Abstract 14612: The Relationship Between Left Ventricular Geometry and Respiratory Sinus Arrhythmia in Patients With Vasovagal Syncope

Introduction: The study was prompted by our observation that a significant number of patients with vasovagal syncope (VVS) have marked respiratory sinus arrhythmia as well as thin left ventricular (LV) walls. We hypothesized that the geometry of the LV walls may play a role in the pathogenesis of VVS. Hypothesis: The aim of this study was to assess LV geometry in relationship to respiratory sinus arrhythmia in patients with VVS M ethods: We included 191 patients (age 52±20 years, 101 women) with VVS who had either a positive or negative response to tilt table testing TTT (n=64 TTT+, and n=127 TTT-). The VVS group was compared to a group of 75 patients with no syncope (NL) and similar age, sex and BMI distributions. Standard 12-lead electrocardiograms (ECG), vectorcardiograms, and transthoracic echocardiograms were performed to assess electrical activation as well as ventricular geometry and function. The magnitude of respiratory sinus rhythm arrhythmia was measured as the maximum percent change in RR interval on a 10 second 12-lead ECG (dRR) performed before the TTT. Results: When compared to NL group patients with VVS had significantly higher dRR and LV end diastolic diameter (12 ±8% vs 10±8%, p=0.047 and 44±5 vs 46±6mm p=0.006 respectively) The end-diastolic thickness of the interventricular septum (IVS) and that of the LV posterior wall (PWT) in the VVS group were significantly smaller than in the NL group (8.9±1.7mm vs 9.6±1.8mm p value=0.003 and 8.4±1.5mm vs 9.2±1.6mm p value=0.0002). The magnitude of respiratory sinus arrhythmia expressed as dRR correlated inversely and significantly with IVS (r=-0.32; p value=0.042). The was however no significant correlation between dRR and PWT. These results suggest that a more pronounced respiratory sinus arrhythmia could be related to more ample variations in right and left ventricular filling due to increased ventricular interdependence via a thinner and more compliant ventricular septum. Conclusions: The geometry of the LV as well as the cardiovascular impact of respiratory movements may play a role in the pathogenesis of VVS.