Alvarez Chikezie K, Cronin Edmond, Baker William L, Kluger Jeffrey
Montefiore Medical Center, Albert Einstein College of Medicine, 111 East 210th Street, Bronx, NY, 10467, USA.
University of Connecticut School of Medicine, Farmington, CT, USA.
J Interv Card Electrophysiol. 2019 Dec;56(3):229-247. doi: 10.1007/s10840-019-00623-x. Epub 2019 Oct 9.
Heart failure (HF) is a major cause of morbidity and mortality with more than 5.1 million individuals affected in the USA. Ventricular tachyarrhythmias (VAs) including ventricular tachycardia and ventricular fibrillation are common in patients with heart failure. The pathophysiology of these mechanisms as well as the contribution of heart failure to the genesis of these arrhythmias is complex and multifaceted. Myocardial hypertrophy and stretch with increased preload and afterload lead to shortening of the action potential at early repolarization and lengthening of the action potential at final repolarization which can result in re-entrant ventricular tachycardia. Myocardial fibrosis and scar can create the substrate for re-entrant ventricular tachycardia. Altered calcium handling in the failing heart can lead to the development of proarrhythmic early and delayed after depolarizations. Various medications used in the treatment of HF such as loop diuretics and angiotensin converting enzyme inhibitors have not demonstrated a reduction in sudden cardiac death (SCD); however, beta-blockers (BB) are effective in reducing mortality and SCD. Amongst patients who have HF with reduced ejection fraction, the angiotensin receptor-neprilysin inhibitor (sacubitril/valsartan) has been shown to reduce cardiovascular mortality, specifically by reducing SCD, as well as death due to worsening HF. Implantable cardioverter-defibrillator (ICD) implantation in HF patients reduces the risk of SCD; however, subsequent mortality is increased in those who receive ICD shocks. Prophylactic ICD implantation reduces death from arrhythmia but does not reduce overall mortality during the acute post-myocardial infarction (MI) period (less than 40 days), for those with reduced ejection fraction and impaired autonomic dysfunction. Furthermore, although death from arrhythmias is reduced, this is offset by an increase in the mortality from non-arrhythmic causes. This article provides a review of the aforementioned mechanisms of arrhythmogenesis in heart failure; the role and impact of HF therapy such as cardiac resynchronization therapy (CRT), including the role, if any, of CRT-P and CRT-D in preventing VAs; the utility of both non-invasive parameters as well as multiple implant-based parameters for telemonitoring in HF; and the effect of left ventricular assist device implantation on VAs.
心力衰竭（HF）是发病和死亡的主要原因，在美国有超过510万人受其影响。室性快速心律失常（VAs），包括室性心动过速和心室颤动，在心力衰竭患者中很常见。这些机制的病理生理学以及心力衰竭对这些心律失常发生的作用是复杂且多方面的。心肌肥大以及前负荷和后负荷增加导致的心肌拉伸，会使早期复极时动作电位缩短，终末复极时动作电位延长，这可能导致折返性室性心动过速。心肌纤维化和瘢痕可为折返性室性心动过速创造条件。衰竭心脏中钙处理的改变可导致促心律失常的早期和延迟后去极化的发生。用于治疗HF的各种药物，如袢利尿剂和血管紧张素转换酶抑制剂，尚未显示出能降低心源性猝死（SCD）；然而，β受体阻滞剂（BB）在降低死亡率和SCD方面是有效的。在射血分数降低的心力衰竭患者中，血管紧张素受体脑啡肽酶抑制剂（沙库巴曲/缬沙坦）已被证明可降低心血管死亡率，特别是通过降低SCD以及因HF恶化导致的死亡。在HF患者中植入植入式心脏复律除颤器（ICD）可降低SCD风险；然而，接受ICD电击的患者随后的死亡率会增加。对于射血分数降低且自主神经功能障碍的患者，预防性ICD植入可降低心律失常导致的死亡，但在急性心肌梗死（MI）后时期（少于40天）并不能降低总体死亡率。此外，虽然心律失常导致的死亡减少了，但这被非心律失常原因导致的死亡率增加所抵消。本文综述了上述心力衰竭中心律失常发生的机制；HF治疗（如心脏再同步治疗（CRT））的作用和影响，包括CRT-P和CRT-D在预防VAs中的作用（如有）；用于HF远程监测的非侵入性参数以及多种基于植入物的参数的效用；以及左心室辅助装置植入对VAs的影响。
