[The effect of some antiarrhythmic drugs on systolic time intervals in normal subjects (author's transl)].

Eleven healthy volunteers (mean age 30.1 +/- 4.3 yrs.) were repeatedly studied by measurement of systolic time intervals (QS2c, PEPc, LVETc, PEP/LVET) and arterial blood pressure (cuff method) before and after 24-hour oral application of four antiarrhythmic drugs (quinidine, disopyramide, prajmaliumbitartrate, propafenone) and two beta-blocking agents (propranolol, atenolol). The studies were repeated in the same group of volunteers with a different drug after an interval of one week. PEPc significantly increased after all antiarrhythmic agents at therapeutic doses by 6.1 to 9.4 ms (p less than 0.05 and p less than 0.01 resp.), whereas LVETc did not change significantly. PEP/LVET increased on an average by 0.033 +/- 0.006 (p less than 0.01). QS2c increased by 7.5 and 7.6 ms resp. (p less than 0.05) after prajmaliumbitartrate and propafenone. Heart rate remained unchanged after disopyramide and propafenone whereas it increased significantly (p less than 0.05) after quinidine and prajmaliumbitartrate. Blood pressure did not change significantly after any of these antiarrhythmic drugs. After application of the two beta-blocking agents propranolol and atenolol, no significant changes in STI could be observed. Mean arterial blood pressure significantly dropped after both, propranolol (minus 2.8 mm Hg) and atenolol (minus 9.7 mm Hg; p less than 0.05 and p less than 0.01, resp.). Heart rate decreased by minus 8.1 b.p.m. after propranolol (p less than 0.01) and minus 11.5 b.p.m. after atenolol (p less than 0.01). The results clearly indicate that at the dosage used, the four antiarrhythmic agents (quinidine, disopyramide, prajmaliumbitartrate, propafenone) exert a negative inotropic effect on left ventricular function as far as it can be judged from the measurement of STI. The lack of a significant negative inotropic effect of an oral treatment with beta-blocking agents on the STI can be explained by opposing effects of a decrease in blood pressure and a negative inotropic action.