アポリポプロテインE4と喫煙する中年男性における冠動脈疾患:前向きな研究
S E Humphries1, P J Talmud, E Hawe
1Centre for Cardiovascular Genetics, Department of Medicine, Royal Free and University College London Medical School, Rayne Institute, WC1E 6JJ, London, UK. rmhaseh@ucl.ac.uk
Lancet (London, England)
|July 21, 2001
まとめ
喫煙は,すべてのアポリポプロテインE (APOE) ゲノタイプにおける冠動脈疾患のリスクを大幅に高めます. APOE epsilon4アレルを持つ男性は,タバコを吸うと特にリスクが高まります.
科学分野:
- 心血管遺伝学 心血管遺伝学
- エピデミオロジー エピデミオロジー
- 脂質代謝 脂質代謝とは
背景:
- アポリポプロテインE (apoE) のイソフォーム (E2,E3,E4) は,脂質レベルと冠動脈疾患 (CHD) リスクに影響します.
- APOE epsilon4アレルは,心血管疾患の既知の危険因子である.
- 喫煙とAPOE遺伝子型が心血管疾患のリスクに及ぼす相互作用については,さらなる調査が必要である.
研究 の 目的:
- APOE遺伝子型が喫煙と冠動脈疾患のリスクとの関連をどのように変化させるかを調べる.
- 喫煙が心血管疾患に与える影響が,様々なAPOE遺伝子型を持つ個体によって異なるかどうかを判断する.
主な方法:
- 前科性心血管疾患のない3052人の中年男性の将来的な心血管監視 (ノースウィックパーク心臓研究II).
- 喫煙習慣の評価は,アンケートと,PCRと制限酵素消化によるAPOEゲノタイプ化によるものです.
- 心筋梗塞,冠動脈外科手術,静かな心筋梗塞を含むCHDのエンドポイントのモニタリング.
主要な成果:
- 喫煙者は,他の危険因子とは関係なく,決して喫煙しない人と比較して,心臓病のリスクが1.94倍増加しました.
- 禁煙者では,異なるAPOE遺伝子型においてCHDリスクが類似していた.
- APOE epsilon4 アレルを持つ喫煙者は,非喫煙者と比較してCHDのリスクが著しく上昇 (2.79倍) しており,強い遺伝子環境相互作用 (p=0.007) を示しています.
結論:
- 喫煙は,すべてのAPOE遺伝子型における冠動脈疾患の重要な危険因子です.
- APOE epsilon4アレルを持つ個人は,喫煙すると,不釣り合いの高い心血管疾患リスクの増加を経験します.
- これらの発見は,心血管疾患における遺伝的傾向 (APOE遺伝子型) とライフスタイル要因 (喫煙) の間の重要な相互作用を強調しています.
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