[Achievement of goal resting heart rate in patients with stable angina and hypertension at the background of therapy with -adrenoblockers in real clinical practice].

ß-Adrenoblockers improve quality of life and in a number of cases life prognosis in patients with stable angina (SA). Dose of -adrenoblockers is considered optimal if at the background of treatment resting heart rate (rHR) is persistently decreased down to 55-60 bpm. But according to data of international registries rate of achievement of target rHR (trHR) in real clinical practice does not exceed 22%. Aim of this study was to determine what portion of patients with SA and arterial hypertension (AH) achieves trHR at the background of therapy with -adrenoblockers in routine practice in this country. Twenty centers in 6 towns in Russian Federation recruited 399 patients (mean age 64+/-10 years) with class I-III angina and concomitant primary AH. These patients for at least 2 months received any -adrenoblocker and did not change its dose during 4 weeks before inclusion into the program. Portion of patients with trHR was 15.5%. There were no significant differences between average daily doses of most frequently used -adrenoblockers (metoprolol, bisoprolol, carvediolol) in groups of patients who achieved and did not achieve trHR. Quality of life of patients who achieved was comparable with that of those who did not achieve trHR. Attainment of trHR was associated with significant decrease of short acting requirement nitrates. There was a significant direct correlation between attainment of trHR and target arterial pressure.

[A possibility to interchange heart rate-slowing therapy with ivabradine and atenolol in patients with stable angina pectoris].

AIM: To evaluate the efficiency and safety of an interchange of atenolol and ivabradine in patients who had stable angina pectoris without myocardial infarction in the history and left ventricular (LV) systolic dysfunction. SUBJECTS AND METHODS: The trial enrolled 31 patients less than 70 years of age who had sinus rhythm, functional classes II-I angina on exertion without clinical signs of LV systolic dysfunction. At the first stage, 15 patients were randomized to ivabradine with its dose titration during 2 weeks; the other 16 patients were to atenolol. At the second stage, 10 patients were switched from ivabradine used at Stage 1 to atenolol 100 mg/day, other 10 patients who were on atenolol were switched to ivabradine 15 mg/day, and 11 patients received combination therapy with ivabradine + atenolol in half doses. All the patients underwent treadmill exercise testing and applanation tonometry. RESULTS: Atenolol, unlike ivabradine, lowered brachial blood pressure and unchanged the central index of its increment, which was associated with LV systolic elongation. On the contrary, ivabradine decreased the central increment index and exerted no significant effect on the duration of LV systole. By comparatively lowering heart rate, ivabradine as well as atenolol reduced pulse wave propagation velocity. CONCLUSION: If ivabradine or atenolol is insufficiently effective or poorly tolerated, there may be an interchange of the drugs, as well as their combination in half doses without substantially affecting their therapeutic action in patients with stable angina pectoris without LV systolic dysfunction.

[Immunoinflammatory changes (myocarditis?) in chronic heart failure in alcoholic patients].

AIM: To estimate the contribution of immuno-inflammatory changes to the formation of clinical and hemodynamic features in alcoholic patients with chronic heart failure (CHF). SUBJECTS AND METHODS: Forty-five males with CHF in the presence of alcohol-induced heart damage (AIHD) who had been admitted to therapeutic units for decompensated heart failure were examined. A control group consisted of 20 men with the CHF severity comparable with the NYHA classification in the presence of prior myocardial infarction. All the patients underwent examination of the immune-inflammatory status--the cytokines: interleukin (IL) 6, IL-8, IL-12, tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta1, endotoxin, cellular immune parameters, and cardiac structure and function by echocardiography. RESULTS: The patients with CHF in the presence of AIHD, as compared to those with ischemic cardiomyopathy, showed the higher levels of inflammatory cytokines (IL-6, TNF-alpha, IL-12, and endotoxin) and cell-mediated immunity changes (the smaller count of suppressor T cells, natural killer cells, and a shift of the T-helper/T-suppressor ratio towards the T-helper population). The magnitude of these changes correlated with the severity of CHF and cardiac morphofunctional changes. CONCLUSION: The relationship of immuno-inflammatory changes to the severity of CHF and the morphofunctional state of the heart irrespective of the etiology of heart failure demonstrated the role of immune inflammation in its pathogenesis particularly in alcoholic patients who were found to have more marked immuno-inflammatory changes than in those with ischemic cardiomyopathy.

