Yokota Takashi, Osanai Tomohiro, Hanada Kenji, Kushibiki Motoi, Abe Naoki, Oikawa Koichi, Tomita Hirofumi, Higuma Takumi, Yokoyama Jin, Hanada Hiroyuki, Okumura Ken
Department of Cardiology, Hirosaki University Graduate School of Medicine, Zaifu-cho 5, Hirosaki 036-8562, Japan.
Heart Vessels. 2010 Nov;25(6):460-8. doi: 10.1007/s00380-010-0013-4. Epub 2010 Oct 5.
Enalapril is effective in the suppression of left ventricular remodeling after acute myocardial infarction (AMI), but the effect of telmisartan is unclear. The consecutive 163 AMI patients underwent primary percutaneous coronary intervention and were randomized to telmisartan (n = 82) or enalapril (n = 81). Left ventriculography was performed in the acute and chronic (6 months) phases. Matrix metalloproteinase (MMP)-2 and MMP-9 activities were measured by zymography in the acute (days 1, 7, and 14) and chronic (6 months) phases. Plasma pentraxin3 (PTX3), a marker of vascular inflammation, was also measured. There were no adverse effects in the telmisartan group. The analysis of the left ventriculograms in the acute and chronic phases revealed no difference between the two groups. MMP-9 activities at days 7 and 14 and in the chronic phase were decreased compared to that at day 1 in both groups. MMP-2 activity was also decreased in the acute phase, but increased in the chronic phase in both groups. There was no difference in the plasma PTX3 level in the acute phase, but in the chronic phase, PTX3 was significantly lower in telmisartan than in enalapril group (2.6 ± 1.4 vs. 3.2 ± 1.6 ng/ml, p = 0.04). Telmisartan is well tolerated, shows similar effects on the markers of left ventricular remodeling to those of enalapril, and suppresses vascular inflammation more effectively than enalapril in AMI patients. Telmisartan can be an alternative to angiotensin converting enzyme inhibitor in patients with AMI.
依那普利可有效抑制急性心肌梗死(AMI)后的左心室重构,但替米沙坦的效果尚不清楚。163例连续的AMI患者接受了直接经皮冠状动脉介入治疗,并随机分为替米沙坦组(n = 82)或依那普利组(n = 81)。在急性期和慢性期(6个月)进行左心室造影。通过酶谱法在急性期(第1、7和14天)和慢性期(6个月)测量基质金属蛋白酶(MMP)-2和MMP-9活性。还测量了血管炎症标志物血浆五聚体3(PTX3)。替米沙坦组无不良反应。急性期和慢性期左心室造影分析显示两组之间无差异。两组第7天和第14天以及慢性期的MMP-9活性均较第1天降低。两组急性期MMP-2活性也降低,但慢性期升高。急性期血浆PTX3水平无差异,但慢性期替米沙坦组PTX3显著低于依那普利组(2.6±1.4 vs. 3.2±1.6 ng/ml,p = 0.04)。替米沙坦耐受性良好,对左心室重构标志物的影响与依那普利相似,且在AMI患者中比依那普利更有效地抑制血管炎症。替米沙坦可作为AMI患者中血管紧张素转换酶抑制剂的替代药物。