The Evolving Science on Sudden Cardiac Death—The Marriage of Left Ventricular Hypertrophy and QT-Dispersion

IF 1.6 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS
James Ker
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引用次数: 0

Abstract

The first description of sudden cardiac death was made by Hippocrates in the 4th century BC [1]. Such cases of sudden collapse and death have intrigued both the public and medical science for centuries and a practical definition is that sudden cardiac death is the unexpected and natural death from a cardiac cause within a short period, usually less than 1 h from the onset of symptoms, in a person without any known prior condition [1, 2]. Sudden cardiac death (SCD) is clearly the end-result of a wide variety of cardiac conditions—both congenital and acquired. However, the most common mechanism for the event of SCD is ventricular fibrillation [1].

Understandably, SCD can afflict both the athlete and the non-athlete and is the cause of 13%–20% of all deaths in Western countries [2]. In athletes older than 35 years of age atherosclerotic coronary artery disease is the most common cause of SCD, while primary cardiomyopathies and ion channelopathies are more commonly found in the young athlete with SCD [2]. However, this is an evolving field of study and the recent study published by Stojanovic et al. [3] is of great importance as it links two well-known risk factors for SCD—left ventricular hypertrophy (LVH) and QT-dispersion [4]. The strong association between LVH and overall cardiovascular mortality first emerged from the Framingham heart study [4]. Initially, after this observation, several studies have confirmed the strong association between LVH and cardiovascular mortality, but the specific association with sudden cardiac death (SCD) came later with the Oregon Sudden Unexpected Death Study (Oregon SUDS)–one of the first to confirm the link between LVH and SCD [4, 5]. The development of LVH creates various pathways to ventricular arrhythmogenesis, which include ventricular ectopy, in fact, every additional millimeter of left ventricular wall thickness increases the risk of ventricular ectopy 2- to 3-fold [4]. LVH is the cause of significant cellular and interstitial remodeling of the myocardium which promotes ventricular arrhythmogenesis from both re-entry and triggered activity [4]. An increase in left ventricular mass (LVH) results in various myocardial alterations resulting in electrical remodeling with resultant prolonged QRS intervals, prolonged OT intervals, interstitial fibrosis with re-entry, sub-endocardial ischemia and increased sensitivity to pro-arrhythmia due to an increase in left ventricular wall stress [4]. In fact, all forms of left ventricular hypertrophy, concentric, eccentric, and even concentric remodeling without hypertrophy are all associated with an increased risk for sudden cardiac death [6].

The QT interval—the interval from the beginning of the QRS complex to the end of the T wave on the surface ECG—represents the period of global ventricular de- and repolarization [7]. Prolongation of this interval is strongly associated with an increased risk of lethal arrhythmia [7]. Regional differences in ventricular repolarization facilitate re-entry and is strongly associated with ventricular arrhythmias [7]. QT dispersion—the difference between the longest and shortest QT interval on the surface ECG—is indicative of such regional differences in ventricular repolarization and numerous publications support this association with lethal arrhythmia [7]. Normal QT dispersion (QTd) is between 20 and 40 ms in normal individuals, with some authors proposing up to 65 ms [8].

It has been shown that LVH in patients with hypertension is associated with an increase in QT dispersion and that both these parameters can be normalized with anti-hypertensive therapy [9].

The finding by Stojanovic et al. [3] that septal thickness in both athletes and sedentary men are associated with increased QTd is concerning and future studies need to clarify if we need to keep the septum thin at all costs with more exercise for some and less for others.

不断发展的心脏性猝死科学--左心室肥大与 QT 弥散的结合。
公元前 4 世纪,希波克拉底首次描述了心脏性猝死[1]。几个世纪以来,这种突然倒地和死亡的病例一直吸引着公众和医学科学界,一个实用的定义是,心脏性猝死是指在短时间内,通常是在症状出现后 1 小时内,在没有任何已知先兆的情况下,因心脏原因导致的意外自然死亡[1, 2]。心脏性猝死(SCD)显然是多种心脏疾病(包括先天性和后天性)的最终结果。然而,SCD 最常见的发病机制是心室颤动[1]。可以理解的是,SCD 可同时困扰运动员和非运动员,是西方国家 13%-20% 死亡的原因[2]。在 35 岁以上的运动员中,动脉粥样硬化性冠状动脉疾病是导致 SCD 的最常见原因,而原发性心肌病和离子通道病则更常见于患有 SCD 的年轻运动员[2]。然而,这是一个不断发展的研究领域,Stojanovic 等人最近发表的研究[3]将两个众所周知的 SCD 危险因素--左心室肥厚(LVH)和 QT 弥散[4]联系在一起,因而具有重要意义。LVH 与心血管总死亡率之间的密切关系最早出现在弗雷明汉心脏研究中[4]。在这一观察结果之后,又有多项研究证实了 LVH 与心血管死亡率之间的密切联系,但与心脏性猝死(SCD)之间的具体联系则是在俄勒冈州意外猝死研究(Oregon Sudden Unexpected Death Study,Oregon SUDS)中出现的,该研究是最早证实 LVH 与 SCD 之间联系的研究之一 [4,5]。事实上,左心室壁厚度每增加一毫米,室性异位的风险就会增加 2 到 3 倍[4]。左心室肥厚是心肌细胞和间质重塑的重要原因,而细胞和间质重塑会促进再入和触发活动导致的室性心律失常[4]。左心室质量(LVH)的增加会导致各种心肌改变,从而引起心电重塑,导致 QRS 间期延长、OT 间期延长、间质纤维化并伴有再入、心内膜下缺血,以及由于左室壁应力增加而导致对原心律失常的敏感性增加 [4]。事实上,所有形式的左心室肥厚、同心性肥厚、偏心性肥厚,甚至是无肥厚的同心性重构,都与心脏性猝死的风险增加有关[6]。QT 间期--表面心电图上从 QRS 波群开始到 T 波结束的间期--代表心室整体去极化和复极化的周期[7]。该间期的延长与致命性心律失常风险的增加密切相关[7]。心室再极化的区域性差异有利于再入,与室性心律失常密切相关[7]。QT 弥散--体表心电图上最长和最短 QT 间期之间的差异--表明心室复极化存在这种区域差异,许多出版物都支持这种差异与致死性心律失常有关 [7]。正常人的正常 QT 弥散(QTd)在 20 至 40 毫秒之间,有些学者认为可达 65 毫秒[8]。Stojanovic 等人[3]发现,运动员和久坐男性的室间隔厚度都与 QTd 增加有关,这一发现令人担忧,未来的研究需要明确我们是否需要不惜一切代价保持室间隔的厚度,让一些人多运动,而另一些人少运动。
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来源期刊
CiteScore
2.40
自引率
6.70%
发文量
211
审稿时长
3-6 weeks
期刊介绍: Echocardiography: A Journal of Cardiovascular Ultrasound and Allied Techniques is the official publication of the International Society of Cardiovascular Ultrasound. Widely recognized for its comprehensive peer-reviewed articles, case studies, original research, and reviews by international authors. Echocardiography keeps its readership of echocardiographers, ultrasound specialists, and cardiologists well informed of the latest developments in the field.
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