Classification According to Tachycardia Morphology

Monomorphic VT has a single stable QRS morphology from beat to beat, indicating repetitive ventricular depolarization with the same activation sequence ( Fig. 22.1 ).

Surface Electrocardiogram of Different Types of Ventricular Tachycardia (VT) .

Multiple monomorphic VTs refers to more than one morphologically distinct monomorphic VT, occurring as different episodes or induced at different times.

Polymorphic VT has clearly defined QRS complexes with a continuously changing morphology or multiform QRS morphology (i.e., no constant morphology for more than five complexes, no clear isoelectric baseline between QRS complexes, or QRS complexes that have different morphologies in multiple simultaneously recorded leads), indicating a variable sequence of ventricular activation and no single site of origin.

Torsades de pointes is a polymorphic VT associated with a long QT interval, and is electrocardiographically characterized by twisting of the peaks of the QRS complexes around the isoelectric line during the arrhythmia.

Pleomorphic VT has more than one morphologically distinct QRS complex occurring during the same episode of VT, but the QRS morphology is not continuously changing.

Bidirectional VT is a VT associated with a beat-to-beat alternans in the QRS frontal plane axis, often associated with digitalis toxicity or catecholaminergic VT.

Ventricular flutter is a term that has been applied to a rapid (250 to 350 complexes/min) VT that has a sinusoidal QRS configuration that prevents clear identification of the QRS morphology.

Ventricular fibrillation (VF) is a rapid (usually greater than 300 complexes/min), chaotic tachycardia without consistently identifiable QRS complexes.

Classification According to Tachycardia Duration

Sustained VT lasts for more than 30 seconds or requires termination (e.g., cardioversion) in less than 30 seconds because of hemodynamic compromise, whereas nonsustained VT is a tachycardia at more than 100 beats/min lasting for three or more complexes but for less than 30 seconds and not requiring termination.

During electrophysiological (EP) testing, nonsustained VT is defined as more than five or six complexes of non–bundle branch reentrant (BBR) VT, regardless of morphology. BBR complexes are frequent (50%) in normal individuals in response to ventricular extrastimulus (VES) and have no relevance to clinical nonsustained VT.

Repetitive polymorphic responses are also common (up to 50%) during programmed ventricular stimulation, especially in response to multiple (three or more) VESs with very short coupling intervals (less than 180 milliseconds). The clinical significance of induced polymorphic nonsustained VT is questionable.

Incessant VT is a continuous sustained VT that recurs promptly over several hours despite repeated interventions (e.g., electrical cardioversion) for termination. Less commonly, incessant VT manifests as repeated bursts of VT that spontaneously terminate for a few intervening sinus beats, followed by the next tachycardia burst. The latter form is more common with the idiopathic VTs ( see Fig. 23.1 ).

Classification According to QRS Morphology in Lead V ₁

Monomorphic VT can be classified as having one of two patterns: a right bundle branch block (RBBB)–like pattern or a left bundle branch block (LBBB)–like pattern. VTs with an LBBB-like pattern have a predominantly negative QRS polarity in lead V ₁ (QS, rS, qrS), whereas VTs with a RBBB-like pattern have a predominantly positive QRS polarity in lead V ₁ (rsR′, qR, RR, R, RS). Importantly, this classification pertains to QRS morphology only in lead V ₁ ; the VT may not show features consistent with the same BBB configuration in other leads. Also, the determination that the VT has an RBBB-like pattern or an LBBB-like pattern does not, by itself, assist in making a diagnosis; however, this assessment should be made initially because it has further implications for evaluating several other features on the ECG, including the QRS axis, the QRS duration, and the QRS morphology.

Classification According to Tachycardia Mechanism

Focal VT has a point source of earliest ventricular activation with a centrifugal spread of activation from that site. The mechanism can be abnormal automaticity, triggered activity, or microreentry. Scar-related reentrant VT describes arrhythmias that have characteristics of reentry and originate from an area of myocardial scar identified from electrogram characteristics or myocardial imaging. Large reentry circuits that can be defined over several centimeters are commonly referred to as “macroreentry” circuits.

Mechanisms of Ventricular Arrhythmias Associated With Acute Ischemia

Acute myocardial ischemia leads to local tissue hypoxia, depletion of adenosine triphosphate (ATP), and anaerobic glycolysis causing intracellular acidosis. ATP depletion impairs the function of the ATP-dependent Na ⁺ -K ⁺ pump, causing net K ⁺ leakage from the myocyte and elevation of extracellular K ⁺ concentration. This results in depolarization of the resting membrane potential of the surviving Purkinje fibers and, as a consequence, abnormal automaticity.

In addition, intracellular acidification and accumulation of H ⁺ ions activate the Na ⁺ -H ⁺ exchanger, which extrudes H ⁺ in exchange for Na ⁺ entry, causing increased intracellular Na ⁺ concentration. The latter activates the Na ⁺ -Ca ²⁺ exchanger in the reverse mode, which extrudes Na ⁺ in exchange for Ca ²⁺ entry, causing intracellular Ca ²⁺ overload in the ischemic myocardium which, in turn, leads to delayed afterdepolarizations (DADs) and triggered arrhythmias.

