East Asian variant aldehyde dehydrogenase type 2 genotype exacerbates ischemia/reperfusion injury with ST-elevation myocardial infarction in men: possible sex differences

• Published in: Heart and vessels Vol. 37; no. 2; pp. 184 - 193
• Main Authors: Ishida, Toshifumi, Arima, Yuichiro, Mizuno, Yuji, Harada, Eisaku, Yamashita, Takayoshi, Sueta, Daisuke, Sakamoto, Kenji, Suzuki, Satoru, Kaikita, Koichi, Yamada, Yoshihiro, Shimomura, Hideki, Oniki, Kentaro, Saruwatari, Junji, Hokimoto, Seiji, Yasue, Hirofumi, Tsujita, Kenichi
• Format: Journal Article
• Language: English
• Published: Tokyo Springer Japan 01.02.2022; Springer Nature B.V
• Subjects: Aged; Aldehyde dehydrogenase; Aldehyde Dehydrogenase, Mitochondrial - genetics; Aldehydes; Asians - genetics; Biomedical Engineering and Bioengineering; Cardiac Surgery; Cardiology; Creatine; Creatine kinase; Dehydrogenase; Dehydrogenases; Female; Gender aspects; Gender differences; Genotype; Genotypes; Genotyping; Heart attacks; Humans; Injuries; Ischemia; Male; Medicine; Medicine & Public Health; Men; Middle Aged; Mitochondria; Myocardial infarction; Myocardial Reperfusion Injury - genetics; Original Article; Patients; Plasma levels; Reperfusion; Sex Characteristics; Sex differences; ST Elevation Myocardial Infarction - genetics; Vascular Surgery; Women; Variant; ST-elevation myocardial infarction; Ischemia/reperfusion injury; Reactive aldehydes; East Asians; Variant ALDH22
• ISSN: 0910-8327; 1615-2573; 1615-2573
• DOI: 10.1007/s00380-021-01907-x

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 ( χ 2 = 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.