The article presents the results of a 6-month long-term therapy with angiotensin II receptor blocker Valsacor and aldosterone receptor blocker Spironolactone in patients with chronic heart failure (CHF) against a background of ischemic and/or post-infarction left ventricular remodelling. The results show that the renin-angiotensin-aldosterone system (RAAS) blockade in the combination therapy slows down the pathological remodelling of the left ventricle (LV) and thus prevents progression of CHF in a majority of patients with myocardial infarction (MI).

Нарушение периферической гемоциркуляции яв-ляется одним из существенных механизмов возникно-вения и/или неблагоприятного течения инсулинорези-стентности, с одной стороны, и усугубления последней при применении многих препаратов, предназначенных для лечения распространенных социально значимых заболеваний, развивающихся на фоне инсулинорези-стентности, — с другой [1—6]. При этом упрощенную схему патогенеза инсулинорезистентности, в которой проблема рассматривается исключительно в плоско-сти изменения кровотока в системе микроциркуляции, можно представить в виде четырехчленной формулы: патология микроциркуляции → снижение кровотока в микроциркуляторном русле скелетных мышц, жировой ткани, печени, поджелудочной железы → неадекватная утилизация глюкозы с компенсаторной гиперинсулине-мией → развитие и/или прогрессирование инсулиноре-зистентности.С учетом изложенного выше, при выборе препарата для эффективной и безопасной коррекции ассоцииро-ванных с инсулинорезистентностью артериальной ги-пертензии, коронарной и сердечной недостаточности предпочтение следует отдавать лекарственным сред-ствам, оказывающим позитивное действие на основную функцию микроциркуляции — транскапиллярный об-мен веществ [7—11]. В наибольшей степени для этого подходят периферические вазодилататоры, особенно блокаторы медленных кальциевых каналов дигидропи-ридинового ряда, которые в отличие, например от боль-шинства β-адреноблокаторов (за исключением препара-тов с дополнительной вазодилатирующей активностью), способны препятствовать снижению кровотока в систе-ме микроциркуляции [12—14]. Доказано положительное влияние антагонистов кальция, в частности адалата, на тканевый кислородный режим у больных ишемической болезнью сердца (ИБС), которое проявляется увеличе-нием напряжения кислорода (рО

Effect of 6 months treatment with carvedilol (25 mg/day) on blood levels of cytokines (interleukins 1alpha, 2, 6, 8, tumor necrosis factor alpha) and clinical symptoms of heart failure was studied in patients with cardiac dysfunction after myocardial infarction. Patients with NYHA class II heart failure, ejection fraction 50% and moderately lowered tolerance to physical exercise (n=21) initially had enhanced cytokine expression: blood content of interleukin (IL) 2 was 2.8 times, tumor necrosis factor (TNFalpha) 78%, IL-1alpha 60% above normal level. Therapy with carvedilol in this group was associated with decreases of Il-2 (-23.8%), TNFalpha (-16.7%), IL-1alpha (-12.5%) (p<0.05-0.01). This was accompanied by alleviation of clinical symptoms and improved exercise tolerance. Patients with NYHA class III heart failure (n=16) with low left ventricular ejection fraction (30+/-2.7%) and low exercise tolerance had high levels of all studied cytokines. Levels of IL-2, TNFalpha and IL-1alpha were most elevated (3.1, 2.8 and 2 times higher than normal values, respectively). Therapy with carvedilol was associated with improvement of clinical symptoms and exercise tolerance (+35%, p<0.05)), increase of ejection fraction (+15%, p<0.05), decrease of left ventricular end systolic volume (-17.5%, p<0.05), and lowering of blood levels of TNFalpha (-31%), IL-2 (-17.4%), IL-1alpha (-15.6%). However cytokine levels remained substantially elevated compared with normal values. Carvedilol was well tolerated, and did not cause negative metabolic effects or other complications.

Aim. To study free radical processes in patients with myocardial infarction (MI) aggravated by heart. failure.Material and methods. Forty seven patients taken to the clinic within the first 5 hours of MI were examined. The patients were divided into 2 groups: 1) those with left ventricular failure-complicated IM (n = 25); 2) those with uncomplicated MI (n = 22). A control group included 17 apparently healthy males. The activity of lipid peroxidation (LPO) and blood antioxidative defense was determined in the. patients' red blood cells prewashed off the plasma with saline solution at a temperature of 4degreesC.Results. The tension of free radical lipid oxidation mechanisms in patients with MI aggravated by circulatory insufficiency is followed by an increased antiradical activity. In patients with uncomplicated higher LPO activity is attended the less marked activation of antioxidative enzymes. The examinees were found. to show a correlation of the global systolic function of the left ventricle with the concentration of LPO products and with the activity of antioxidative enzymes.Conclusion. More significant LP activation coupled with. left ventricular systolic dysfunction was noted in patients with MI aggravated by acute heart failure.

AIM To study a relationship between reduced heart rate variability and ventricular ectopic activity in patients with coronary artery disease and also efficiency of atenolol in suppression of ventricular arrhythmias and increase of heart rate variability. MATERIAL AND METHODS 32 men with stable angina of effort (functional class II-III) after the first myocardial infarction (mean age 52.9 years). 24-h ECG monitoring was carried out in 25 patients before and 3 weeks after treatment with atenolol in the dose 50-100 mg/day for 3 weeks. RESULTS The mean standard deviation of the R-R intervals in 24 hours was much lower in patients with ventricular arrhythmias. In the majority of the patients with frequent ventricular premature beats (> 10 VPB/hour), the changes in vegetative homeostasis manifested mainly by activation of sympathetic nervous system. Atenolol given for 3 weeks to these patients proved effective. CONCLUSION Low heart rate variability correlated with increased frequency of ventricular premature beats. Atenolol can be recommended for the treatment of such patients.