Matsunaga Toshiro, Abe Naoki, Kameda Kunihiko, Hagii Jhoji, Fujita Norio, Onodera Hiroyuki, Kamata Takaatsu, Ishizaka Hiroshi, Hanada Hiroyuki, Osanai Tomohiro, Okumura Ken
Second Department of Internal Medicine, Hirosaki University School of Medicine, 5 Zaifu, Hirosaki, Aomori, Japan.
Int J Cardiol. 2005 Nov 2;105(2):203-8. doi: 10.1016/j.ijcard.2005.01.011.
Matrix metalloproteinase (MMP) plays an important role in the development of ventricular remodeling in an animal model of acute myocardial infarction (AMI). We examined whether circulating MMP activity can predict left ventricular (LV) remodeling after AMI in humans.
We measured the circulating level of MMP-2 and MMP-9 activities (gelatinase activity) at 14 days after the onset of AMI by gelatin zymography in 52 consecutive patients (age 62+/-2). All patients underwent direct PTCA and stenting at an acute stage, and were treated subsequently with losartan or enalapril. Biplane left ventriculography was performed at admission, and 2 weeks and 6 months after the onset of AMI.
We expressed gelatinolysis activity as the ratio to MMP-2 standard. Mean gelatinase activity was 0.721+/-0.013. We divided patients into two groups, groups with gelatinolysis activity <0.72 (low group, n=27) and >0.72 (high group, n=25). Either change in LV end-diastolic volume index (LVEDVI, ml/m(2)) or end-systolic volume index (LVESVI, ml/m(2)) from admission to 2 weeks was not different between the two groups. Changes in both LVEDVI and LVESVI from 2 weeks to 6 months were greater in high gelatinolysis activity group than those in low activity group. Moreover, circulating level of gelatinolysis activity was positively correlated with changes in LVEDVI and LVESVI from 2 weeks to 6 months.
These results demonstrate that circulating level of gelatinase activity can predict LV remodeling after AMI. Inhibition of gelatinase activity at the acute phase may be a therapeutic strategy for the prevention of remodeling after AMI.
基质金属蛋白酶（MMP）在急性心肌梗死（AMI）动物模型的心室重构发展过程中起重要作用。我们研究了循环MMP活性是否能预测人类AMI后的左心室（LV）重构。
我们通过明胶酶谱法在52例连续患者（年龄62±2岁）AMI发病后14天测量了MMP - 2和MMP - 9活性（明胶酶活性）的循环水平。所有患者在急性期均接受了直接经皮冠状动脉腔内血管成形术（PTCA）和支架置入术，随后接受氯沙坦或依那普利治疗。在入院时、AMI发病后2周和6个月进行了双平面左心室造影。
我们将明胶酶解活性表示为与MMP - 2标准的比值。平均明胶酶活性为0.721±0.013。我们将患者分为两组，明胶酶解活性<0.72的组（低活性组，n = 27）和>0.72的组（高活性组，n = 25）。从入院到2周，两组间左心室舒张末期容积指数（LVEDVI，ml/m²）或收缩末期容积指数（LVESVI，ml/m²）的变化无差异。从2周到6个月，高明胶酶解活性组的LVEDVI和LVESVI变化均大于低活性组。此外，明胶酶解活性的循环水平与从2周到6个月的LVEDVI和LVESVI变化呈正相关。
这些结果表明，循环明胶酶活性水平可预测AMI后的LV重构。急性期抑制明胶酶活性可能是预防AMI后重构的一种治疗策略。
