[I-AEPCYIA-03] The Impact of the Obesity on the Fontan Hemodynamics during Transition to the Adult
Keywords:Fontan, obesity, end-organ dysfunction, FALD
BACKGROUND AND AIM:Obesity is a risk for developing heart failure in the adults, where increased circulatory volume as well as augmented ventricular afterload exacerbates cardiovascular remodeling. Since the characteristic feature of Fontan circulation including augmented afterload and compromised preload reserve attributes Fontan related end-organ dysfunction, obesity during adolescence may further accelerate organ dysfunction. We tested our hypothesis that obesity in the Fontan circulation additively increase the cardiovascular load and compromise organ function. METHOD:The consecutive 54 Fontan patients older than 13 years old were enrolled in this study. The patients were categorized into 3 groups based on the Japanese obesity criteria using body mass index (BMI); obesity (>25, n=7), lean (<18.5, n=21), and moderate (18.5-25, n=26). The hemodynamic data and its interaction with markers for end-organ dysfunction were analyzed. RESULTS:The age for each group was similar (17±3, 16±5, 18±5 years old). While cardiac index, systemic vascular resistance, and blood pressure (BP) were similar, central venous pressure (CVP 12.7±2.1*, 11.8±1.7, 10.8±2.0 mmHg), pulmonary resistance (Rp 2.2±1.0*, 2.0±0.8, 1.5±0.5 mmHg), hepatic wedge pressure (HCWp 14.0±1.6*, 12.2±1.6, 11.7±2.1 mmHg) were markedly high in the obese patients (*: p<0.05 as compared with moderate. Indeed, the BMI was positively correlated with CVP, HCWp and trans-hepatic pressure. Interestingly, blood volume (BV, ml/kg) measured by dye dilution and CVP augmentation by contrast load (mmHg/ml) were positively correlated with BMI (p= 0.031, 0.023, respectively), suggesting saturated vascular bed in the patients with high BMI. In addition, BP suppression with general anesthesia induction were closely correlated with higher BMI, but independent of BV, suggesting reactive vascular constriction as the contributor of BP augmentation in the obese patients (p= 0.0079, ANCOVA). Although BMI was independent of eGFR, serum hepatic fibrosis markers (procollagen type III peptide, type IV collagen 7s, hyaluronic acid) and hepatic elasticity markers (Shear wave elasticity, Dispersion slope), it was closely corelated with suppressed hepatic function as represented by ICG clearance rate (p=0.029). CONCLUSIONS:The Fontan patients with obesity had unfavorable vascular hemodynamics including reactive BP augmentation and CVP elevation with saturated vascular bed. Although hepatic fibrosis was unaffected in adolescence, additive hemodynamic load was associated with hepatic dysfunction.