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The results of our study suggest that thrombolysis may favorably affect the clinical outcome of hemodynamically stable patients with major pulmonary embolism.

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1. Haemodynamic studies were performed in six patients with hypertension, hyperaldosteronism and low plasma renin (five patients with a solitary adrenocortical adenoma, one patient with bilateral adrenocortical nodular hyperplasia), and in ten normotensive control subjects.2. Studies in the chronic phase of hypertension uniformly showed elevated total peripheral resistance while cardiac output was not increased.3. In four patients haemodynamics were studied in the early phase of hypertension following a normotensive period induced by spironolactone. Under these latter conditions the raised blood pressure was associated with increased cardiac output whereas total peripheral resistance was normal. It is suggested that the haemodynamic pattern observed during the phase of the renewed elevation of blood pressure is similar to that at the onset of aldosterone-induced hypertension.4. Serial measurements in two patients revealed that the haemodynamic characteristics were dependent on the phase of hypertension: during the chronic phase total peripheral resistance was increased whereas cardiac output was not. The new rise in blood pressure following discontinuation of spironolactone therapy was associated with increased cardiac output while total peripheral resistance was normal. 5. Although limited, the findings suggest that the initial step in the development of aldosterone-induced hypertension is a rise in cardiac output. This may be an important factor for the final elevation of total peripheral resistance.

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Clinical and experimental investigations have demonstrated an inverse relation between heart rate and myocardial performance in patients with congestive heart failure. Accordingly, this study was designed to investigate the hemodynamic effect of the novel bradycardic compound tedisamil in patients with heart failure. We hypothesized that tedisamil would reduce heart rate and thereby improve hemodynamic parameters of failing hearts with an inverse force-frequency relation. Tedisamil was administered intravenously in nine patients with dilated cardiomyopathy (NYHA II-III). Hemodynamic measurements by right heart catheterization were carried out at time points -30, 10, 20 min, 1, 2, 4, and 6 h. Tedisamil decreased heart rate significantly from 84 +/- 6 beats/min to 73 +/- 4 beats/min (at 10 min; p < 0.05). Stroke volume index remained unchanged, and cardiac index tended to decrease transiently. Mean blood pressure increased from 98 +/- 5 to 104 +/- 6 mm Hg (p < 0.05) because of an increase in systemic vascular resistance from 1,619 +/- 145 to 2,079 +/- 198 dyn x s x cm(-5) (at 20 min; p < 0.05). Diastolic pulmonary pressure and pulmonary vascular resistance showed similar changes. Pulmonary capillary wedge pressure increased from 12 +/- 3 to 16 +/- 4 mm Hg (at 20 min; p < 0.05). Although tedisamil resulted in a significant heart-rate reduction, this was not associated with an improvement of hemodynamics. This may be due to increased afterload of the left and right ventricle. In these patients, tedisamil increased vascular resistance, which is unwanted in the treatment of congestive heart failure.

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