目的: 评估急性前壁ST段抬高心肌梗死(acute anterior ST elevation myocardial infarction，STEMI)患者直接经皮冠状动脉介入术(primary percutaneous coronary intervention，PPCI)后微循环阻力指数(index of microcirculatory resistance，IMR)与1年后左心室不良重构(left ventricular adverse remodeling，LVAR)之间的关系。方法: 采用单中心回顾性队列研究，连续选择2014年1月至2017年8月在北京大学第三医院住院的前壁STEMI并行PPCI患者，术后即刻通过压力/温度导丝测量IMR。利用血清肌酸激酶(creatine kinase，CK)峰值评估梗死面积，心肌梗死(myocardial infarction，MI)后1 d和1年时评估超声心动图，将左心室舒张末期容积(left ventricular end-diastolic volume，LVEDV)较基线增加≥20%定义为LVAR。结果: 共入选43例患者，平均年龄(58.7±12.4)岁。根据IMR正常参考值将患者分为两组，IMR>25(n=23)组较IMR≤25组(n=20)患者冠状动脉造影显示梗死相关血管完全闭塞率(95.7% vs. 65.0%, P=0.029)更高，血清CK峰值水平更高[4 090(383, 15 833)vs. 1 580(396, 5 583), P=0.004]，室壁瘤发生率更高(30.4% vs. 5.0%，P=0.021)。MI后1 d两组LVEDV差异无统计学意义[(111.0±18.8) mL vs. (115.0±23.6) mL，P=0.503]，而1年后IMR>25组LVEDV明显高于IMR≤25组[(141.5±33.7) mL vs. (115.9±27.9) mL, P=0.018]。IMR>25组LVAR发生比例更高(47.4% vs. 11.8%, P=0.024)。二元Logistics回归显示IMR[B=0.079，exp(B) (95%CI) 为1.082 (1.018~1.149), P=0.011]和血清甘油三酯(triglyceride，TG)水平[B=1.610，exp(B) (95%CI)为5.005 (1.380~18.152), P=0.014]是患者MI后1年发生LVAR的预测因素，IMR对1年后发生LVAR具有良好的预测价值(曲线下面积=0.749, P=0.019)，IMR>29为良好的临界点，敏感性81.8%，特异性68.0%。结论: STEMI患者PPCI术后即刻测定IMR可以反映微血管功能，而微血管功能障碍是STEMI后1年左心室不良重构的有力预测指标。

Objective: To evaluate whether index of microcirculatory resistance (IMR) is associated with left ventricular (LV) remodeling in acute anterior ST elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PPCI). Methods: This was a single-center retrospective cohort study. The patients with first anterior STEMI who received PPCI from January 2014 to August 2017 in Peking University Third Hospital was enrolled. After PPCI, IMR was measured immediately by using pressure/temperature guidewire. The success rate of IMR measurement was 100%. Also we collected some related clinical data from the medical records and laboratory results. Infarct size [assessed as creatine kinase (CK) peak], echocardiography at baseline and 1 year follow-up were assessed. LV adverse remodeling (LVAR) was defined as ≥20% increase in LV end-diastolic volume (LVEDV). Results: A total of forty-three patients were enrolled, with an average age of (58.7±12.4) years.The patients were divided into two groups as IMR ≤25 and IMR>25 by normal values recommended by previous literature. Compared with IMR ≤25 group, IMR>25 group had a higher percentage of initial thrombolysis in myocardial infraction (TIMI) grade 0 (95.7% vs. 65.0%, P=0.029), higher serum CK peak value [4 090 (383, 15 833)vs. 1 580 (396, 5 583), P=0.004]. The IMR>25 group suffered higher rates of ventricular aneurysm (30.4% vs. 5.0%, P=0.021). There was no difference in LVEDV [(111.0±18.8) mL vs. (115.0±23.6) mL, P=0.503] between the two groups 1 day after MI, but after 1 year, LVEDV in IMR>25 group was significantly higher than in IMR≤25 group [(141.5±33.7) mL vs. (115.9±27.9) mL, P=0.018]. The incidence of LVAR was more significant in IMR>25 group (47.4% vs. 11.8%, P=0.024). Binary Logistics regression showed that IMR [B=0.079, exp(B) (95%CI)=1.082 (1.018－1.149), P=0.011] and serum triglyceride level [B=1.610, exp(B) (95%CI)=5.005 (1.380－18.152), P=0.014] were the predictors of LVAR 1 year after MI. IMR had a good predictive value for LVAR 1 year after MI [area under the curve (AUC)=0.749, P=0.019], IMR>29 was a good cutoff value with sensitivity 81.8% and specificity 68.0%. Conclusion: Our study elaborates that immediate measurement of IMR after PPCI in patients with STEMI can reflect the microvascular function.And IMR could be used as a quantitative biomarker to predict LVAR after STEMI.