Fibrosis and Cardiac Arrhythmias

被引：269

作者：

de Jong, Sanne ^{[1
]}

van Veen, Toon A. B. ^{[1
]}

van Rijen, Harold V. M. ^{[1
]}

de Bakker, Jacques M. T. ^{[1
,2
,3
]}

机构：

[1] Univ Med Ctr, Dept Med Physiol, Utrecht, Netherlands

[2] Heart Failure Res Ctr, Dept Expt Cardiol, Amsterdam, Netherlands

[3] Interuniv Cardiol Inst Netherlands, Utrecht, Netherlands

来源：

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY | 2011年 / 57卷 / 06期

关键词：

fibrosis; collagen; arrhythmias; electrophysiology; CARDIOVASCULAR MAGNETIC-RESONANCE; IDIOPATHIC DILATED CARDIOMYOPATHY; ALTERED CONNEXIN43 EXPRESSION; DELAYED CONTRAST ENHANCEMENT; LATE GADOLINIUM ENHANCEMENT; GAP JUNCTIONAL CONDUCTANCE; HYPERTROPHIC CARDIOMYOPATHY; MYOCARDIAL FIBROSIS; HEART-FAILURE; VENTRICULAR-TACHYCARDIA;

D O I：

10.1097/FJC.0b013e318207a35f

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

In this review article about fibrosis and arrhythmias, we show that the amount of collagen, a normal element of the heart muscle, increases with age and in heart disease. The relation between fibrosis and electrophysiological parameters such as conduction, fractionation of electrograms, abnormal impulse initiation as well as arrhythmogenicity is discussed. Next to the amount of fibrosis, we offer data suggesting that collagen texture too plays a role in conduction slowing and arrhythmia vulnerability. Data are shown revealing that fibrosis can also be induced by reduced sodium channel and connexin43 expression. Finally contrast-enhanced magnetic resonance to detect fibrosis and ventricular tachycardia vulnerability in a noninvasive way as well as a reduction of fibrosis and arrhythmogenicity by inhibition of the renin-angiotensin-aldosterone system is discussed.

引用

页码：630 / 638

页数：9

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