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A Murine Model of Increased Coronary Sinus Pressure Induces Myocardial Edema with Cardiac Lymphatic Dilation and Fibrosis.

AIMS
Myocardial edema is a consequence of many cardiovascular stressors including myocardial infarction, cardiac bypass surgery, and hypertension. The aim of this study was to establish a murine model of myocardial edema without infarct, and elucidate the response of cardiac lymphatics and the myocardium in the resolution of edema.


METHODS AND RESULTS
Myocardial edema without infarction was induced in mice by cauterizing the coronary sinus, increasing pressure in the coronary venous system and inducing myocardial edema. In male mice, there was rapid development of edema 3 hours following coronary sinus cauterization (CSC), with associated dilation of cardiac lymphatics. By 24 hours, males displayed significant cardiovascular contractile dysfunction. In contrast, female mice exhibited a temporal delay in the formation of myocardial edema, with onset of cardiovascular dysfunction by 24 hours. Furthermore, myocardial edema induced a ring of fibrosis around the epicardial surface of the left ventricle in both sexes that included fibroblasts, immune cells, and increased lymphatics. Interestingly, the pattern of fibrosis and the cells that make up the fibrotic epicardial ring differ between sexes.


CONCLUSIONS
A novel surgical model of myocardial edema without infarct was established in mice. Cardiac lymphatics compensated by exhibiting both an acute dilatory and chronic growth response, that temporally differs between sexes. Transient myocardial edema was sufficient to induce a robust epicardial fibrotic and inflammatory response, again with distinct sex differences, which underscores the sex-dependent differences that exist in cardiac vascular physiology.