Furthermore, membrane depolarization causes Na ⁺ channel inactivation and, as a result, reduced fast Na ⁺ current and reduced action potential upstroke, leading to slowed conduction and altered refractoriness.

Although an initial prolongation of the action potential duration can be observed (likely caused by an increase in the late Na ⁺ current), abbreviation of the action potential duration develops shortly afterward secondary to reduced Na ⁺ entry (due to Na ⁺ channel inactivation), reduced Ca ²⁺ entry (due to inhibition of Ca ²⁺ channels by acidosis), and enhanced K ⁺ efflux (due to activation of ATP-sensitive potassium current, IK-ATP, caused by reduced intracellular ATP).

Importantly, the effects of ischemia on the EP properties of myocardial cells are heterogeneous. Shortening of the action potential duration and reduction of upstroke velocity and amplitude are more pronounced within the central zone of ischemia and subepicardium than within the border zone and subendocardium. On the other hand, the surrounding normal myocardium can have an increase in conduction velocity (secondary to increased catecholamines) and decrease in refractoriness. This heterogeneity of action potential duration and dispersion of refractoriness provide a substrate for an injury current to flow between the ischemic and the nonischemic cells located at the border zone. In addition, myocardial ischemia causes disruption of gap junctions, leading to cellular uncoupling, with consequent slow and anisotropic conduction, and unidirectional conduction block, providing a substrate for reentry.

High levels of catecholamines, endothelin-1 activation, increased lysophosphatidylcholine (a phospholipid that accumulates in ischemic myocardium), mechanical stretch (induced by the viable myocardium surrounding the infarct zone), electrolyte abnormalities (particularly hypokalemia and hypomagnesemia), preexisting myocardial abnormalities (e.g., prior myocardial infarction [MI], hypertrophy, depressed ejection fraction), and genetic predisposition (likely mediated by mutations or polymorphism in genes encoding ion channels), can all significantly modify the EP properties of the substrate and contribute to arrhythmogenesis. Prolonged and severe acute ischemia and delayed or unsuccessful revascularization increase the risk of ventricular arrhythmias during an acute ischemic event.

Experimental studies demonstrated that arrhythmia mechanisms undergo dynamic changes in the early minutes and hours after onset of myocardial ischemia. Two temporally distinct phases of ventricular arrhythmia develop in response to ischemic injury: phase 1 is the reversible phase of acute MI, whereas phase 2 is the infarct evolution phase ( eFigs. 22.1 and 22.2 ).

Biochemical and Electrophysiological Characteristics of Phase 1 and Phase 2 Ischemia-Mediated Ventricular Arrhythmias.

APD , Action potential duration; I _Na , sodium channel current; I _Ca , inward calcium current; I _{K – ATP} , ATP-sensitive potassium current.

(From Di Diego JM, Antzelevitch C. Ischemic ventricular arrhythmias experimental models and their clinical relevance. Heart Rhythm. 2011;8:1963–1968.)

Temporal Distribution and Genesis of Ischemic Ventricular Arrhythmias.

AA, Abnormal automaticity; EADs, early afterdepolarizations; DADs, delay afterdepolarizations; PFs, Purkinje fibers; VF, ventricular fibrillation; VT, ventricular tachycardia.

(From Di Diego JM, Antzelevitch C. Ischemic ventricular arrhythmias experimental models and their clinical relevance. Heart Rhythm. 2011;8:1963–1968.)

Mechanisms of Ventricular Arrhythmias Associated With Healed Infarction

Most post-MI sustained monomorphic ventricular tachycardias (SMVTs) are caused by macroreentry involving the region of the ventricular scar. Left ventricular (LV) remodeling begins almost immediately after acute MI. Experimental studies suggest that the EP substrate for monomorphic VT gradually forms in the subacute phase (in the first week) following acute MI and once established, appears to remain stable into the chronic phase. EP and electroanatomical characteristics demonstrated no difference between induced VT during the subacute and chronic phases, with comparable sites of earliest presystolic activation. These sites are located predominantly in the border zone adjacent to dense injury areas in both phases.

