Abstract 16876: Saturated Arterial Vasoconstriction in the Fontan Circulation

Abstract

Background: Cardiac afterload in the Fontan circulation is enhanced due to sequentially connected pulmonary circulation to the systemic circulation. As the augmentation of afterload, which includes both of venous and arterial components, markedly compromise stroke volume in the Fontan patients, identification of primary culprit is vitally important to determine therapeutic targets in preserving circulation and end-organ function. We tested our hypothesis that the augmentation of cardiac afterload in the Fontan circulation is attributed by the compensative arterial constriction in addition to the venous congestion. Methods: Transient inferior vena-caval occlusion (IVCO) was applied to induced venous congestion in 23 Fontan and 87 postoperative biventricular circulation patients(BVC), and augmentation of arterial elastance (Ea) was measured with constructing ventricular pressure-volume relationship. Results: As compared with BVC patients, lower cardiac output in the Fontan patient was attributed by the augmented afterload with similar contractile function. While increase of CVP was augmented in the Fontan pts as compared to those with BVC (p=0.0016), increase of Ea was similar in both groups, suggesting suppressed response of increasing Ea in the Fontan pts. This was further supported by the negative relationship between CVP increase and Ea augmentation (p=0.048). Consistent with this, increase of Ea by induced venous congestion was negatively correlated with mean circulatory filling pressure (p=0.025) as well as systemic vascular resistance (p=0.047). Importantly, augmentation of Ea was independent of renin-angiotensin-aldosterone system (RAAS). Conclusions: Augmentation of afterload by induced venous congestion was rather saturated in the Fontan circulation, suggesting chronic activation of excessive compensatory vasoconstriction at baseline, which involves entire vascular system. As this response was independent of RAAS activity, in addition to RAAS blockade, structural and functional interventions to suppress cardiovascular remodeling should be implemented for the further reduction of cardiac afterload.