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Trimetazidine has been shown to improve anginal symptoms and exercise tolerance in patients with coronary artery disease (CAD). To determine the hemodynamic effects of trimetazidine, systemic hemodynamics were studied in 15 patients suffering from CAD (12 male, 3 female, mean age +/- SEM = 58.6 +/- 1.8 years). Cardiac index was determined by thermodilution method. Left ventricular and aortic pressures were measured using micromanometers (Miller Instruments). After basal measurements, patients were randomly given either placebo (n = 5) or one of two therapeutic doses of trimetazidine 1 mg.kg-1 (n = 5) or trimetazidine 1.5 mg.kg-1 (n = 5) in a double-blind procedure. Data were recorded 5, 10 and 20 min after intravenous drug bolus. Throughout the procedure, the evolution of systemic hemodynamic parameters was not statistically different between the three groups, in particular heart rate, cardiac index, systolic, diastolic and mean aortic pressures, end-diastolic ventricular pressure, mean capillary wedge pressure, pulmonary artery pressures or systemic vascular resistances. We conclude that, unlike other antianginal drugs (particularly beta-blockers, nitrates and calcium-channel inhibitors), trimetazidine does not modify systemic hemodynamics in patients with CAD. These results are consistent with a direct effect of trimetazidine on the ischemic myocardial cell previously reported.

A better selection of patients referred for cardiac transplantation should lead to better surgical results. The presence of severe and irreversible pulmonary hypertension is an important factor and its pretransplantation assessment requires pharmacodynamic testing with vasodilators and dobutamine. The aim of this study of 10 patients in congestive cardiac failure referred for cardiac transplantation was to evaluate enoximone in this indication by comparing it with sodium nitroprussiate (3 micrograms/kg/mn). Intravenous enoximone (total dose of 1.5 mg/kg) increased the cardiac index (+49%; p less than 0.01), slightly reduced the mean systemic blood pressure (-8%; p less than 0.05) whilst inducing a greater reduction in systemic arterial resistances (-36%; p less than 0.01); the fall in mean blood pressure was less than with sodium nitroprussiate (-23%; p less than 0.01). Myocardial oxygen consumption (rate-pressure product) did not increase in contrast to the effect of dobutamine (+21%; p less than 0.01). There was a significant reduction in pulmonary arteriolar resistances (p less than 0.01) with all three drugs but the interpretation of this response and its prognostic significance in patients with a low cardiac output and persistent pulmonary hypertension are discutable even when pulmonary arteriolar resistances are less than 6 Wood units. The value of using an inotropic agent such as Dobutamine or Enoximone is to unmask fixed pulmonary hypertension which may be missed in patients with low cardiac output even with vasodilator drugs, and also to mimic the haemodynamic result of transplantation. In this indication Enoximone may be used like Dobutamine but with the advantage of not increasing myocardial oxygen consumption and being probably less arrhythmogenic.

The acute effects of captopril on haemodynamics, coronary flow and myocardial metabolism were studied in 12 patients with chronic severe cardiac failure (primary cardiomyopathy: 10 cases; ischaemic: 2 cases) in functional Classes III or IV of the NYHA. All patients were male and their average age was 51.3 +/- 14.1 years (range 27 to 68 years). Measurements were carried out under basal conditions and 90 minutes after a single dose of 50 mg (5 cases) or 100 mg (7 cases) of captopril. Captopril administration leads to an increase in cardiac index from 2.05 +/- 0.32 to 2.34 +/- 0.35 l/min/m2 (p less than 0.05) and a greater increase in systolic index from 23.9 +/- 6.7 to 29.8 +/- 6.9 ml/syst/m2 (p less than 0.01), because the heart rate decreased slightly (p less than 0.05). These changes were the result of a decrease in afterload: mean aortic pressure fell from 85 +/- 11.8 to 68 +/- 19.6 mmHg (p less than 0.01) and systemic arterial resistance fell from 2 886 +/- 745 to 2 010 +/- 610 dynes/cm-5/sec/m-2 (p less than 0.01). Captopril also led to a fall in venous tone, i.e. pre-load: left ventricular end diastolic pressure fell from 26.9 +/- 6.1 to 20.8 +/- 6.6 mmHg: p less than 0.01. There was no change in contractility as shown by the absence of variation of the V.max (0.92 +/- 0.18 under basal conditions, and 0.90 +/- 0.15 after 90 minutes).(ABSTRACT TRUNCATED AT 250 WORDS)

A study has been made of the haemodynamic affects of a single intravenous injection of amiodarone chorhydrate (5 mg/kg); the injection was given at rest to six normal subjects and six patients with coronary insufficiency due to atherosclerosis. The effects of the drug are most marked at the fifteenth minute after injection, and are: slowing of the heart rate; lessened cardiac output and left ventricular effort; a significant increase in mean pulmonary arterial pressure and diastolic pressure; slight variations in flow in the coronary sinus, with an increase in the ratio of coronary sinus flow to cardiac output. Amiodarone chlorhydrate appears to exert a favourable action upon the heart because, while it maintains myocardial perfusion, it tends to diminish the myocardial oxygen requirement by decreasing the rate of contraction and the contractility of the myocardium.

The haemodynamic and myocardial metabolic effects of intravenous Labetalol were studied in 7 normotensive coronary patients with at least one significant stenosis on the left anterior descending artery. The study consisted of 5 successive observation periods: basal (I); during atrial pacing at the theoretical maximal heart rate or when anginal pain occurred (II); return to basal conditions (III); 20 minutes after an injection of 1.5 mg/kg of Labetalol over 3 minutes into the pulmonary artery (IV); during repeat atrial pacing at the rate achieved during phase II (V). There was no significant difference between phases I and III except for a slightly faster heart rate in phase III. The effects of Labetalol were assessed by comparing the results during phases III and IV between phases II and V and by analysing the variations between phases I, II, IV and V. In comparison with basal conditions (phase III), Labetalol (phase IV) induced a slight decrease in cardiac output (p less than 0.05), a decrease in aortic pressure and systemic arterial resistances (p less than 0.01) and of the double product. Coronary sinus flow did not change but myocardial oxygen consumption fell by an average of 11% (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)