In 19 patients with hypertrophic cardiomyopathy (15 males, 4 females, mean age 49.2 ± 10.8 years) left ventricular function was studied with radionuclide ventriculography at rest and during exercise in a crossover design without intervention and after disopyramide and propranolol treatment. 15 of the 19 patients had a resting or latent intraventricular gradient of more than 30 mm Hg. Left ventricular function at rest and during exercise was evaluated before medication, 90 min after oral administration of 200 mg disopyramide or 160 mg propranolol and after 3 weeks of oral therapy with disopyramide 200 mg 2 times a day or propranolol 80 mg 4 times a day. After long-term treatment with disopyramide, resting ejection fraction decreased from 72 ± 12 to 69 ± 14% (p < 0.01) and peak ejection rate (PER) decreased from 3.46 ± 135 to 3.24 ± 65 end-diastolic volume (EDV)·s-<sup>1</sup> (p < 0.01). Peak filling rate (PFR) at rest decreased from 3.01 ± 0.8 to 2.77 ± 0.63 EDV·S”<sup>1</sup> (p < 0.05). Time to peak filling rate (TPFR) at rest and during exercise after acute and chronic therapy did not change compared to control values. Acute and long-term administration of propranolol lead to a significant reduction in heart rate at rest and during exercise. During exercise, PFR was significantly reduced: from 5.76 ± 1.32 (at baseline) to 4.27 ± 1.0 (acute therapy; p < 0.01) and 4.34 ± 0.97 EDV·s-<sup>1</sup> (chronic therapy); TPFR was significantly prolonged: from 122 ± 32 (at baseline) to 144 ± 22 (acute therapy) and 149 ± 39 ms (chronic therapy, p < 0.01) and PFR/PER was significantly lower after acute and long-term therapy with propranolol. The data indicate that disopyramide has a slight negative inotropic activity on systolic ventricular function. Diastolic filling is also impaired. Propranolol reveals a strong negative chronotropic effect and in addition a negative influence on systolic and diastolic ventricular function.