Development of right ventricular (RV) failure in patients after ST-segment elevation myocardial infarction (STEMI) is common. However, a systematic analysis of chamber-specific changes in the expression of genes linked to cardiac function, apoptosis, fibrosis, receptor responsiveness, and inflammation is lacking. Postischemic remodeling was analyzed in rats that received STEMI in the closed chest mode. Rats were sacrificed at day 1, 3, 7, and 120 after surgery. The mRNA expression of genes was quantified by a real-time RT-PCR. Echocardiography was performed after 120 days. Organ weights and systemic blood pressure were determined in addition. Rats developed left and RV dysfunction within 7 days after ischemia/reperfusion and this lasted until the end of the experiments. However, adaptation to ischemia/reperfusion differed significantly between both ventricles. In the LV, a high expression of MMP12, a neutrophile-specific elastase, indicated a significant inflammatory responsiveness that did not occur in RV. A number of differentially regulated genes in the RV exceeded that of the LV at day 3. Postinfarction RV failure is common in rats with ischemia/reperfusion of the left arterial descending aorta. It is associated with severe RV remodeling that occurred delayed to that of the LV. Changes in RV are independent of the initial inflammation.
Part of the book: Visions of Cardiomyocyte