BACKGROUND: We hypothesized that endothelial cell integrity in the risk area would influence left ventricular remodeling after acute myocardial infarction. PATIENTS AND METHODS: Twenty patients (61 +/- 8 y.o.) with acute myocardial infarction underwent 99mTc-tetrofosmin imaging in the subacute phase and three months after successful primary angioplasty due to myocardial infarction. All patients were administered angiotensin-converting enzyme inhibitor after revascularization. Cardiac scintigraphies with quantitative gated SPECT were performed at the sub-acute stage and again 3 months after revascularization to evaluate left ventricular (LV) remodeling. The left ventricular ejection fraction (EF) and end-systolic and end-diastolic volume (ESV, EDV) were determined using a quantitative gated SPECT (QGS) program. Three months after myocardial infarction, all patients underwent cardiac catheterization examination with coronary endothelial function testing. Bradykinin (BK) (0.2, 0.6, 2.0 microg/min) was administered via the left coronary artery in a stepwise manner. Coronary blood flow was evaluated by Doppler flow velocity measurement. Patients were divided into two groups by BK-response: a preserved endothelial function group (n = 10) and endothelial dysfunction group (n = 10). RESULTS: At baseline, both global function and LV systolic and diastolic volumes were similar in both groups. However, LV ejection fraction was significantly improved in the preserved-endothelial function group, compared with that in the endothelial dysfunction group (42 +/- 10% to 48 +/- 9%, versus 41 +/- 4% to 42 +/- 13%, p < 0.05). LV volumes progressively increased in the endothelial dysfunction group compared to the preserved-endothelial, function group (123 +/- 45 ml to 128 +/- 43 ml, versus 111 +/- 47 ml to 109 +/- 49 ml, p < 0.05). CONCLUSION: In re-perfused acute myocardial infarction, endothelial function within the risk area plays an important role with left ventricular remodeling after myocardial infarction.
BACKGROUND: We hypothesized that endothelial cell integrity in the risk area would influence left ventricular remodeling after acute myocardial infarction. PATIENTS AND METHODS: Twenty patients (61 +/- 8 y.o.) with acute myocardial infarction underwent 99mTc-tetrofosmin imaging in the subacute phase and three months after successful primary angioplasty due to myocardial infarction. All patients were administered angiotensin-converting enzyme inhibitor after revascularization. Cardiac scintigraphies with quantitative gated SPECT were performed at the sub-acute stage and again 3 months after revascularization to evaluate left ventricular (LV) remodeling. The left ventricular ejection fraction (EF) and end-systolic and end-diastolic volume (ESV, EDV) were determined using a quantitative gated SPECT (QGS) program. Three months after myocardial infarction, all patients underwent cardiac catheterization examination with coronary endothelial function testing. Bradykinin (BK) (0.2, 0.6, 2.0 microg/min) was administered via the left coronary artery in a stepwise manner. Coronary blood flow was evaluated by Doppler flow velocity measurement. Patients were divided into two groups by BK-response: a preserved endothelial function group (n = 10) and endothelial dysfunction group (n = 10). RESULTS: At baseline, both global function and LV systolic and diastolic volumes were similar in both groups. However, LV ejection fraction was significantly improved in the preserved-endothelial function group, compared with that in the endothelial dysfunction group (42 +/- 10% to 48 +/- 9%, versus 41 +/- 4% to 42 +/- 13%, p < 0.05). LV volumes progressively increased in the endothelial dysfunction group compared to the preserved-endothelial, function group (123 +/- 45 ml to 128 +/- 43 ml, versus 111 +/- 47 ml to 109 +/- 49 ml, p < 0.05). CONCLUSION: In re-perfused acute myocardial infarction, endothelial function within the risk area plays an important role with left ventricular remodeling after myocardial infarction.