Left ventricular performance in ischemic right ventricular dysfunction.

Ventricular Dysfunction To the Editor: Brookes et al1 reported decreased left ventricular (LV) systolic performance during right ventricular (RV) ischemia in the pig and concluded that “The hemodynamic compromise seen in association with acute RV dilatation within an intact pericardium is partly attributable to impaired LV systolic performance and cannot be wholly ascribed to changes in either LV preload or compliance.” They also stated that “. . . no studies to date have examined LV systolic performance in this context.” However, my colleagues and I reported LV systolic and diastolic performance during ischemic RV dysfunction in the dog.2 This study was unfortunately ignored by Brookes et al.1 We demonstrated that ischemic RV dysfunction induced by right coronary artery (RCA) occlusion resulted in a significant leftward shift of the LV end-diastolic pressure-volume relation, which was markedly exaggerated by the presence of an intact pericardium. This finding agrees with that of Brookes et al.1 More important, when we compared the indexes of LV systolic performance (ie, cardiac output, LV systolic pressure, peak LV dP/dt, and percent systolic shortening) during RCA occlusion with those during inferior vena caval occlusion at a matched LV end-diastolic volume, they were the same. This indicates that the primary mechanism of decreased cardiac output during RCA occlusion is caused by decreased LV preload (ie, end-diastolic volume) due to decreased LV chamber compliance rather than by decreased LV contractility. Because RCA occlusion in the dog causes isolated RV free wall ischemia,2 our results represent a pure RV ischemia model. In contrast, because occlusion of a dominant RCA in the pig probably causes ischemia in the inferior interventricular septum, the decreased LV contractility (ie, decreased slopes of both the preloadrecruitable stroke work and end-systolic pressure-volume relation) seen in Brookes et al’s study1 may be explained by concomitant LV myocardial ischemia. Thus, the hemodynamic compromise seen in Brookes et al’s study1 is attributable to the combined mechanisms of decreased LV preload and acute LV ischemia.