Persistent coronary occlusion typically leads to a central core of dense transmural scar in the territory supplied by the occluded artery, surrounded by a thin rim (border zone) where fibrotic tissue and viable myocardial fibers are intermixed. Conversely, early reperfusion (achieved by thrombolytics or coronary intervention) can lead to a more complex substrate, with nontransmural myocardial necrosis (primary subendocardial necrosis and variable epicardial sparing depending on the duration of coronary occlusion) and heterogeneous (and even patchy) scarring with multiple channels of viable myocardium embedded within the scar region, and complex border zones. The scar and fibrosis resulting from MI are distinctly different from nonischemic etiologies. Compared with post-MI VT, the scar in dilated cardiomyopathy (DCM) tends to be smaller and less confluent, with less endocardial involvement and less transmurality. Whereas ischemia produces a predictable wedge-shaped wavefront of necrosis progressing from subendocardium to epicardium (and scar areas larger endocardially than epicardially), usually confined to a specific coronary vascular territory, scars in nonischemic DCM have been shown to have a predilection for the midmyocardium and epicardium. In contrast to the dense post-MI scar with isolated surviving myocardial bundles, scarring in nonischemic DCM is patchy with fewer fixed boundaries and protected channels or isthmuses, which can alter the extent of local conduction slowing.

Generally, the reentrant circuit arises in areas of a dense fibrotic scar interspersed with bundles of viable myocytes with poor intercellular coupling (due to altered gap junctions), producing a zigzag course of activation along a pathway lengthened by branching and merging bundles of surviving myocytes, leading to nonuniform anisotropic conduction ( see Fig. 3.18 ). Heterogeneity in tissue composition and autonomic innervation in these regions can create areas of slow conduction and block, which promote reentry.

Buried in the arrhythmogenic substrate is the common central pathway (critical isthmus), which is a narrow path of tissue with abnormal conduction properties, causing slowing of impulse propagation and allowing reentry to occur. The isthmus itself can be surrounded by dead ends or branches that do not participate in the common pathway of the main reentrant circuit (i.e., bystander channels). The critical isthmus is typically protected by boundaries formed of both fixed and functional conduction block. Fixed conduction barriers are anatomically determined by the heterogeneous scar geometry or a valvular annulus. Development of functional conduction block is a prerequisite for initiation of VT in most cases, forming at least one border of the diastolic pathway. Evidence indicates that formation of functional block leading to reentry is associated with a large dispersion in refractory periods over short anatomical distances.

Depolarization of the small mass of tissue within the isthmus is usually not detectable on the surface ECG and constitutes the electrical diastole between QRS complexes during VT. The wavefront leaves the isthmus at the exit site and propagates out to depolarize the remainder of the ventricles, producing the QRS complex. After leaving the exit of the isthmus, the reentrant wavefront can return to the entrance of the isthmus through an outer loop or an inner loop ( see Fig. 5.16 ). An outer loop is a broad sheet of myocardium along the outer border of the infarct. The reentrant wavefront propagates though the outer loop while at the same time activating the rest of the myocardium, corresponding to electrical systole (QRS complex) on the surface ECG. Reentrant circuits can have one or more outer loops. An inner loop is a conduction pathway within scars, communicating with the common central pathway (critical isthmus) forming a circuit. The inner loop can serve as an integral part of the reentrant circuit or function as a bystander pathway. The dominant loop is the circuit loop outside the common central pathway with the shortest conduction time. If conduction through the inner loop is slower than conduction from the exit to entrance sites (through the outer loop), the inner loop will serve as a bystander, and the outer loop will be the dominant loop. If conduction through the inner loop is faster than conduction through the outer loop, it will form an integral component of the reentrant circuit and is designated as the dominant inner loop. Bystander loops can serve as a potential component of a new reentrant circuit if the dominant loop is ablated. This may manifest as sudden slowing of the VT rate without changing QRS morphology during ablation of the dominant nonisthmus loop.

Studies using electroanatomic substrate mapping found that ischemic cardiomyopathy patients without clinical SMVT had markedly smaller endocardial low-voltage areas, fewer scar-related electrograms (i.e., fractionated, isolated, and very late potentials, which represent electrically viable sites within the scar), and fewer putative conducting channels compared with patients with spontaneous SMVT, despite equally severe LV dysfunction as well as similar infarct age and distribution. These differences in the myocardial EP substrate can play an important role in VT arrhythmogenesis in the chronic post-MI context. Both the extent of the scar areas (electrogram voltage less than 0.5 mV) and the presence of numerous channels within this zone seem to be critical to the development of VT. Although the border zone region of the scar (electrogram voltage, 0.5 to 1.5 mV) did not differ in area between the two groups, this zone also had a significantly higher prevalence of putative conducting channels in the SMVT patients. This suggests a fundamentally different scar composition (more “arrhythmogenic”) in the SMVT patients. As noted, inhomogeneous scarring with varying degrees of subendocardial myocardial fiber preservation within dense zones of fibrosis leads to slowed conduction, nonuniform anisotropy, and the potential for channels within the scar zone—conditions necessary for the development of reentry.

It is common for patients with post-MI VT to have more than one VT morphology. Even in patients presenting with a single SMVT, multiple distinct uniform VTs can be induced in the EP laboratory, especially in patients receiving antiarrhythmic therapy. The induction of multiple VT morphologies during an ablation procedure suggests that the arrhythmogenic substrate can support multiple reentrant circuits or different exit sites from a single circuit. Distinct VT morphologies (as defined by the 12-lead ECG and tachycardia cycle length [TCL]) often share a common isthmus but differ in propagation direction or location across the isthmus perimeter during reentry, but can also arise from distinct, usually adjacent, circuits.

