Search

Antihypertensive therapy with sequential addition of drugs (noliprel, noliprel-forte, metoprolol, amlodipine) for achievement of target blood pressure (BP) below 140/90 mm Hg was used in the treatment of 99 patients with arterial hypertension (AH) with (n=51) or without left ventricular (LV) hypertrophy (LVH). At initial Doppler study of transmitral blood flow all patient with LVH had type 1 (n=48) or type 2 (n=3) diastolic LV dysfunction. Among patients without LVH 13 had minor type 1 diastolic LV dysfunction. After 12 - 14 months of antihypertensive therapy in all 44 patients with moderate LVH (myocardial mass index below 140 g/m2) BP corresponded to target level. This was associated with 6% decrease of myocardial mass index (MMI) and its normalization in 2/3 of patients, restoration of diastolic function in 3/4 of patients and its improvement in other patients, decrease of functional class, in rease of 6 min walking distance, and improvement of quality of life according to questionnaire for patients with CHF. In 7 patients with pronounced LVH (MMI 140 g/m2) target BP was not achieved, LVMMI, diastolic function, and functional class did not change, however tolerance to physical effort and quality of life improved. Thus in all patients with AH without LVH target BP level was achieved. In minor initial diastolic dysfunction diastolic function restored to normality, functional class, tolerance to physical work and quality of life improved.

Aim: To assess effect of trimetazidine on clinical course of postinfarction period and restoration of left ventricular myocardium., Material and Methods: 1.5-2.0 months after acute myocardial infarctions 123 patients receiving conventional therapy (aspirin, beta-blockers, angiotensin converting enzyme inhibitors, nitrates) were divided into 2 groups. Patients of group 1 (n=62) were given 60 mg/day of trimetazidine and patients of group 2 (n=61) were not. All patients were followed up for 12 months after onset of myocardial infarction., Results: 12 months after myocardial infarction decreases of average heart failure and angina classes, increase of left ventricular ejection fraction, reduction of left ventricular end systolic and end diastolic volumes and left atrial dimensions occurred in group 1. Ejection fraction in this group became significantly higher while left ventricular end systolic and end diastolic volumes and left atrial dimensions significantly lower than in group 2. Index of diastolic function V(e)/V(a)ased in trimetazidine treated patients with normal and hypertrophic types of transmitral diastolic blood flow and became higher than in group 2., Conclusion: Trimetazidine facilitates restoration of systolic and diastolic left ventricular function after myocardial infarction.

Bicycle ergometry and echocardiography were conducted in 54 patients with primary uncomplicated large-focal myocardial infarction (MI), while their central hemodynamic parameters were examined radiocardiographically on days 10, 20 and 30 of the disease. About 70% of patients were doing exercise until they were fatigued or showed a submaximum pulse rate, whereas 20% developed angina pectoris. In the course of recovery, threshold capacity increased in most of the patients and as the cumulative group result (with a 16% increment from day 10 to day 20). No basic changes in hemodynamic response to exercise could be registered between days 10, 20 and 30 of the disease. Most patients showed reduced stroke index during exercise, and their cardiac index grew at the expense of increased heart rate. Exercise-induced rise in the cardiac index was insignificant in anginal cases. Left-ventricular ejection fraction increased significantly: from 48.6 +/- 1.8 on days 1-3, to 55.4 +/- 2.3 on day 30 (p less than 0.01), the magnitude of the increase showing no correlation with threshold capacity parameters and being basically similar in all groups of patients where exercise had to be discontinued for different reasons.

Ultrasonic scanning of the heart was carried out on days 1, 10, 20 and 30 of uncomplicated myocardial infarction (MI) in 46 patients whose total and segmental ejection fraction (EF) (5 segments by a two-chamber projection from the apex) were then calculated. Total left-ventricular EF was moderately reduced on day 1 (48.6 +/- 1.8%) and increased significantly by day 30 (55.4 +/- 2.3%, p less than 0.01). All patients showed impaired segmental contractility in infarcted areas. Segmental EF was essentially reduced in segments 3, 4 and 5 in anterior MI, and in segments 1 and 2 in posterior MI. Recovery was associated with increasing EF in asynergic segments, that nevertheless remained diminished on day 30, as compared to unaffected areas. The rise in left-ventricular total EF is attributed to better contractility of asynergic segments.

In a coronary club, physical trainings (30-60 lessons) by using bicycle ergometry were performed in 242 patients with various types of coronary heart disease, two thirds having a history of myocardial infarction. In 58% of the patients, the interval between the onset of myocardial infarction and the initiation of the trainings ranged 1 to 3 months. The trainings were found to be beneficial in 99.4% of the patients who had sustained myocardial infarction. After 30 training lessons, the threshold exercise capacity showed a 36.3% increase. Beneficial trainings depended on the number of trainings and, to a lesser degree, on patients' age. The trainings were followed by favorable changes in plasma lipid levels and hemorheology.

