Syncope and the risk of sudden cardiac death: Evaluation, management, and prevention

Abstract

Syncope is a clinical syndrome defined as a relatively brief self-limited transient loss of consciousness (TLOC) caused by a period of inadequate cerebral nutrient flow. Most often the trigger is an abrupt drop of systemic blood pressure. True syncope must be distinguished from other common non-syncope conditions in which real or apparent TLOC may occur such as seizures, concussions, or accidental falls. The causes of syncope are diverse, but in most instances, are relatively benign (e.g., reflex and orthostatic faints) with the main risks being accidents and/or injury. However, in some instances, syncope may be due to more worrisome conditions (particularly those associated with cardiac structural disease or channelopathies); in such circumstances, syncope may be an indicator of increased morbidity and mortality risk, including sudden cardiac death (SCD). Establishing an accurate basis for the etiology of syncope is crucial in order to initiate effective therapy. In this review, we focus primarily on the causes of syncope that are associated with increased SCD risk (i.e., sudden arrhythmic cardiac death), and the management of these patients. In addition, we discuss the limitations of our understanding of SCD in relation to syncope, and propose future studies that may ultimately address how to improve outcomes of syncope patients and reduce SCD risk.

Keywords: Risk assessment; Sudden cardiac death; Syncope.

Fig. 1

12-lead ECG of a patient with 2:1 AV block. The conducted beats have a long PR interval and a left bundle branch block morphology, indicating severe underlying conduction system disease.

Fig. 2

12-lead ECG showing a prolonged QTc in a patient with Long QT type 1 syndrome. The long QT syndromes may be associated with a particular form of polymorphous ventricular tachycardia (i.e., torsade de pointe). Torsades may be non-sustained and, in such cases, could be the cause of syncope. However, torsades may also degenerate into VF and, thereby, be responsible for SCD.

Fig. 3

12-lead ECG of a patient with catecholaminergic polymorphic ventricular tachycardia (CPVT). Note that the QRS axis alternates with every other beat, and consequently this arrhythmia is referred to as bidirectional VT. Digitalis toxicity may cause a similar arrhythmia.

Fig. 4

12-lead ECG of a patient with early repolarization of the inferolateral leads. This ECG finding has recently been associated with increased SCD propensity.