Key result
The J wave in early repolarization syndrome is driven by a transmural voltage gradient from transient outward current (Ito), which is exacerbated by bradycardia and ICa inhibition, potentially triggering phase 2 reentry and ventricular fibrillation.
Why the study?
The J wave has garnered attention due to its association with the onset of ventricular fibrillation, prompting a review of its origin based on the repolarization hypothesis.
This review elucidates the repolarization abnormality mechanisms underlying J waves and early repolarization syndrome, highlighting the role of Ito and phase 2 reentry in arrhythmogenesis.
Supports repolarization theory for J-wave VF risk; leaves open therapeutic targeting pending prospective validation.
J波が心室細動（ventricular fibrillation：VF）発症と関連することが判明し，注目を集めている．本稿では，再分極説に基づきJ波の成因を解説する．2008年にHaïssaguerreらは，“早期再分極（J波）を呈する症例のなかに，VFを発症するリスクの高い症例が少なからずいる”ことを示し，「早期再分極症候群（early repolarization syndrome：ERS）」という疾患概念を提唱した．一過性外向き電流（transient outward current：Ito）は活動電位1相で急速に流れる外向き電流であり，オーバーシュート直後のノッチを形成する．Itoは心外膜で電流量が多く，心内膜では少ない．この心外膜から心内膜にかけての貫壁性電位勾配が大きいと，J波が顕著になる．Itoの不活性化からの回復が遅い際は，徐脈時にJ波は増高する．J波がVFを生じる機序としては，“phase 2 reentry”が有力である．自験例（30代後半のVF既往ERS患者）で，心血管作動薬の投与に対するJ波の反応を観察した．プロプラノロールおよびベラパミルはJ波振幅を増高させた．これは内向きCa電流（ICa）抑制効果で説明可能と思われた．一方，イソプロテレノールはJ波振幅を減高・消失させた．これはICa増強および心拍数増加にともなう二次性のIto抑制によるものと思われた．
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Naohiko Takahashi (2022) conducted a review in Early repolarization syndrome. Pharmacological modulation (propranolol, verapamil, isoproterenol) was evaluated on J wave amplitude and ventricular fibrillation risk. The J wave in early repolarization syndrome is driven by a transmural voltage gradient from transient outward current (Ito), which is exacerbated by bradycardia and ICa inhibition, potentially triggering phase 2 reentry and ventricular fibrillation.
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