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September 25, 2018 Circulation. 2018;138:e272–e391. DOI: 10.1161/CIR.0000000000000549 e284 CLINICAL STATEMENTS AND GUIDELINES ventricular myocytes and Purkinje fibers, and may also enhance normal automaticity in Purkinje fibers in the ischemic zone. 3.3 Triggered Activity Early afterdepolarizations occur during late phase 2 or early phase 3 of the action potential,S3.4-3–S3.4-5 usually in the setting of action potential prolongation due to an increase in inward currents (the late sodium current, the inward calcium current or the sodium calcium exchange current) or a decrease in repolarizing potassium currents. Under these conditions, early afterdepolarizations may be initiated when reactivation of the inward L-type calcium channel occurs before the membrane has returned to a more negative potential than that required for calcium channel reactivation. Spontaneous calcium release from the sarcoplasmic reticulum may also result in activation of a depolarizing sodium/calcium exchange current. Early afterdepolarizations are the trigger for torsades de pointes VT associated with QT prolongation either induced by medications or other acquired factors or due to mutations of ion channels causing the long QT syndrome. In these cases, it is possible that the early afterdepolarization/triggered activity sequence is the trigger that culminates in polymorphic VT/VF. Delayed afterdepolarizations occur after complete membrane repolarization and develop under conditions of intracellular calcium overload. Factors contributing to elevated intracellular calcium load include tachycardia, catecholamines, hypokalemia, digoxin toxicity, cardiac hypertrophy, and HF.S3.4-6,S3.4-7 Elevated sarcoplasmic calcium content or increased sensitivity of the ryanodine receptor can initiate spontaneous calcium release, which activates a transient inward current driven predominantly by the sodium–calcium exchange current. If the membrane depolarization is sufficiently large, the inward sodium current is activated resulting in a triggered action potential. Delayed afterdepolarizations are the underlying mechanism for VT in the setting of digoxin toxicity, catecholaminergic polymorphic VT, and idiopathic outflow tract VA. Delayed afterdepolarizations are also considered to be an important trigger of VA in the setting of HF. Purkinje cells are more susceptible to spontaneous sarcoplasmic reticulum calcium release than ventricular myocytes suggesting that delayed afterdepolarizations may be an important mechanism for some Purkinje fiber-related VA.S3.4-3,S3.4-8,S3.4-9 3.4 Reentry Reentry is the underlying mechanism for most sustained VA in the presence of structural heart disease.S3.4-1–S3.4-3,S3.4-10–S3.4-12 Reentry may occur around a fixed anatomical obstacle, such as scar after an MI or surgically repaired congenital heart disease. In this setting, an excitable gap separates the excitation wavefront from its tail of refractoriness. The existence of structural reentrant substrates provide the rationale for VT ablation in scar-related VTs.S3.4-11,S3.4-12 Functional reentry around areas of functional block without anatomical obstacles can also occur. Two main models of functional reentry have been proposed.S3.4-2,S3.4-3 The leading circle model has a functionally refractory core and no excitable gap. Spiral wave reentry is driven by a rotor with a curved wavefront and wavetail pivoting around an excitable but unexcited core. There remains much debate about the precise mechanism(s) of VF (rotor versus multiple wavelet reentry). Both mechanisms may be operational in different phases of VF.S3.4-10 Phase 2 reentry may occur due to heterogeneity of ventricular repolarization. Electrotonic currents may flow from endocardial sites with longer action potential durations to the epicardium with shorter action potential durations which can result in reexcitation when these sites have recovered from refractoriness. This is believed to be one potential mechanism of VT/VF in Brugada syndromeS3.4-3 and may also be operative during ischemia. 4 GENERAL EVALUATION OF PATIENTS WITH DOCUMENTED OR SUSPECTED VA 4.1 History and Physical Examination Recommendation for Syncope* Referenced studies that support the recommendation are summarized in Online Data Supplement 1. COR LOE Recommendation I B-NR 1. Patients presenting with syncope for which VA is documented, or thought to be a likely cause, should be hospitalized for evaluation, monitoring, and management.S4.1-1–S4.1-4 *This section covers practices that are well accepted, and a new recommendation was determined to only be warranted for syncope. Synopsis VA can produce a wide spectrum of symptoms, and the severity of symptoms does not necessarily reflect the extent of structural heart disease or the potential risk of SCD. Symptoms of VA include palpitations, either skipped or extra beats or sustained palpitations, shortness of breath, chest pain, dizziness, near syncope, and syncope.S4.1-5,S4.1-6 Palpitations may correlate with VA but are frequently reported during normal rhythm.S4.1-7 The differential diagnosis of exercise intolerance, chest pain, dyspnea, presyncope, and syncope includes VA but also includes other etiologies. Nonetheless, more dramatic Downloaded from http://ahajournals.org by on October 7, 2026