Question: 

Revascularization of occluded coronary vessels has significantly reduced infarct associated mortality but the subsequently induced cardiac remodelling caused by reperfusion remains a clinical problem due to the development of heart failure. Infarcts of the free left ventricular wall require a compensatory reaction of the septum thereby also interfering with right ventricular hemodynamics. The subsequent consequences fort he right ventricle are not known. Because a better understanding of interventricular interference will be the basis for an improvement of post-infarct therapy we established an in vivo model of left ventricular ischemia/reperfusion and analyzed the effect on the right ventricle.

Methodology: 

7 days prior tot he infarction a suture was placed around the LAD and fixed under the skin. Seven days later wound healing of the surgery procedure has been completed. At that time the suture was remobilized and the LAD was occluded for 30 min and subsequently re-opened. The success was monitored by ST elevation. All rats were analyzed fort he next 120 days.

Results: 

In the first three days after infarction, LVDP was significantly reduced (-12%) but this was compensated after 7 days. At day 120 a thinning oft he free left ventricular wall was found (Echo data) and a slightly impaired EF. Blood pressure and body weight were not different between infarct and sham. In the left ventricle there was an activation of the transcriptosome within 24 hours that was normalized thereafter. However, in the right ventricle there were remarkable changes in the mRNA expression within the next 3–7 days in genes linked to apoptosis, fibrosis, cardiac hypertrophy, and calcium handling. At day 120 the right ventricle had developed a severe right ventricular hypertrophy (46.0 vs. 35.4 mg/mm tibia length). In the lung we found a significant down-regulation of PTHrP and eNOS that is responsible for the afterload oft he right ventricle.

Conclusion: 

The non-infarcted right ventricle shows an adaptive cardiac hypertrophic remodelling in response to non-fatal ischemia/reperfusion of the left ventricle. Therefore, the right ventricle has the possibility to respond adequately to hemodynamic changes caused by left ventricular-dependent infarction. This is be triggered by down-regulation of vasodilatory proteins in the lung.