The electrophysiological properties of alinidine were studied in 18 patients. Four of these patients were pretreated with intravenous propranolol, 0.2 mg kg-1, and atropine, 0.04 mg kg-1, to induce autonomic blockade. Alinidine produces a sustained bradycardiac effect at a dose of 40 mg intravenously. The sinus node recovery time increased in patients with and without autonomic blockade, while the corrected sinus node recovery time was unaffected by alinidine in patients without autonomic blockade and increased in patients with autonomic blockade. The effective refractory period of the right atrium, the atrioventricular node and the right ventricle, as well as the functional refractory period of the atrioventricular node, were unaffected by alinidine in both groups of patients. Intraatrial, atrioventricular and intraventricular conduction was also not altered by this drug. Thus the electrophysiological profile of alinidine differs from other bradycardia-inducing agents such as beta-blockers or calcium antagonists. Furthermore we evaluated alinidine efficacy in 14 patients with angiographically proven coronary artery disease and stable angina during a 10-week placebo-controlled randomized double-blind trial. Alinidine (40 mg three times a day) reduced the number of anginal attacks and the average number of nitroglycerine capsules consumed. The double product was slightly lowered during rest but more pronounced during exercise. This effect was mainly due to decreased heart rate. The ischaemic ST-segment depression was diminished. Exercise tolerance was clearly improved in 6, slightly improved in 2, and unchanged in 4 patients.