Determinants of the recovery of right ventricular performance following experimental chronic right coronary artery occlusion.

Abstract

BACKGROUND Patients with acute ischemic right ventricular dysfunction often develop hemodynamic compromise, yet most manifest spontaneous early clinical improvement and later recovery of global right ventricular performance. This study was designed to delineate the determinants of right ventricular performance following chronic right coronary artery occlusion. METHODS AND RESULTS Thrombotic right coronary artery occlusion was induced in 16 closed-chest dogs. Acute occlusion depressed right ventricular free wall motion (motion score, 1.0 +/- 0.0 to 3.4 +/- 0.1*) and global performance (right ventricular fractional area change, 29.2 +/- 1.8% to 2.3 +/- 1.9%*). There was right ventricular dilatation and reversed septal curvature, with elevated and equalized diastolic filling pressures. At 5 days, despite persistent severe right ventricular free wall dysfunction (motion score, 3.4 +/- 0.1 to 2.7 +/- 0.1*), global right ventricular performance improved (fractional area change, 2.3 +/- 1.9% to 17.0 +/- 3.8%*), in part due to reduced right ventricular free wall dyskinesis associated with increased right ventricular free wall end-diastolic thickness. At 7 weeks, collateral flow had restored right ventricular free wall perfusion to baseline values. The increased right ventricular free wall thickness had resolved, right ventricular free wall motion was improved (2.7 +/- 0.1 to 1.6 +/- 0.1*), and global right ventricular performance had recovered further (17.0 +/- 3.8 to 20.9 +/- 0.9). Right ventricular dilatation was reduced, septal curvature normalized, and there was resolution of equalized filling pressures. Histopathological analysis demonstrated minimal right ventricular infarction. CONCLUSIONS Acute right coronary artery occlusion results in right ventricular free wall dyskinesis and depressed global right ventricular performance. Global right ventricular function improves early, in part due to reduced right ventricular free wall dyskinesis associated with increased right ventricular free wall diastolic thickness. Collateral restoration of perfusion facilitates late recovery of right ventricular free wall function (*P < .05).