[Influence of long-term therapy with enalapril on late postinfarction remodeling and functional state of the left ventricle in patients with diastolic heart failure.].

Enalapril (average dose 7,0+/-0.8 mg) was given for 12 weeks to 15 patients with preserved left ventricular (LV) systolic function who had survived large focal myocardial infarction small i, Ukrainian6 months before that. The use of enalapril was associated with 49% lessening of severity of clinical signs of heart failure (p<0.001) and 47% increase of tolerance to physical exercise. It also provided dose dependent 17.8% reduction of LV myocardial mass (p<0.05), normalization of initially "hypertrophic" type of transmitral flow, 21% lowering of LV end diastolic pressure (p<0.05) without effect on LV volume, geometry, global and local systolic function.

[Effect of long-term myocardial unloading with beta1-adrenoblocker atenolol on the state of the left ventricle in patients with moderate ischemic dysfunction of the heart as shown by doppler echocardiography]. / Vliianie beta1-adrenoblokatora atenolola na sostoianie levogo zheludochka u bol'nykh s umerenno vyrazhennoi ishemicheskoi disfunktsiei serdtsa (doppler-ékhokardiograficheskoe issledovanie).

Effects of 12-month therapy with a beta1-adrenoblocker atenolol on the process of late postinfarction remodeling of the heart and parameters of intracardiac hemodynamics were assessed in an open noncomparative study on 55 survivors of macrofocal myocardial infarction. Therapy with atenolol was associated with: (1) reduction of myocardial hypertrophy in patients with increased left ventricular myocardial mass without effect on its volume, cavity geometry and global systolic function; (2) normalization of initially 'hypertrophic' type of transmitral blood flow. Affecting mainly the demand component of the myocardial oxygen supply/demand ratio atenolol promoted inclusion of hibernating cardiomyocytes into active contraction.

[Effect of atenolol and trimetazidine on dispersion of cardiac rhythm in patients with moderately expressed postinfarction left ventricular dysfunction]. / Vliianie atenolola i trimetazidina na dispersiiu ritma serdtsa u bol'nykh s umerenno vyrazhennoi postinfarktnoi disfunktsiei levogo zheludochka.

AIM: To study effects of atenolol and trimetazidine on heart rhythm variability in postmyocardial infarction patients with moderate left ventricular dysfunction. MATERIAL AND METHODS: Fifty postmyocardial infarction (PMI) patients participated in a 3-week randomized blind trial. They were divided into two groups given atenolol or trimetazidine. Time and spectral analyses of heart rhythm dispersion on short ECG parts (5 min) were done before and after treatment with atenolol (76.9 +/- 6.6 mg/day) or trimetazidine (60 mg/day). RESULTS: Only course therapy with atenolol raised heart rhythm variability registered both by time and spectral analysis. CONCLUSION: Studying heart rhythm variability enables efficient non-invasive control over effectiveness of neurohumoral heart unloading in the course of pharmacotherapy of ischemic left ventricular dysfunction.

[Role of left ventricular systolic and diastolic dysfunction in clinical manifestations of chronic heart failure in patients with prior myocardial infarction]. / Rol' sistolicheskoi i diastolicheskoi disfunktsii levogo zheludochka v klinicheskoi manifestatsii khronicheskoi serdechnoi nedostatochnosti u bol'nykh, perenesshikh infarkt miokarda.

AIM: To study the impact of systolic and systolic dysfunction of the left ventricle (LV) on the clinical manifestations of chronic heart failure (HF) in patients with prior myocardial infarction (MI). MATERIALS AND METHODS: 102 patients (mean age 47.4 +/- 0.7 years) who had sustained large focal IM at least 6 months before were examined. LV echocardiography was made to define systolic-diastolic relationships in HF. RESULTS: Analyzing the prevalence of primary diastolic HF in patients with its different clinical manifestations, it may be concluded that LV diastolic dysfunction is of the leading pathogenetic value at early stages of ischemic heart dysfunction. A complex relationship between the clinical manifestations of HF and a number of parameters characterizing the systolic and diastolic function of LV was estimated by the multiple regression analysis and presented as a trinomial equation. CONCLUSION: The results of the regression analysis have shown that the clinical manifestation of HF intensifies as relaxation slows down and transmitral blood flow redistributes to the left atrial systole; the severity of HF also increases with the depletion of compensatory mechanisms responsible for LV contractility.

[Depression of diurnal dispersion of sinus rhythm in patients after myocardial infarct]. / Depressiia sutochnoi dispersii sinusovogo ritma u bol'nykh, perenesshikh infarkt miokarda.

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.