In experimental conditions, exercise increased electrical stability of the heart in trained rats, promoted an improvement of heart electrical stability in hypoxic hypoxia and under the effect of dextran, which is known to worsen blood rheologic properties, and had no effect on heart electrical stability in curantyl-treated rats. In 50 postmyocardial-infarction coronary patients, exercise was conductive to a drop in erythrocyte cholesterol/phospholipid ratio and total plasma cholesterol, and a rise in alpha-cholesterol level. In 10 untrained control coronary patients, erythrocyte cholesterol/phospholipid ratio remained unchanged.

Two months after myocardial infarction, 30 patients were subjected to a 10-week physical training course. Following the training, their threshold capacity grew by 46%. The effect of training (increased threshold capacity, reduced double product at submaximum effort) persisted for 1 year after myocardial infarction. In 28 control-group patients, changes of threshold capacity and double product at submaximum effort were not significant over the first post-infarction year. A relatively early post-infarction physical training is not associated with complications and largely speeds up physical rehabilitation.

The psychological effect of short exercise on a bicycle trainer (30 sessions over 10 weeks) was assessed in 20 postmyocardial infarction patients, while spontaneous mental changes were assessed in 21 untrained controls. Exercise was started 2 to 2.5 months after the attack. Mental states were assessed by the brief multifactorial personality assessment questionary (the BMPAQ test) and the neuroticism scale (NS). Physical exercise contributed to a more rapid psychological rehabilitation, as evidenced by the BMPAQ and NS testing. The mentality of the control patients improved less rapidly as shown by the BMPAQ test, while their NS parameters remained unchanged. Mental parameters of trained and untrained patients were basically similar within 12 months, after myocardial infarction as evidenced by the BMPAQ test.

This is a report on the results of physical training in 52 patients who had myocardial infarction and in 8 patients with angina pectoris of effort who had not suffered infarction. The training lasted 10 weeks, 3 times a week using a bicycle ergometer. 75% of the patients have accomplished the entire program of training. Patients who had myocardial infarction showed threshold capacity increased by 22%, which is considerably higher than in the group with no training. The work equivalent to the exercise was performed after training with lower pulse rate and systolic arterial pressure. In the majority of patients the volume of the heart decreased, as determined by X-ray and the amplitude coefficient of apex cardiogram diminished which justifies the assumption of improvement in the state of the myocardium in these patients. In patients with angina pectoris of effort there was an increase of threshold capacity which is explained by decreased pulse rate and systolic arterial pressure after physical loading.

The substantiation and the indications and contraindications for the physical training of patients who have had myocardial infarction are discussed on the basis of the experience gained at the Clinic of Internal Diseases of the Medical Department of K. Marx University in Leipzig (DDR) and the First Chair of Hospital Therapy of the N.I. Pirogov Second Moscow Medical Institute. On the strength of their own findings and the information in the current literature, the authors name, among other precoditions for training, diminution of capacity for muscular work, psychologic instability and the persisting threat of the progression of ischemic heart disease. The methods of functional diagnosis, which is also a necessary precondition for the physical rehabilitation of the patients are bicycle ergometry, auxiliary tests for the gaseous composition of blood and exhaled air, determination of the heart volume by means of X-ray, catheterization of the pulmonary artery with a floating catheter, ventriculography, and coronarography.

Results of physical training in 37 patients with the ischaemic heart disease with angina of effort are given, 31 one them had had myocardial infarction. Training on bicycle ergometer lasted 2 1/2 to 10 months. After exercise 75% of patients showed enhanced threshold capability, the "double product" (the heart rate x systolic AP) decreased at the expense of the pulse deceleration and decrease of the systolic AP with the standard exercise of 50 W. The maximum size of the "double product" under exercise and also with the appearance of angina remained unchanged. The heart volume after exercises did not change. Changes in haemodynamics depended on the initial functional state of the myocardium, which was evaluated by the degree of rise of the diastolic pressure in the pulmonary artery (DPPA) with 50 W exercise and according to the functional curves of the left ventricle traced by comparing DPPA and the minute volume. In patients with "good" myocardial function (DPPA not lower than 30 mm Hg) after exercises the stroke and minute volumes increased with the threshold exercise, DPPA decreased with 50 W, functional curve of the left ventricle approached the functional curve of healthy individuals. Patients with "bad" function (DPPA over 30 mm Hg and higher did not show) changes in haemodynamics and in the functional curve of the left ventricle.