A focal mechanism of VT (abnormal automaticity or triggered activity) has been implicated in the setting of acute ischemia. Focal VT can also occur in the absence of an acute ischemic event in patients with chronic ischemic heart disease. In one study, a focal mechanism was present in up to 9% of VTs that were induced in patients with ischemic heart disease during EP study for radiofrequency (RF) ablation.

Infrequently, SMVT in the setting of chronic coronary artery disease (CAD) is related to a nonischemic arrhythmogenic substrate rather than a healed infarct. CAD can coexist with nonischemic cardiomyopathy, in which setting, arrhythmogenic substrate is inconsistent with the distribution of CAD, with VT morphologies originating in the periannular basal ventricular segments and frequent epicardial VT exits.

Premature Ventricular Complexes

Premature ventricular complexes (PVCs) are seen in most cases of acute MI. Early PVCs (within the first 48 hours) do not appear to affect the prognosis. In contrast, repetitive complex PVCs (ventricular bigeminy, couplets, or multiform PVCs) occurring beyond 48 hours after acute MI can be associated with increased arrhythmic risk, particularly in patients with larger infarctions and impaired LV function.

Accelerated Idioventricular Rhythm

Accelerated idioventricular rhythm occurs in up to 50% of patients with acute MI, predominantly occurring in the first 12 hours after admission for acute MI. Although more common in patients with successful reperfusion therapy, accelerated idioventricular rhythm is neither a sensitive nor a very specific marker for successful reperfusion.

Reperfusion Arrhythmias

Ventricular arrhythmias upon reperfusion typically manifest as bursts of PVCs with long coupling intervals and accelerated idioventricular rhythms occurring at the moment of reperfusion, and are hemodynamically well tolerated. These arrhythmias originate within the reperfusion zone and likely reflect myocellular reperfusion injury. Reperfusion injury produces a second peak of myocardial necrosis, which depends on the duration of the preceding ischemia. Alteration of the EP substrate and, in particular, intracellular Ca ²⁺ overload combined with increased catecholamines, likely play a central role in reperfusion arrhythmias. Abnormal automaticity is the likely mechanism.

In conjunction with thrombolytic therapy, reperfusion ventricular arrhythmias were considered as a noninvasive marker of successful infarct artery recanalization; however, current evidence suggests that those arrhythmias are neither specific nor sensitive. In the more contemporary era of primary percutaneous coronary intervention (PCI), the presence of ventricular arrhythmia bursts timed closely to reperfusion appears to predict larger infarct size in patients presenting with ST-segment elevation MI and treated with primary PCI resulting in brisk epicardial flow restoration (TIMI 3 flow) and rapid and complete ST-segment resolution.

Nonsustained Ventricular Tachycardia

Nonsustained VT is observed in 1% to 7% of acute MI patients. Nonsustained VT occurring early (within the first 2 to 3 hours) following acute MI does not appear to predict poor prognosis. Arrhythmic episodes occurring later (after the first 24 hours, and particularly after the first week), in the course of acute MI portend a worse prognosis. Beyond the periinfarct period, nonsustained VT is common in ischemic heart disease, recorded in 30% to 80% of patients during long-term ambulatory monitoring, or detected by cardiac implanted devices.

Polymorphic Ventricular Tachycardia

Polymorphic VT, which occurs in 0.3% to 2% of patients, is usually due to abnormal automaticity or triggered activity associated with ischemia or reperfusion. In the setting of coronary disease, polymorphic VT is generally considered a marker of ongoing ischemia and is often suppressed by antiischemic interventions. Unlike monomorphic VT, polymorphic VT is rarely seen in patients with healed MI in the absence of acute myocardial ischemia.

Ventricular Fibrillation

VF occurs in 3.7% of all acute ST-elevation MIs in the first 48 hours, and this is likely an underestimation because prehospital events are not included. When all VF events, before and after 48 hours, were included, VF was found to occur in 6.7% of ST-elevation MI patients and in 1.3% of non-ST-elevation MI patients. The majority of arrhythmic episodes occur early (within the first 48 hours) in the course of acute MI.

Primary VF (i.e., VF that occurs during the first 48 hours of an uncomplicated MI, without recurrent ischemia or heart failure), is associated with an up to fivefold increase in hospital mortality (greater than 50% due to LV failure or cardiogenic shock) but appears to have little effect on long-term mortality in patients who survived to hospital discharge. Conversely, nonprimary VF (i.e., VF that occurs beyond the first 48 hours following MI or in the setting of recurrent ischemia or heart failure) is associated with marked increases in both 30-day mortality and 6-month mortality. The temporal cutoff between “early” and “late” arrhythmias at 48 hours following MI, however, is arbitrary to some extent; data to suggest that this should be at 24 hours or even earlier exist.

