Matsuo Shinro, Nakae Ichiro, Matsumoto Tetsuya, Horie Minoru
Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Japan.
Ann Nucl Med. 2006 Jan;20(1):57-62. doi: 10.1007/BF02985592.
We hypothesized that endothelial cell integrity in the risk area would influence left ventricular remodeling after acute myocardial infarction.
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).
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).
In re-perfused acute myocardial infarction, endothelial function within the risk area plays an important role with left ventricular remodeling after myocardial infarction.
我们推测，危险区域的内皮细胞完整性会影响急性心肌梗死后的左心室重塑。
20例急性心肌梗死患者（年龄61±8岁）在亚急性期及因心肌梗死成功进行直接血管成形术后三个月接受了99mTc-替曲膦显像。所有患者在血运重建后均接受了血管紧张素转换酶抑制剂治疗。在亚急性期及血运重建后3个月进行定量门控单光子发射计算机断层扫描（SPECT）心脏显像，以评估左心室（LV）重塑。使用定量门控SPECT（QGS）程序测定左心室射血分数（EF）、收缩末期和舒张末期容积（ESV、EDV）。心肌梗死后三个月，所有患者均接受了冠状动脉内皮功能检测的心脏导管检查。缓激肽（BK）（0.2、0.6、2.0微克/分钟）通过左冠状动脉逐步给药。通过多普勒流速测量评估冠状动脉血流。根据BK反应将患者分为两组：内皮功能保留组（n = 10）和内皮功能障碍组（n = 10）。
基线时，两组的整体功能以及左心室收缩和舒张容积相似。然而，与内皮功能障碍组相比，内皮功能保留组的左心室射血分数显著改善（42±10%至48±9%，而41±4%至42±13%，p < 0.05）。与内皮功能保留组相比，内皮功能障碍组的左心室容积逐渐增加（123±45毫升至128±43毫升，而111±47毫升至109±49毫升，p < 0.05）。
在再灌注急性心肌梗死中，危险区域内的内皮功能在心肌梗死后的左心室重塑中起重要作用。
