Mitochondrial aldehyde dehydrogenase 2 (ALDH2) detoxifies toxic aldehydes generated during ischemia/reperfusion (I/R) injury in ST-elevation myocardial infarction (STEMI). The deficient variant ALDH2 genotype (ALDH2*2) is prevalent among East Asians. Whether ALDH2*2 exacerbates I/R injury of in patients with STEMI is not known. The study subjects comprised 218 Japanese patients with STEMI (158 men and 60 women, mean age 67.9 ± 11.9) who underwent successful percutaneous coronary intervention. Of these, 120 (55.0%) were the carriers of variant ALDH2*2 and 98 (45.0%) those of wild ALDH2*1/*1 on genotyping. There were no differences in clinical characteristics between the ALDH2*2 and ALDH2*1/*1 group except lower alcohol habit (14.2% vs 46.3%, P < 0.001) in the ALDH2*2 group. The peak plasma levels of creatine phosphokinase myocardial binding (CKMB), a marker of myocardial injury, however, were significantly higher in the patients with ALDH2*2 than in those with ALDH2*1/*1 [a median 275.0 (175.8–407.5) vs 177.5 (126.9–344.3) U/L, P = 0.001] among men but not among women (P = 0.811). There was a significant interaction between men (male sex) and ALDH2*2 for I/R injury (χ2 = 4.425, P = 0.040). The variant ALDH2*2 was associated with more severe I/R injury than the wild ALDH2*1/*1 in STEMI patients in men with possible sex differences.

线粒体醛脱氢酶 2 (ALDH2) 可解毒 ST 段抬高心肌梗死 (STEMI) 缺血/再灌注 (I/R) 损伤期间产生的有毒醛。缺乏变异的ALDH2基因型 ( ALDH2*2 ) 在东亚人中普遍存在。尚不清楚ALDH2*2是否会加剧 STEMI 患者的 I/R 损伤。研究对象包括 218 名接受成功经皮冠状动脉介入治疗的日本 STEMI 患者（158 名男性和 60 名女性，平均年龄 67.9 ± 11.9）。其中，ALDH2*2变异体携带者120人（55.0%），野生ALDH2*1/*1携带者98人（45.0%）。ALDH2*2和ALDH2*2的临床特征没有差异ALDH2*1/*1组除了低酒精习惯（14.2% vs 46.3%，P  < 0.001）在ALDH2*2组。然而， ALDH2*2患者的肌酸磷酸激酶心肌结合 (CKMB) 峰值血浆水平显着高于ALDH2 *1/*1患者[中位数 275.0 (175.8–407.5)] vs 177.5 (126.9–344.3) U/L, P  = 0.001] 在男性中，但在女性中没有（P  = 0.811）。对于 I/R 损伤，男性（男性）和ALDH2*2之间存在显着的交互作用（ χ 2 = 4.425，P  = 0.040）。变体ALDH2*2在可能存在性别差异的男性 STEMI 患者中，与野生ALDH2*1/*1相比，I/R 损伤与更严重的 I/R 损伤相关。