AN ABNORMAL NEURAL REFLEX PLAYS A ROLE IN CAUSING SYNCOPE IN SINUS BRADYCARDIA

Objectives. This study investigates the role of an abnormal neural reflex in causing syncope in patients with sinus bradycardia. Background. Syncope is commonly considered an indication of severity in sinus bradycardia. However, the occurrence of syncope is unpredictable, and the prognosis appears to be similar in patients with and without syncope. Methods. Head-up tilt testing (60-degrees for 60 min), carotid sinus massage in the supine and standing positions, 24-h Holter ambulatory electrocardiographic (ECG) recording and electrophysiologic study before and after pharmacologic autonomic blockade were performed in 25 patients with sinus bradycardia and syncope (group I, sinus rate <50 beats/min, age 71 +/- 12 years) and 25 patients with sinus bradycardia and no neurologic symptoms (group II, sinus rate <50 beats/min, age 67 +/- 16 years). Results. Clinical characteristics and ambulatory ECG monitoring data were similar in the two study groups. A positive response (induction of syncope or presyncope with hypotension and/or bradycardia) was obtained by head-up tilt testing in 15 group I (60%) and in 3 group II (12%) patients (p < 0.001) and by carotid sinus massage in 11 group 1 (44%) and 6 group II (24%) patients (p = NS). Results of at least one test (head-up tilt testing or carotid sinus massage, or both) were positive in 19 group 1 (76%) and 9 group II (36%) patients (p < 0.01). Basal and intrinsic corrected sinus node recovery time did not differ significantly between the two groups. An abnormal intrinsic heart rate was present in 66% of group I and 26% of group II patients (p < 0.01). The different percentage of positive findings on head-up tilt testing and carotid sinus massage in the two groups was independent of the presence of intrinsic sinus node dysfunction. Conclusions. These results indicate that an abnormal neural reflex plays a role in causing syncope in patients with sinus bradycardia. This reflex seems to be unrelated to the severity of sinus node dysfunction, even if the latter could enhance the cardioinhibitory response.