[Efficacy of ivabradin in combined treatment of patients with postinfarction systolic chronic cardiac failure].

AIM: To study effects of ivabradin on clinicohemodynamic and prognostic parameters in patients after myocardial infarction (MI) with systolic chronic cardiac failure (SCCF). MATERIAL AND METHODS: A population-based randomized prospective trial enrolled 49 patients (40 males--81.6%, mean age 63.1 +/- 8.1 years) with sinus rhythm and a longer than 3 month history of MI. The patients were randomized into 2 groups: 23 patients of group 1 received standard treatment plus ivabradin, 26 patients of group 2 received standard treatment alone. Follow-up was 36.1 +/- 6.2 months. We analysed the trend in heart rate (HR), blood pressure (BP), parameters of echocardiography, ECG, levels of electrolytes, creatinin in blood plasma, frequency of hospitalizations, recurrent non-fatal MI and lethality (combined endpoint). RESULTS: In the end of the trial ivabradin significantly decreased HR from 71 to 64 b/m. Frequency of combined end point of efficacy was 30.4 and 50% in group 1 and 2, respectively. In group 1 primary end point in high baseline HR occurred more frequently than in HR < 70 b/m in 6 (50%) and 1 (9.1%) cases, respectively, but these differences were not significant (p = 0.068). In group 2 the differences were significant--9 (90%) and 4 (25%) cases, respectively (p = 0.004). By none of the parameters of ECG, plasma electrolytes, creatinine level significant intergroup differences were found. CONCLUSION: In the same trend in BP and ECG, group 1 patients showed significant and more pronounced HR lowering than group 2 patients. Addition of ivabradin to standard treatment of SCCF after MI promoted less frequency of hospitalizations, recurrent non-fatal MI, fatal cardiovascular events. This effect was especially strong in high baseline HR.

[Inflammation and chronic heart failure. The role of statins].

Immune inflammation is an important link in pathogenesis of chronic heart failure (CHF). It has been proven that hyperproduction of proinflammatory cytokines (TNFa, IL-6, IL-1, etc) with associated endothelial dysfunction and oxidative stress affect unfavorably clinico-hemodynamic parameters and prognosis of life of patients. However attempt to augment efficacy of treatment of CHF by means of inclusion of TNFa activity inhibitors in the complex of main remedies turned out unsuccessful. At present under discussion are perspectives of application in this category of patients of statins--lipid lowering drugs with pleiotropic properties most important of which is antiinflammatory action. Theoretical obstacles for the use of statins constitute available epidemiological data on reverse relationship between cholesterol level and mortality of patients with CHF in a framework of endotoxin-lipoprotein theory. At the same time preclinical and clinical experience has been accumulated evidencing for perspectiveness of such approach. Final solution of the problem of safety and feasibility of application of statins in CHF is expected after completion of prospective randomized trials GISSI-HF and CORONA.

[Treatment of ventricular arrhythmias in patients with manifestations of heart failure]. / Lechenie zheludochkovykh aritmii u bol'nykh s proiavleniiami serdechnoi nedostatochnosti.

A comparative study of the efficiency of digoxin and "pure" antiarrhythmic agents was carried out in 56 patients with ventricular arrhythmias and signs of circulatory insufficiency (CI). Digoxin had arrhythmogenic effect in 20% of the patients, which was twice as frequent in the marked CI group. "Pure" anti-arrhythmic agents were effective in 47% (ritmilen) to 71% (cordaron), and etmozin, in 63% of the patients, while adverse myocardial inotropic effect was only produced by ritmilen. Combined use of etmozin, ritmilen or cordaron with digoxin increases their antiarrhythmic efficiency.

[Digoxin in the treatment of patients with ventricular disorders of cardiac rhythm]. / Digoksin v lechenii bol'nykh s zheludochkovymi narusheniiami ritma serdtsa.

A study of digoxin antiarrhythmic effect in 44 patients with recurrent ventricular extrasystole showed the drug to be effective in an average 34% of patients, the effect being more marked in patients with originally impaired ventricular function.