Abstract 17013: Preceding Contraction of Less Distensible Ventricular Compartment Plays a Key Role in the Pathogenesis of Mechanical Dyssynchrony in the Univentricular Heart

Abstract

Background: Septal flash motion is the key to mechanical dyssynchrony in the left bundle branch block in biventricular physiology. In univentricular Fontan circulations, however, morphological variations of systemic ventricles make it difficult to evaluate the negative impact of asynchronous contraction with widened QRS duration on hemodynamics. Methods: A computational simulation of Fontan circulation using a time-varying elastance chamber model combined with a three-element Windkessel vascular model was performed. Systemic ventricles were divided into two ventricular compartments (Vnt 1 , Vnt 2 ) by large ventricular septal defects (VSD), which had various ratios of end-diastolic volumes (EDV 1 /EDV 2 , α) and contractilities (Emax 1 /Emax 2 , β). We introduced delayed contraction onset of Vnt 2 from Vnt 1 (T dys , ms) and simulated hemodynamic changes. We also studied 44 consecutive postoperative Fontan patients with wide QRS (28 male, 1-37 years; median age 16.2 years) and examined their clinical profiles including the analysis of focal ventricular wall motion with 2D speckle tracking echocardiography, hemodynamic parameters in cardiac catheterization, plasma levels of brain natriuretic peptide (BNP, pg/mL) and exercise capacities (peak VO 2 , mL/kg/min). Results: In silico , compared with the ventricles with α > 1 and β < 1, those with α < 1 and β > 1 exhibited significantly decreased cardiac output as T dys increased, and relatively impaired output reserve when tachycardia developed. These deteriorations were characterized by the increased reverse flow from Vnt 2 to Vnt 1 through VSD during mid-systole. Also in vivo , reverse flow during mid-systole via VSD, flash motion during isovolumic contraction time and lower peak systolic strain of smaller ventricular compartment were associated with higher central venous pressures, elevated BNP levels and decreased peak VO 2 (p < 0.05). Conclusion: Delayed contraction in more distensible ventricular compartment can exacerbate the mechanical dyssynchrony characterized by preceding “flash” contraction and subsequent dyskinetic dilation of less distensible compartment, which contributes to the pathogenesis of heart failure in the univentricular heart.