Acute and chronic response of the right ventricle to surgically induced pressure and volume overload

We aimed to determine the response of the right ventricle (RV) to surgically induced pressure and volume overload in both acute and chronic settings. Four-month-old sheep were operated via left anterior thoracotomy. Pressure overload of the RV was established by banding of the pulmonary trunk. Volume overload was induced by the implantation of a transannular patch to the right ventricular outflow tract. Right ventricular function was obtained with conductance catheters before and after surgery as well as three months postoperatively. Acute pressure overload resulted in an increase of end-systolic volume (ESV) (P=0.002) and end-diastolic volume (EDV) (P=0.004), increments in contractile indexes [maximal slope of systolic pressure increment (dP/dt(max)), P=0.002; slope of end-systolic pressure volume relation (Ees), P=0.002; preload recruitable stroke work (PRSW), P=0.002] and an acceleration of early diastole [relaxation time (tau), P=0.012; maximal slope of diastolic pressure decrement (dP/dt(min)), P=0.002]. Acute volume overload revealed better contractility and more prominent increases in preload (ESV, EDV; both P=0.008). Three months postoperatively, pressure overloaded hearts demonstrated superior systolic (Ees, P=0.022; PRSW, P=0.013) and diastolic reserves (dP/dt(min), P=0.013; slope of end-diastolic pressure volume relation (Eed), P=0.005; P(20), P=0.003) than volume overloaded hearts. Acute pressure overload leads to enhanced contractility of the RV as a result of the Anrep effect and the Frank-Starling mechanism whereas volume overload institutes only the latter. The chronically pressure overloaded RV exposes more contractile and elastic reserves than the chronically volume overloaded RV under stress conditions.