Induction of heat shock proteins prevents the arrhythmogenic substrate for atrial fibrillation

被引：14

作者：

Takahashi, Naohiko ^{[1
]}

Wakisaka, O. ^{[2
]}

Yoshimatsu, H. ^{[2
]}

Saikawa, T. ^{[1
]}

机构：

[1] Oita Univ, Fac Med, Dept Lab Examinat & Diagnost, Yufu City, Oita 8795593, Japan

[2] Oita Univ, Fac Med, Dept Internal Med, Yufu City, Oita 8795593, Japan

来源：

INTERNATIONAL JOURNAL OF HYPERTHERMIA | 2009年 / 25卷 / 08期

关键词：

atrial refractory period; atrial fibrosis; atrial fibrillation; ISCHEMIA/REPERFUSION INJURY; INDUCED EXPRESSION; HEAT-SHOCK-PROTEIN-72; MECHANISMS; CARDIOPROTECTION; EPIDEMIOLOGY; DYSFUNCTION; CORRELATE; PROTECTS; FIBROSIS;

D O I：

10.3109/02656730903070949

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Atrial fibrillation (AF) is the commonest arrhythmia. Studies have shown that atrial tachypacing (artificial persistent AF) causes electrical remodelling. This is characterised by the shortening of the atrial effective refractory period (ERP), in which reduction in L-type Ca2+ channel current plays an essential part. Atrial fibrosis, a feature of structural remodelling, is induced by continuous infusion of angiotensin II, and has been associated with conduction delay in atria, which promotes AF. Acute atrial ischaemia, frequently observed during development of acute coronary syndrome, has been associated with atrial conduction heterogeneity, which also promotes AF. Induction of heat shock proteins (Hsp72 and Hsp27) by hyperthermia and/or geranylgeranylacetone has demonstrated to protect the heart against such atrial remodelling. The potent protective role of Hsp72 and Hsp27 against clinical AF in patients who underwent open heart surgery has been shown. Taken together, interventions that induce heat shock responses (including induction of Hsp72 and Hsp27) may prevent newly developed AF and delay the progression of paroxysmal AF to persistent AF.

引用

页码：641 / 646

页数：6

共 37 条

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