Myocardial infarction potentially alters mitral valve (MV) protein synthesis resulting in MV deterioration. Angiotensin converting enzyme (ACE) inhibitors may decrease MV protein synthesis following infarction, thereby delaying surgical intervention and facilitating repair. To investigate this hypothesis Lewis rats were randomized into five groups: non-surgical (n=7), sham surgery (n=7), sham surgery ACE-inhibitor (n=7), infarct (n=10), and infarct ACE-inhibitor (n=10). For both infarct groups, the left anterior descending artery was ligated. Both ACE-inhibitor groups received Captopril. At sacrifice, the MVs were evaluated for heat shock protein 70 (HSP-70) and procollagen. MV HSP-70 levels were significantly increased in both infarct groups (p<0.05). Procollagen was increased in both infarct groups (p=0.07). Trends towards decreased HSP-70 and procollagen in the infarct group treated with ACE-inhibitors were observed. In summary, myocardial infarction increases MV HSP-70 (stress protein) and procollagen synthesis. Pharmocologic manipulation (ACE inhibition) may impact surgical management and prove beneficial in controlling the MV disease process following infarction.