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


OBJECTIVE
To investigate the relation between autonomic nervous dysfunction and syncope in cases of sinus bradycardia (SB).


METHODS
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.


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Nomura
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A
First Department of Internal Medicine, Nippon Medical School, Tokyo, Japan.
Saitoh
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Atarashi
H
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Hayakawa
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H
D000293:Adolescent; D000328:Adult; D000368:Aged; D001146:Arrhythmia, Sinus / Q000150:complications*; D001285:Atropine / Q000494:pharmacology; D001341:Autonomic Nervous System / Q000187:drug effects*; D001919:Bradycardia / Q000150:complications*; D002545:Brain Ischemia / Q000209:etiology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010276:Parasympatholytics / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D013565:Sympatholytics / Q000494:pharmacology; D013566:Sympathomimetics / Q000494:pharmacology; D013575:Syncope / Q000209:etiology*; D014661:Vasoconstriction / Q000502:physiology
D010276:Parasympatholytics; D011942:Receptors, Adrenergic, alpha; D013565:Sympatholytics; D013566:Sympathomimetics; D010656:Phenylephrine; D001285:Atropine; D011433:Propranolol; D010646:Phentolamine