Accentuated Vagal Antagonism of /3-Adrenergic Effects on Ventricular Repolarization Evidence of Weaker Antagonism in Hostile Type A Men

men. Methods and Results. Responses to two 5-minute intravenous isoproterenol infusions (0.01 ug/kg/min and 0.02 pg/kg/min) were evaluated in six type A and six type B men after pretreatment with either dextrose placebo or atropine (1.2 mg). Atropine significantly potentiated T wave attenuation in the recovery period after isoproterenol infusion (0.30±0.07 mV) compared with placebo (0.54±0.09 mV, p<O.OOl). Atropine also potentiated the heart rate increase to isoproterenol (39±3 beats per minute versus 20±2 beats per minute after placebo). Atropine enhanced decreases in systolic, diastolic, and mean arterial pressures as well as pulse pressure to isoproterenol. Atropine enhancement of many of these responses was increased among subjects with high scores on various hostility/anger scales. Isoproterenol alone produced greater T wave attenuation in type A than in type B men. However, atropine enhancement of T wave attenuation and blood pressure falls by isoproterenol was present only in type B men. Conclusions. These findings indicate that there is accentuated parasympathetic antagonism of T wave attenuation and blood pressure responses induced by f3-adrenergic stimulation. Relative weakness of this antagonism of sympathetic effects on the heart in hostile type A individuals may contribute to their higher coronary disease risk. (Circulation 1992;85:2045-2053)