Abstract 16230: Fenestration in the Fontan Circulation Secures Circulatory Reserve~Potential for Chronic Cardio-protective Strategy~
Background: Fontan patients are increasingly subjected to advanced heart failure therapies due to end organ failure, which stems from Fontan specific hemodynamics. Since fenestrated Fontan (FF) procedure accelerates recovery from operation insults and preserves exercise capacity, it may liberate patients from the factors driving circulatory compromise. We hypothesized that FF possesses hemodynamic advantages over preservation of preload.
Methods and Results: Thirty Fontan pts (age 4.0±2.0 yrs) with constructed pressure volume relationship under dobutamine infusion (DOB) and/or transient fenestration occlusion (TFO) were enrolled. In FF pts (n=19), TFO suppressed end diastolic volume, stroke volume (SV) and cardiac index (CI), with increasing heart rate (HR), afterload (Ea) and ventricular chamber stiffness β (p<.05 for all), while contractility (Ees, PRSW) remained unchanged. As compared to FF, non-FF pts had a similar but more mild cardiovascular phenotype of FF with TFO. Only HR (baseline 109±6 vs 96±16 bpm, DOB 123±12 vs 105±24 bpm, p<.05) and central venous pressure (CVP, 14±3 vs 11 ±3 mmHg) were particularly higher than FF. To delineate the impact of FF with increasing HR, response to rapid atrial pacing (+20, 40, 60 bpm to pre-TFO HR) with/without TFO was monitored (figure). Marked decline of CI by TFO at baseline was compensated by the increase of HR by 20 bpm. While the product of CI and arterial oxygen saturation (SaO2), as a surrogate of arterial oxygen content, was constant, TFO consistently raised CVP regardless of HR.
Conclusions: As compared with non-FF, CI preservation in FF was mediated by not only preload reserve, but also low afterload and relative decreased ventricular stiffness. In addition, FF pts can achieve circulatory homeostasis with lower levels of HR and CVP than non-FF pts. Since somatic growth ultimately diminishes R-L shunt related to FF, the FF procedure might be a promising strategy to avoid factors driving cardiovascular remodeling.
Author Disclosures: H. Saiki: None. S. Kuwata: None. C. Kurishima: None. Y. Iwamoto: None. H. Ishido: None. S. Masutani: None. H. Senzaki: None.
- © 2016 by American Heart Association, Inc.