Healing human myocardial infarction associated with increased chymase immunoreactivity

We studied the immunoreactivity of the chymase protein in normal human myocardium and in human myocardial infarctions at various postinfarction times using immuno-histochemistry. In noninfarcted hearts chymase was mainly present in cardiomyocytes and endothelial cells. At 6 h after infarction the ischemic cardiomyocytes had lost their chymase immunoreactivity. A portion of the smooth muscle alpha-actin-expressing myofibroblasts and some of the CD-68-positive macrophages, which both appear 4-6 days after infarction, contained chymase. Chymase was also found in mast cells, which were present in the normal myocardium and the healing scar. These data show that chymase, a protein that mediates the conversion of angiotensin I to angiotensin II via a non-angiotensin-converting-enzyme-dependent pathway is present in the normal adult human myocardium and is upregulated in the healing tissue after myocardial infarction.