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The sustained haemodynamic effects of prazosin (20-30 mg) and metoprolol (400-800 mg) alone and combined (half-dose) were evaluated in five patients with hypertension, left ventricular hypertrophy, and radiological cardiac enlargement. Measurements were made at rest and during isometric handgrip exercise. Blood pressure at rest was equally well controlled on each regimen. The heart rate and cardiac output (thermodilution) were reduced by metoprolol, even when combined with prazosin. Systolic ejection time was prolonged by metoprolol, but there were no changes in left ventricular dimensions at rest. During isometric handgrip the pressure increments were similar on each of the three regimens, although absolute diastolic pressure was lower on combined therapy. The arterial pressure increment on prazosin therapy was predominantly due to a rapid rise in heart rate and cardiac output, whereas with metoprolol and combined therapy the major contribution to the response was by peripheral vasoconstriction. Moreover, with the latter regimens there was a rapid rise in pulmonary artery occluded pressure, which did not occur with prazosin therapy. In conclusion, metoprolol alone, or combined with prazosin, caused significant depression of cardiac function, which was apparent only when the patients were subjected to the haemodynamic stress of isometric exercise.

The antiarrhythmic effect of intravenous disopyramide phosphate was assessed in a multicentre open study of 141 patients admitted to coronary care units. Disopyramide was administered in a bolus dose of 2 mg/kg over 10 min with an optional second bolus of 1 mg/kg and infusion of 0.4 mg/kg hour. Atrial fibrillation was terminated in 57% of 56 patients, supraventricular tachycardia in 82% of 11 patients, ventricular tachycardia in 88% of 17 patients and premature ventricular contractions were controlled in 85% of 55 patients. Atrial flutter was terminated in only 2 of 17 patients (12%). Side effects occurred in 38% of the patients, the most frequent being those relating to anticholinergic properties of the drug (15%) or systemic hypotension (13%). Occasionally worsening of the arrhythmia (4%), QRS widening (3) or apparent hypertension (2%) were noted. It was concluded that intravenous disopyramide is an effective antiarrhythmic agent in the coronary care unit setting, but that side effects require close monitoring of dosage.