Cardiac fibrosis in three dimensions - mechanistic insights into arrhythmic risk due to hypertrophy.
Cardiac fibrosis in three dimensions - mechanistic insights into arrhythmic risk due to hypertrophy.
复制标题
三个维度的心脏纤维化 - 对肥厚引起的心律失常风险的机制见解。
DOI：
10.1113/jp283710
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发表时间：
2023
期刊：
影响因子：
--
通讯作者：
Harvey,Robert
中科院分区：
文献类型：
--
作者：
Shivkumar,Kalyanam;Qu,Zhilin;Harvey,Robert
Sudden cardiac death, predominantly due to ventricular tachycardia and fibrillation (VT/VF), has a staggering death toll, by some estimates up to 10 million deaths/year worldwide (Rubart & Zipes, 2005). Underlying heart disease increases the risk of VT/VF and arrhythmic death.(Rubart & Zipes, 2005) Physiological (uniform/orderly) impulse propagation in the myocardium is critically dependent on proper organization of the myocardial bundles and cell-cell communication.(Kleber & Rudy, 2004) Myocardial fibrosis is a major structural alteration of the myocardium as a result of various disease processes. Cardiac injury (eg infarction, focal inflammation) results in the formation of a fibrotic scar.(Rutherford et al., 2012) Other cardiac diseases such as hypertension that are associated with cardiac hypertrophyare also associated with myocardial fibrosis. Fibrosis is a central problem in arrhythmia biology, by distorting myocardial architecture and interrupting electrical propagation pathways it setsthe stage for non-uniform impulse propagation. These altered ‘zig zag’conduction pathways form reentrant circuits that sustain VT/VF.(Nguyen et al., 2014) The pattern and location of fibrosis also profoundly influences the formation of arrhythmogenic circuits in the heart.(Nguyen et al., 2014) Fibrotic scars secondary to myocardial infarction have been the subject of intense study over several decades. These scars (usually encompassing a perfusion bed of a coronary artery) contain strands of viable myocardial bundles interspersed with fibrotic tissue that can create reentrant circuits (Janse & Wit, 1989). The translational potential of understanding myocardial scars by the experimental mapping of reentry in experimental models has resulted in substantial clinical benefit.(Ajijola et al., 2013) Clinical translation of these experimental findings resulted in mapping of VT circuits in humans. The development of catheter ablation of VT as a clinical therapy followed and is an excellent example of the direct beneficial consequence of these scientific advances.(Shivkumar, 2019)
