Right ventricular cardiomyocyte apoptosis in patients with acute myocardial infarction of the left ventricular wall.

Cardiac remodeling after acute myocardial infarction (AMI) is characterised by molecular and cellular mechanisms involving both left (LV) and right ventricular (RV) walls. Cardiomyoycte apoptosis in the peri-infarct and remote LV myocardium plays a central role in cardiac remodeling. Whether apoptosis also occurs in the right ventricle of patients with ischemic heart disease has not been investigated. Aim of the current study was to investigate the presence of cardiomyocyte apoptosis in the right ventricle in patients with AMI. We assessed the number of apoptotic cardiomyocytes by multiple samplings in the LV and RV walls of 12 patients selected at autopsy who died 4 to 42 days after AMI. Five patients without cardiac disease were also selected at autopsy as controls. Apoptotic rates were calculated from the number of cardiomyocytes showing double positive staining for in situ end-labeling of DNA fragmentation – TUNEL – and for activated caspase-3. Potentially false positive results (DNA synthesis and RNA splicing) were excluded from the cell counts. The apoptotic rate in the RV in patients with AMI was significantly higher than in control hearts (0.8% [0.3–1.0] vs 0.01% [0.01–0.03], P<0.001). RV apoptosis was significantly correlated with parameters of global adverse remodeling such as cardiac diameter-to-LV free wall thickness (R=+0.57, P=0.050). RV apoptosis was significantly higher in 5 cases (42%) with infarct involving the ventricular septum and an adjacent a small area of the RV walls (1.0% [0.8–2.2] vs 0.5% [0.2–1.0], P=0.048; P<0.001 vs controls). The association between apoptotic rate in RV and cardiac remodeling was apparent even after exclusion of cases with RV AMI involvement (R=+0.82, P=0.023 for diameter-to-LV wall thickness ratio; and R=−0.91, P=0.002 for RV free wall thickness). In conclusion, patients with cardiac remodeling after AMI have a significant increase in RV apoptosis even when ischemic involvement of the RV wall is not apparent.