Vasovagal syncope in patients with reduced left ventricular function

Vasovagal syncope (VVS) is mediated by arterial mechanoreceptors, resulting in reflexive changes in heart rate and vascular tone. The Bezold–Jarisch reflex was originally described as enhanced contraction and activation of left ventricular mechanoreceptors, but later studies implicated other triggers, including coronary, carotid, and cerebral arterial mechanoreceptors. VVS is uncommon in patients with left ventricular dysfunction. We hypothesized that VVS could occur in this subset and examined patient characteristics and hemodynamic responses during tilt table testing. From 1996 through 1998, 128 consecutive patients with ejection fraction <40% underwent tilt table testing (70°, 45 min). A total of 15 patients (11.7%) had a positive neurocardiogenic response thought to be the cause of syncope. Clinical data and hemodynamic responses were reviewed. Mean patient age (±SEM) was 70.1 ± 12.2 years. Nine patients were male. Mean ejection fraction was 27.7% ± 7.1%. Thirteen had electrophysiologic studies with normal findings or abnormal findings insufficient to account for syncope. Hemodynamic analysis of 14 patients who had a vasovagal response during passive tilt table testing showed a mean time to positive response of 17.6 ± 12.7 min. Cardioinhibitory responses (pauses >3 sec or heart rate < 40 beats/min for ≥10 sec) were not observed. Five responses were classified as mixed type (>10% decrease in heart rate without a cardioinhibitory response) and 9 as vasodepressor type (≤10% decrease in heart rate). VVS occurs in patients who have clinically significant left ventricular dysfunction. Although this study had a small cohort size, the predominantly vasodepressor response without a cardioinhibitory component warrants further investigation into mechanisms of VVS in these patients.