Tohoku J. Exp. Med., 1999, 187 (4)

The Role of Alcohol Dehydrogenase 2 and Aldehyde Dehydrogenase 2 Genotypes in Alcohol-Induced Vasospastic Angina

TAKAFUMI SEKI, HIROSHI OKAYAMA, SHOGEN ISOYAMA, YUTAKA KAGAYA, KUNIO SHIRATO, KEI MUNAKATA,1 MASAHARU KANAZAWA,1 KENJI TAMAKI,2 TETSUYA HIRAMOTO,3 MICHIKO OKAYAMA4 and SHINYA KASAHARA4

The First Department of Internal Medicine, Tohoku University School of Medicine, Sendai 980-8574, 1Cardiology Division, Sendai City Medical Center, Sendai 983-0824, 2Cardiology Division, Iwate Prefectural Central Hospital, Morioka 020-0066, 3Cardiology Division, Tohoku Kosai Hospital, Sendai 980-8674, and 4Sendai Cardiovascular Center, Sendai 981-3107

  • Alcohol ingestion often provokes attacks in patients with vasospastic angina. Type 2 aldehyde dehydrogenase (ALDH2) deficiency, which is based on a single point mutation (Glu487Lys) of the ALDH2 gene, is common in the Japanese population, but rare among the Caucasian population. We investigated how the genotype of ALDH2 affects the characteristics of alcohol-induced vasospastic angina. Ninety-one patients with vasospastic angina who had ingested alcohol daily or occasionally were studied. Patients had been diagnosed as vasospastic angina by a provocation test with an intracoronary injection of ergonovine or acetylcholine during coronary angiography. The Glu487Lys mutation was detected by allele specific PCR. We interviewed the patients to obtain information concerning the relationship between alcohol ingestion and anginal attacks. Alcohol ingestion induced attacks in 16 of 66 patients without the Glu487Lys mutation, 8 of 22 in heterozygotes, and 1 of 3 in mutant homozygotes. The intervals between alcohol ingestion and the onset of anginal attacks were shorter in homozygotes (0.17 hours) and heterozygotes (1.5±0.6 hours) for ALDH2*2 than in normal homozygotes for ALDH2*1 (5.4±0.6 hours). The amount of ethanol which induced attacks was significantly greater in normal homozygotes than in homozygotes (11 ml) and heterozygotes (42.5±7.1 ml) for ALDH2*2 (96.1±13.4 ml in normal patients). The frequency of anginal attacks induced by alcohol ingestion did not differ between ALDH deficient and normal homozygotes. In ALDH deficient patients, however, anginal attacks were induced by a smaller amount of alcohol immediately after its ingestion. Thus, the ALDH2 genotype modifies the characteristics of the anginal attacks as a co-factor for the induction of vasospastic angina after alcohol ingestion.
    Key words--- alcohol ingestion; vasospastic angina; aldehyde dehydrogenase genotype; alcohol dehydrogenase genotype
    © 1999 Tohoku University Medical Press

    Tohoku J. Exp. Med., 1999, 187, 311-322
    Address for reprints: Shogen Isoyama, M. D., Ph. D., Faculty of Medical Science and Welfare, Tohoku Bunka Gakuen University, 6-45-16 Kunimi, Aoba-ku, Sendai 981-8550, Japan.
    e-mail: shogen@rehab.tbgu.ac.jp

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