EFFECTS OF AORTIC CONSTRICTION DURING EXPERIMENTAL ACUTE RIGHT-VENTRICULAR PRESSURE LOADING - FURTHER INSIGHTS INTO DIASTOLIC AND SYSTOLIC VENTRICULAR INTERACTION

Background Acute right ventricular (RV) hypertension may result in hem odynamic collapse. The associated reduction in left ventricular (LV) e nd-diastolic volume is thought to result from reduced RV output (secon dary to RV ischemia) and adverse direct ventricular interaction. Aorti c constriction improves cardiac function in these circumstances; this has been attributed to a reversal of the RV ischemia caused by an incr eased coronary perfusion pressure. We hypothesized that altered ventri cular interaction, potentially via altered septal mechanics, may also contribute to the beneficial effects of aortic constriction. Methods a nd Results We instrumented nine dogs with ultrasonic dimension crystal s to measure RV segment length, septum-to-RV free wall and septum-to-L V free wall diameters, and LV anteroposterior diameter. Catheter-tippe d manometers were used to measure LV and RV pressures. Pericardial pre ssure was measured with hat, liquid-containing balloon transducers. In flatable cuff constrictors were placed on the pulmonary artery (PA) an d aorta, and a flow probe was placed on the PA. The right coronary art ery (RCA) was perfused independently by a roller pump calibrated for f low. During moderate PA constriction, while RCA pressure was maintaine d at control level, RCA flow did not change significantly (15.8+/-6.2 to 16.9+/-11.5 mL/min) and was similar during severe PA constriction ( 18.6+/-9.8 mL/min). During severe PA constriction, RV stroke volume de creased from a control value of 10.3+/-4.9 to 2.3+/-1.4 mL/beat (P<.05 ). When aortic constriction was added while RCA pressure was maintaine d at control level, there was an increase in RV stroke volume to 4.5+/ -2.0 mL/beat (P<.05) with no associated change in RCA flow (17.8+/-9.5 mL/min). However; pressure-dimension loops clearly demonstrated chang es in diastolic and systolic ventricular interaction; with aortic cons triction, there was a large increase in the transseptal pressure gradi ent associated with a rightward septal shift. During either isolated s evere PA constriction or simultaneous severe PA and aortic constrictio n, RCA flow was increased until RCA pressure was approximately equal t o that in the aorta. This produced an increase in RCA flow of 50% (P<. 05); however, this increase in coronary flow was ineffective in improv ing any measure of RV function. Conclusions In this model of acute RV hypertension, aortic constriction improves cardiac function, at least in part, by altering ventricular interaction independent of changes in RCA flow. Changes in RCA flow do not appear to have a significant imp act on cardiac function in this model in which coronary artery pressur e was maintained at normal or increased levels.