Abolishment of chronic volume overload. Implications for diastolic function of the systemic ventricle immediately after Fontan repair.
BACKGROUND
In patients with a univentricular heart, the chronic ventricular volume overload is acutely abolished by the creation of a Fontan circuit. This results in an immediate reduction of the ventricular cavity size but also in an inappropriate degree of ventricular wall thickness, at least in the early postoperative period. The implications for the diastolic properties of the ventricle are poorly understood.


RESULTS
A chronic volume overload through a modified Blalock-Taussig shunt was created in 10 mongrel dogs. Six weeks later, the shunt was occluded percutaneously with a detachable balloon. The left ventricular end-diastolic dimension and posterior wall thickness were measured with transcutaneous echocardiography. Digitized high-fidelity pressure tracings were used to determine the time constant of isovolumic pressure decay, tau. The isovolumic relaxation time (A2-MVO) and time to minimal left ventricular pressure (A2-LVPmin) were recorded. All variables were followed up to 1 month after occlusion of the shunt. One hour after occlusion, there was an incomplete return to baseline values of the echocardiographic left ventricular dimension (+12 +/- 8% of baseline value, p < 0.01). Despite a 31 +/- 14% (p < 0.001) increase of the posterior wall thickness after removal of the volume overload, tau or ventricular relaxation showed no change from control values. In contrast, the early filling wave was blunted, suggesting diminished ventricular suction. A2-MVO (p < 0.01) and A2-LVPmin (p < 0.05) lengthened well above baseline values for up to 1 week after occlusion of the shunt. Over the following month, the volume-induced hypertrophy regressed, and indexes of early ventricular filling resumed control values.


CONCLUSIONS
We conclude that early after removal of a chronic volume overload, the resultant increase of wall thickness is not associated with impaired relaxation but that viscosity and inertia caused by the increased mass-to-volume ratio will impair early ventricular filling.
Gewillig
M
M
Laboratory of Experimental Cardiology, O/N Gasthuisberg, University of Leuven, Belgium.
Daenen
W
W
Aubert
A
A
Van der Hauwaert
L
L
D000818:Animals; D003971:Diastole / Q000502:physiology*; D004285:Dogs; D004452:Echocardiography; D006325:Heart Atria / Q000601:surgery*; D006330:Heart Defects, Congenital / Q000601:surgery; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology*; D011651:Pulmonary Artery / Q000601:surgery*; D016277:Ventricular Function, Left / Q000502:physiology*