Several factors appear to be associated with an increased risk of early VF during the periinfarction period, including ST-elevation MI, larger infarct size, inferoposterior MI, periinfarction angina, incomplete revascularization, hypokalemia, hypotension, male gender, younger age, and history of smoking.

Sudden Cardiac Death

SCD accounts for up to 15% of total mortality in industrialized countries and claims the lives of more than 200,000 to 400,000 people per year in the United States (precise number not known and impacted by how estimates are obtained). Approximately 50% of deaths in patients with prior MI occur suddenly and unexpectedly. Ventricular arrhythmias are responsible for most of these deaths in stable ambulatory populations. Most SCD victims have known heart disease—most frequently CAD or prior MI.

Cardiac arrest is the initial manifestation of heart disease in approximately 50% of cases. Such patients are more likely to have single-vessel coronary disease and normal or mildly abnormal LV systolic function than cardiac arrest victims with prior MI. Although heart failure increases risk for both sudden and nonsudden death, a history of heart failure is present in only approximately 10% of cardiac arrest victims.

Acute MI is a common precipitant of out-of-hospital cardiac arrest, especially in older patients. About 40% of out-of-hospital cardiac arrest survivors develop overt signs of an MI (e.g., ST-segment elevation, Q waves, or elevated cardiac enzymes), and 50% are found to have an acutely occluded coronary vessel on coronary angiography.

The risk for arrhythmic and total mortality is highest in the first month after an acute MI and stays high during the first 6 months after acute MI. After the first year post MI, there appears to be a relatively quiescent period of relatively low rates of SCD, followed by a second peak 4 to 10 years after acute MI. The later occurrence of SCD likely results from delayed ventricular remodeling resulting in the creation or activation of reentrant VT circuits on the infarct border and from heart failure developing late after MI.

Although cardiac arrest and SCD in post-MI patients are predominantly caused by VT or VF, several studies in patients with cardiac arrest have shown that VF as the causative rhythm appears to be decreasing, being replaced by pulseless electrical activity and asystole. The cause of this change is unknown, but it may reflect patients with sicker hearts who are living longer due to better therapy. Hearts with advanced disease may be more likely to develop pulseless electrical activity and asystole than VF.

Sustained Monomorphic Ventricular Tachycardia

“Early” SMVT within the first 24 to 48 hours of acute MI is uncommon, and occurs in about 2% to 3% of ST-elevation MI patients and in less than 1% of non-ST-elevation MI patients. Although early SMVT is associated with an increase in in-hospital mortality, studies showed that mortality at 1 year (among 21- to 30-day survivors) is not increased, suggesting that the arrhythmogenic mechanisms can be transient in early post-MI SMVT. Nevertheless, it is important to understand that data are limited regarding the long-term prognostic significance of SMVT in the early post-MI setting because most studies combined VT and VF or sustained and nonsustained VT without specifying the results for each arrhythmia. Many investigators consider SMVT, even when occurring in the early hours following MI, to be an indicator of the presence of an already established permanent substrate (developing necrosis or preexisting scar) and, hence, an indicator of high long-term risk for arrhythmic events.

On the other hand, the typical patient with SMVT occurring during the subacute and healing phases, beginning more than 48 hours after an acute MI, has had a large, often complicated infarct with a reduced left ventricular ejection fraction (LVEF), and such VT is a predictor of a worse prognosis. SMVT within 3 months of an MI is associated with a 2-year mortality rate of 40% to 50%, with most deaths being sudden. Predictors of increased mortality in these patients include anterior wall MI, frequent episodes of sustained or nonsustained VT, heart failure, and multivessel coronary disease, particularly in individuals with residual ischemia.

Early reperfusion of infarct-related arteries results in less aneurysm formation, smaller scars, and less extensive EP abnormalities, although a significant risk of late VT (often with rapid TCLs) persists. In patients with ST-elevation MI treated with primary PCI, delayed reperfusion (greater than 5 hours after MI) was associated with a sixfold increase in the odds of inducible SMVT by programmed electrical stimulation (performed 6 to 10 days post MI) as well as an increased risk of spontaneous ventricular arrhythmias and SCD (after a mean follow-up of 28 ± 13 months) compared with early reperfusion (≤3 hours), independent of LVEF. It was estimated that each 1-hour delay in reperfusion conferred a 10.4% increase in the odds of inducible VT.

Most episodes of post-MI SMVT occur during the chronic phase. Among all patients presenting with SMVT in the setting of significant structural heart disease, ischemic heart disease is the most frequent etiology, comprising 54% to 59% of patients who receive an implantable cardioverter-defibrillator (ICD) or who are referred for catheter ablation.

