BLOOD-PRESSURE, PLASMA ATRIAL-NATRIURETIC-PEPTIDE AND CATECHOLAMINES DURING RAPID VENTRICULAR PACING AND EFFECTS OF BETA-ADRENERGIC-BLOCKADE IN CORONARY-ARTERY DISEASE

To study neurohumoral control mechanisms of the hemodynamic response to ventricular tachycardia, arterial blood pressure, plasma atrial natriuretic peptide (ANP) and catecholamine levels were monitored during simulated ventricular tachycardia before and after administration of beta-blockade. Tachycardia was simulated by ventricular pacing at 150 beats/min for 150 seconds in 9 patients without and 14 with angiographically demonstrable coronary artery disease (CAD). The effects of intravenous propranolol (0.15 mg/kg) were evaluated in 7 control subjects and in 13 patients with CAD. Arterial blood pressure decreased to its minimum within 5 seconds after onset of pacing in all patients, the decrease being 27 and 30% (p = not significant) in the groups without and with CAD, respectively. Propranolol did not affect the initial decline, but blunted subsequent recovery. The ANP baseline levels were similar in both groups, increasing by 60% (p < 0.05) and 71% (p < 0.02) in the groups without and with CAD, respectively, during ventricular pacing. After administration of propranolol the increase in ANP was 180% in both groups. Rapid ventricular pacing did not affect catecholamine levels before propranolol, but after propranolol norepinephrine increased by 71 (p < 0.02) and 97% (p < 0.01) in patients without and with CAD, respectively. There was a significant correlation (r = 0.53, p = 0.001) between pacing-induced ANP and norepinephrine changes, but changes in arterial blood pressure did not correlate with those in either of these hormones. Thus, beta-adrenergic blockade blunts blood pressure recovery during simulated ventricular tachycardia. However, this is partly counterbalanced by increased circulating norepinephrine levels. The positive correlation between ANP and norepinephrine changes shows that secretion of these hormones is interrelated. The lack of any correlation between hormonal changes and blood pressure changes suggests that other determinants of hemodynamic recovery, such as activation of neuroadrenergic system, exist under these circumstances.