Goal: This manuscript evaluates atrioventric-ular valve regurgitation (AVVR) in babies born with an already very challenging heart condition, i.e., with single ventricle physiology. Although the second surgery that single ventricle patients undergo is thought to decrease AVVR, there is much controversy in the clinical literature about AVVR treatment. Methods: The effect of AVVR on Stage 1 haemodynamics and resulting acute changes from conversion to Stage 2 circulation in single ventricle patients are analyzed through lumped parameter models. Several degrees of AVVR severity are analyzed, for two types of valve regurgitation: incomplete leaflet closure and valve prolapse. Results: The models show that increasing AVVR in Stage 1 induces the following effects: first, higher stroke volume and associated decrease in ventricular end-systolic volume; second, increase in atrial volumes with V-loop enlargement in pressure-volume curves; third, pulmonary venous hypertension. The Stage 2 surgery results in volume unloading of the ventricle, thereby, driving a decrease in AVVR. However, this effect is offset by an increase in ventricular pressures resulting in a net increase in regurgitation fraction (RF) of approximately 0.1 (for example, in severe AVVR, the preoperative RF increases from -60% to 70% postoperatively). Moreover, despite some improvements to sarcomere function early after Stage 2 surgery, it may deteriorate in cases of severe AVVR. Conclusion: In patients with moderate to severe AVVR, restoration of atrioventricular valve competence prior to, or at the time of, Stage 2 surgery would likely lead to improved haemodynamics and clinical outcome as the models suggest that uncorrected AVVR can worsen across Stage 2 surgery. This was found to be independent of the AVVR degree and mechanisms.

A Lumped Parameter Model to Study Atrioventricular Valve Regurgitation in Stage 1 and Changes Across Stage 2 Surgery in Single Ventricle Patients

Corsini C.;Pennati G.;
2018-01-01

Abstract

Goal: This manuscript evaluates atrioventric-ular valve regurgitation (AVVR) in babies born with an already very challenging heart condition, i.e., with single ventricle physiology. Although the second surgery that single ventricle patients undergo is thought to decrease AVVR, there is much controversy in the clinical literature about AVVR treatment. Methods: The effect of AVVR on Stage 1 haemodynamics and resulting acute changes from conversion to Stage 2 circulation in single ventricle patients are analyzed through lumped parameter models. Several degrees of AVVR severity are analyzed, for two types of valve regurgitation: incomplete leaflet closure and valve prolapse. Results: The models show that increasing AVVR in Stage 1 induces the following effects: first, higher stroke volume and associated decrease in ventricular end-systolic volume; second, increase in atrial volumes with V-loop enlargement in pressure-volume curves; third, pulmonary venous hypertension. The Stage 2 surgery results in volume unloading of the ventricle, thereby, driving a decrease in AVVR. However, this effect is offset by an increase in ventricular pressures resulting in a net increase in regurgitation fraction (RF) of approximately 0.1 (for example, in severe AVVR, the preoperative RF increases from -60% to 70% postoperatively). Moreover, despite some improvements to sarcomere function early after Stage 2 surgery, it may deteriorate in cases of severe AVVR. Conclusion: In patients with moderate to severe AVVR, restoration of atrioventricular valve competence prior to, or at the time of, Stage 2 surgery would likely lead to improved haemodynamics and clinical outcome as the models suggest that uncorrected AVVR can worsen across Stage 2 surgery. This was found to be independent of the AVVR degree and mechanisms.
2018
Atrioventricular valve; cardiovascular flow; hypoplastic left heart syndrome; incomplete leaflet closure; lumped parameter model; prolapse; valve regurgitation; Heart Valve Diseases; Heart Valves; Hemodynamics; Humans; Hypoplastic Left Heart Syndrome; Infant; Models, Cardiovascular
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11311/1126270
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