Possible contribution of alpha-adrenergic abnormalities to cerebral ischemia in the patients with sinus bradycardia. Analysis by pharmacologic autonomic nervous test

Abstract

Syncope of patients with bradyarrhythmia is perceived as severe sign of low cardiac output caused by bradycardia and as a major criteria for pacemaker implantation (PMI). However, it has been reported that PMI can not always prevent syncope; it has been suggested that not bradycardia but an abnormality of the autonomic nervous system plays a part in syncope. To investigate the relation between autonomic nervous dysfunction and syncope in cases of sinus bradycardia (SB). Thirty-nine patients with SB were divided into two groups according to the presence (group S, n = 16, 46.9 +/- 20.0 years) or absence (group N, n = 23, 40.4 +/- 17.6 years) of syncope or presyncope. Corrected sinus node recovery time (CSNRT) was measured by electrophysiologic study. Pharmacologic autonomic nervous tests were performed as follows in a quiet room. Increased HR by application of 0.04 mg/kg atropine (para-tone), and by 0.004 microgram/kg/min isoproterenol divided by 0.004 (beta-sens) were evaluated, beta-tone was obtained by subtracting HR after application of propranolol (0.2 mg/kg) from that of atropine. Basal beta-sympathetic activity was evaluated by beta-sec that was obtained by beta-tone/beta-sens. Increased SBP by application of 0.4 microgram/kg/min phenylephrine divided by 0.4 (alpha-sens) was evaluated. alpha-tone was obtained by subtracting minimum SBP after 0.2 mg/kg phentolamine from SBP after application of propranolol. Basal alpha-sympathetic activity was evaluated by alpha-sec, that was obtained by alpha-tone/alpha-sens. There were no significant differences in basal clinical characteristics (age, sex, cardiac function) between the groups. The parameters of the functions of parasympathetic and beta-sympathetic receptors (para-tone, beta-sens, beta-tone, beta-sec) showed no significant differences between the groups, alpha-sens was attenuated (P < 0.01) and alpha-sec was augmented (P < 0.0001) significantly in group S. It was suggested that syncope or presyncope in SB patients could be attributed to failure of vasoconstriction mediated by alpha-sympathetic receptor but to severity of sinus node dysfunction.