VT occurs in 1% to 2% of patients late after MI, but the time interval from MI to first episode of VT is highly variable. The first episode can be seen within the first year post MI, but the median time of occurrence is about 3 years, and SMVT can occur as late as 10 to 15 years after an MI. Late SMVT often reflects significant LV dysfunction and the presence of a ventricular aneurysm or scarring. Late arrhythmias can also result from new cardiac events. The annual mortality rate for SMVT that occurs after the first 3 months following acute MI is approximately 5% to 15%. Predictors of life-threatening ventricular arrhythmias include residual ischemia in the setting of damaged myocardium, LVEF less than 40%, and electrical instability, including inducible or spontaneous VT, particularly in those who present with cardiac arrest.

Recent evidence suggests that coronary revascularization before or shortly after ICD placement in high-risk post-MI patients with LV dysfunction and wide QRS duration can potentially reduce the risk for life-threatening ventricular arrhythmias and appropriate ICD shocks.

The relationship between SMVT and VF is uncertain, and it is not clear how often VF is triggered by SMVT rather than occurring de novo. SMVT can simply be the company kept by VF in a number of patients or, in the appropriate setting such as recurrent ischemia, a rapid VT can develop a wavefront that becomes fractionated, leading to VF.

Evaluation of Type and Burden of Ventricular Arrhythmias

Identifying and quantifying the types and burden of sustained and nonsustained VT and PVCs are necessary. In addition to 12-lead ECG, ambulatory cardiac monitoring (Holter or event monitoring) or implantable loop recorders may be required to document the type, burden, and clinical impact of the arrhythmia. In patients with ICDs, stored device data such as electrogram morphology and TCL can be used to identify the clinical VT.

Evaluation of the Triggers of Ventricular Arrhythmias

Initial testing in patients with post-MI VT should evaluate for reversible causes of the arrhythmia. These include electrolyte imbalances, acute ischemia, heart failure, hypoxia, hypotension, drug effects, and anemia.

Evaluation of Myocardial Ischemia

Although recurrent SMVT is rarely due to acute myocardial ischemia in patients with known CAD, diagnostic evaluation for acute or persistent ischemia is warranted to improve patient outcome, especially if the severity of CAD has not been previously established or prior episodes of VT caused hemodynamic compromise. This may include echocardiographic examination, exercise testing, and cardiac catheterization. In patients with reversible myocardial ischemia, coronary revascularization may be warranted, and can potentially reduce the risk of life-threatening ventricular arrhythmias. However, if the severity of coronary disease has been recently defined and symptoms and hemodynamic tolerance of VT do not suggest significant ischemia, further evaluation may not be required.

Role of Electrophysiological Testing

Invasive EP testing should be considered in post-MI patients presenting with unexplained syncope or sustained palpitations, and those with wide complex tachycardia of uncertain mechanism. In addition, EP testing can be used for risk stratification late after MI in patients with ischemic cardiomyopathy and nonsustained VT (see later). However, EP testing is not recommended in patients with documented sustained VT unless catheter ablation is planned.

Programmed stimulation induces VT in over 90% of patients with a history of VT. Although the rate and QRS morphology of the induced VT can differ from that observed during spontaneous tachycardia, the induction of VT signifies the presence of a fixed anatomical substrate associated with an increased likelihood of future spontaneous events.

Ventricular Arrhythmias

In general, on the basis of large thrombolytic trials, the occurrence of ventricular arrhythmias and cardiac arrest in the early course (within the first 24 to 48 hours) of an uncomplicated acute MI is associated with increased in-hospital and 30-day mortality, but has not been considered a marker of long-term mortality beyond hospital discharge. Early ventricular arrhythmias likely represent a transient, reversible arrhythmogenic event caused by acute ischemia and reperfusion rather than a permanent arrhythmogenic substrate; hence, they do not predict an increased risk for recurrent arrhythmic events in patients who are successfully revascularized. Nonetheless, the long-term prognostic significance of SMVT in the early hours post MI remains uncertain, as most studies combined VT and VF or sustained and nonsustained VT without specifying the results for each arrhythmia. Many investigators consider SMVT, even when occurring in the early hours following MI, to be an indicator of the presence of an already established permanent substrate (developing necrosis or preexisting scar) and, hence, an indicator of high long-term risk for arrhythmic events.

On the other hand, multiple studies confirm that the occurrence of sustained ventricular arrhythmias (VT and VF) late (greater than 48 hours following MI) or in the context of complicated MI is associated with significantly worse long-term prognosis and high risk of SCD, even after successful revascularization. The temporal cutoff between “early” and “late,” however, remains uncertain. Many investigators prefer a 24-hour (rather than 48-hour) cutoff. Furthermore, some more contemporary studies found that both early and late sustained VT/VF were associated with a markedly increased risk of all-cause death at 30 days and 1 year after discharge despite revascularization.

Repetitive complex PVCs (ventricular bigeminy, couplets, or multiform PVCs) occurring beyond 48 hours after acute MI can be associated with increased arrhythmic risk, particularly in patients with larger MIs and impaired LV function. In a recent report evaluating ventricular ectopy on Holter recordings obtained 6 weeks after acute MI in patients with LVEF of 40% or less, frequent PVCs (≥10 per hour), prevalence of repeating forms of PVCs, and low coupling interval variability were potentially useful risk markers of fatal or near-fatal arrhythmias after MI. However, the utility of these risk markers in guiding ICD implantation is limited.

