients than in IHD normotensive patients and in the control group. Lpa in IHD hypertensive patients was significantly higher (p < 0.045) than in the controls as well as TG (p < 0.05). By the other parameters the groups did not differ. CONCLUSION: The blood plasma level of apoB higher than 130 mg/dl is an independent and significant risk factor of ACS in IHD patients especially at the age under 60. The level of apoB over 115 mg/dl is a significant risk factor of IHD. The significance of this lipid factor rises in concomitant hypertension.

[The effect of anaprilin on the reaction of the sympathetic-adrenal system to graded physical loading in healthy subjects and patients with ischemic heart disease]. / Vliianie anaprilina na reaktsiiu simpatiko-adrenalovoi sistemy pri dozirovannoi fizicheskoi nagruzke u zdorovoykh liudei i bol'nykh ishemicheskoi bolezn'iu serdtsa.

The specific features of responses of the sympathoadrenal system during its activation by graded exercise (E), including that along with anaprilin induced blockade of beta-adrenoceptors, were determined from the urinary excretion of norepinephrine, epinephrine, dopamine, and dioxyphenylalanine in 54 healthy males and 22 patients with postinfarction cardiosclerosis concurrent with Functional Class I-II angina pectoris on effort. E caused hyperreactivity of the sympathoadrenal system, as appeared as significantly greater increases in the levels of catecholamines and their precursors in the patients than in the healthy persons. A single anaprilin dose of 40 mg abolished the responsiveness to exercise and improved its tolerance. The revealed features of sympathoadrenal responsiveness to exercise with and without anaprilin suggest that the patients with coronary heart disease have sympathoadrenal dysfunction, which shows one of the possible mechanisms responsible for the cardioprotective effect of beta-adrenoblockers in this disease.

[Blood rheological effects in ischemic heart disease treated with antianginal and thrombolytic agents]. / Gemoreologisheskie éffekty u bol'nykh ishemicheskoi bolezn'iu serdtsa pri lechenii antianginal'nymi i tromboliticheskimi sredstvami.

In 161 patients with different forms of ischaemic heart disease the authors studied changes of the blood viscosity, erythrocyte aggregation and of thrombocytes during treatment with modern antianginal and the thrombolytic agents. Treatment with nitroglycerin in tablets and Sustac revealed no statistically significant differences in the changes of the haemorheological parameters. The mainly thrombocyte disaggregational effect was shown by micristin (aspirin/propranolol in the daily dose of over 120 mg) and verapamil (the daily dose over 160 mg). The use of dipyridamol, trental and nonachlazin was accompanied both by the decrease of functional activity of thrombocytes and by the decrease of the blood viscosity as a result of improvement of the functional properties of erythrocytes. Sodium nitroprusside depressed shortly the aggregation of platelets and decreased the blood viscosity at the expense of the decrease of the haematocrit. The use of streptokinase (avelisine) in patients with acute myocardial infarction was accompanied by defibrinisation of the blood, by marked decrease of the aggregation facility of formed elements of the blood and its viscosity. The results suggest that the haemorheological mechanisms participate in the antianginal effect of the drugs studied.