HEALING HUMAN MYOCARDIAL-INFARCTION ASSOCIATED WITH INCREASED CHYMASEIMMUNOREACTIVITY

We studied the immunoreactivity of the chymase protein in normal human myocardium and in human myocardial infarctions at various postinfarct ion times using immuno-histochemistry. In noninfarcted hearts chymase was mainly present in cardiomyocytes and endothelial cells. At 6 h aft er infarction the ischemic cardiomyocytes had lost their chymase immun oreactivity. A portion of the smooth muscle alpha-actin-expressing myo fibroblasts and some of the CD-68-positive macrophages, which both app ear 4-6 days after infarction, contained chymase. Chymase was also fou nd in mast cells, which were present in the normal myocardium and the healing scar. These data show that chymase, a protein that mediates th e conversion of angiotensin I to angiotensin II via a non-angiotensin- converting-enzyme-dependent pathway is present in the normal adult hum an myocardium and is upregulated in the healing tissue after myocardia l infarction.