The occurrence of nonsustained VT in the subacute and chronic phases post MI has been found to predict an increased risk of cardiovascular death. Nonsustained VT has been used for risk stratification but only in conjunction with moderate to severe LV dysfunction (LVEF ≤40%) and inducible VT at EP study. Nonetheless, the current guidelines do not recommend surveillance cardiac monitoring beyond 24 to 48 hours of hospitalization after an acute coronary event.

Syncope

Patients with syncope (that is thought to be due to ventricular tachyarrhythmia) in the setting of structural heart disease (including LV systolic dysfunction or prior MI) have an increased incidence of SCD and overall mortality. It is recommended that these patients undergo ambulatory cardiac monitoring or invasive EP testing. If sustained VT is detected on cardiac monitoring or is inducible at EP study, an arrhythmic cause of syncope should be considered, and ICD implantation is recommended.

Left Ventricular Ejection Fraction

Multiple studies evaluating survival of patients with prior MI established a clear relationship between reduced LVEF and increased mortality ( Table 22.1 ; eFig. 22.3 ). However, these trials were designed to evaluate the usefulness of ICD in high-risk groups, defined mainly by reduced LVEF, and not to evaluate different variables, including LVEF, as risk stratifiers. In essence, these studies show that a reduced LVEF is associated with an increased SCD risk and that ICD therapy improves survival, but they do not establish LVEF as the optimal risk stratification variable for arrhythmic mortality.

Survival Curves for the Implantable Cardioverter-Defibrillator (ICD) -Only Primary Prevention Trials in Patients With Cardiomyopathy Due to Coronary Artery Disease (CAD) or Acute Myocardial Infarction (MI) .

All curves represent mortality/survival. CABG-Patch, Coronary artery bypass graft-patch; DINAMIT, defibrillator in acute myocardial infarction trial; EPG, electrophysiologically guided; IRIS, immediate risk stratification improves survival study; MADIT, multicenter automatic defibrillator trial; MUSTT, multicenter unsustained tachycardia trial; SCD-HeFT, sudden cardiac death in heart failure trial.

(From Kusumoto FM, Calkins H, Boehmer J, et al. HRS/ACC/AHA expert consensus statement on the use of implantable cardioverter-defibrillator therapy in patients who are not included or not well represented in clinical trials. J Am Coll Cardiol . 2014;64:1143–1177.)

LVEF behaves as a continuous variable, with gradually increasing mortality risk until the LVEF declines to 40% and then markedly increasing risk for values less than 40%. Nevertheless, the exact mechanisms involved in the strong correlation between decreased LV systolic function and increased incidence of SCD are not clearly defined. LVEF is a global measure of heart function and is only loosely correlated with the amount of myocardial scar.

Although low LVEF identifies one patient population at relatively increased risk for SCD, there are clear limitations to LVEF as the ideal risk stratification test for deciding whether to implant an ICD for primary prevention of SCD. LV systolic dysfunction lacks specificity. There is no evidence of any direct mechanistic link between low LVEF and mechanisms responsible for ventricular tachyarrhythmias and no study has demonstrated that reduced LVEF is specifically related to SCD. In fact, in studies that enrolled all patients after MI, patients with LVEF less than 30% to 35% account for no more than 50% of sudden cardiac arrest victims. Thus, although LVEF is a good marker of risk for total mortality, it does not provide insight into how patients are likely to die (sudden vs. nonsudden). Furthermore, patients with low LVEF are not uniform with regard to other prognostic markers, and not all are at high risk for SCD.

Another limitation of LVEF is its poor sensitivity. Although most studies have focused on patients with markedly reduced LVEF, this group currently accounts for only 10% to 15% of MI survivors, and most contemporarily managed post-MI patients who suffer a cardiac arrest have better-preserved LV systolic function (i.e., LVEF ≥35%).

It is also recognized that methods of LVEF determination lack precision. Different imaging modalities can produce significantly different LVEF values, and the accuracy of techniques varies among laboratories and institutions, and there is evidence that prognosis, and hence risk, depends on the method by which the LVEF is measured. It is therefore recommended to use the LVEF determination that clinicians believe is the most clinically accurate and appropriate in their institution.

Invasive Electrophysiological Testing

Inducibility of VT/VF during invasive EP testing identifies patients at risk of spontaneous ventricular tachyarrhythmia and, hence, can enhance the predictive accuracy of reduced LVEF for post-MI patients with high mortality risk. Programmed ventricular stimulation is probably the most effective stratification technique for identification of post-MI patients at high risk for development of monomorphic VT, but the sensitivity is inadequate to predict SCD, especially in patients with severe LV systolic dysfunction.

The first MADIT study demonstrated that those patients with inducible VT/VF and LVEF of 35% or less late after MI are likely to benefit from prophylactic ICD therapy. Moreover, the absolute mortality reduction in MADIT I (26.2% over 27 months) was substantially greater than what was found in either MADIT II or SCD-HeFT. Similar results were found in MUSTT. However, secondary analysis from MUSTT revealed that despite the significant difference in outcome between inducible patients enrolled in the trial and noninducible patients enrolled in a registry, EP inducibility was of limited value because the 5-year mortality rate in inducible patients was 48% compared with 44% in noninducible patients. Later, data from MADIT II showed that there is no need for additional risk stratifiers (including EP testing) when LVEF is so low. In more than 80% of patients randomized to the ICD arm of MADIT II, invasive EP testing with an attempt to induce tachyarrhythmias was performed at the time of ICD placement. VT inducibility, observed in 40% of studied patients, was not effective in identifying patients with cardiac events defined as VT, VF, or death. These observations from both MUSTT and MADIT II subanalyses suggest that in patients with substantially depressed LV function, EP inducibility should not be considered a useful predictor of outcome. It is possible, however, that inducibility might have much better predictive value in post-MI patients with LVEF greater than 30% or greater than 35%.

Furthermore, using inducible VT/VF to guide prophylactic ICD therapy is limited by low sensitivity. Post-MI patients with LVEF of 35% or less and no inducible VT/VF still appear to have a substantial (greater than 25%) risk of serious events over the near term. Furthermore, there are no data to support the use of invasive EP testing in post-MI patients with LVEF values greater than 40% or in the early post-MI period. In fact, the BEST-ICD trial found that inducible VT/VF early after MI does not predict benefit from ICD therapy. In contrast, the CARISMA study found that inducible VT identified 6 weeks following an acute MI was a strong predictor of future life-threatening arrhythmias. In addition, EP testing is invasive and not practical for broad application as a screening tool.

Nonetheless, EP testing can be valuable when used in patients in whom the risk of sustained arrhythmias and SCD is intermediate, and the potential benefit of ICD therapy uncertain. Current guidelines recommend prophylactic ICD therapy in post-MI patients with nonsustained VT and LVEF less than 40% if sustained VT/VF is inducible at EP study.

Measures of Cardiac Repolarization

Microvolt-level T wave alternans (TWA) has emerged as a promising noninvasive marker of risk for SCD. TWA, measured on the surface ECG, detects subtle beat-to-beat oscillations in cardiac repolarization and has been linked to cellular mechanisms of arrhythmogenesis. Initial clinical studies of TWA demonstrated a high negative predictive value (≥95%). In addition, an abnormal TWA was associated with significantly increased mortality risk as well as risk of arrhythmic events, although the positive predictive values were far more variable, depending on the characteristics of the study populations and pretest probability. Although those studies suggested that TWA could potentially provide prognostically useful information beyond the LVEF and help guide selection of appropriate patients for prophylactic ICD therapy, more recently, several large multicenter studies of TWA failed to support these findings. In fact, the latter studies strongly suggested that a negative TWA result should not be used to withhold ICD therapy among patients who meet other standard criteria.

Other noninvasive measures of dispersion of repolarization, including QT dispersion, QT variability, and QT dynamics, have had similar mixed predictive results in studies with limited clinical applicability.

Measures of Autonomic Imbalance

Methods to assess the autonomic nervous system, which has been thought to be a modulator between triggers of ventricular tachyarrhythmias and the underlying substrate (including heart rate variability, baroreflex sensitivity, heart rate turbulence, and deceleration capacity) have been evaluated for SCD risk stratification. Multiple studies have correlated relative excess of sympathetic tone (or deficient parasympathetic tone) with increased mortality in post-MI patients as well as increased propensity for VF during acute ischemia. Although the majority of studies showed no significant difference in relative risk for SCD versus total mortality, a recent meta-analysis found that heart rate turbulence was a powerful predictor of both cardiac death and arrhythmic events in post-acute-MI patients with LVEF greater than 30%, and its performance was improved in combination with TWA. Nevertheless, these measures need further validation to support their use in guiding prophylactic ICD therapy.

Measures of Myocardial Conduction Disorders

Increased QRS duration on a surface ECG has been associated with a higher risk of death after MI and appears to reflect greater LV dysfunction, but association with SCD has not been proven. Similarly, the presence of late potentials on signal-averaged ECG failed to identify patients likely to benefit from ICD therapy. Because of the lack of discrimination in the mode of death, these noninvasive markers of risk have not had widespread adoption.

More recently, fragmentation of the QRS complex on the 12-lead surface ECG (filter range, 0.15 to 100 Hz; AC filter, 60 Hz, 25 mm/s, 10 mm/mV), which likely signifies inhomogeneous ventricular activation due to myocardial scar or ischemia in patients with CAD, has been found to potentially predict increased risk of appropriate ICD therapies in patients who received an ICD for primary and secondary prevention. In a recent meta-analysis, fragmented QRS was found to be an indicator of all-cause mortality and SCD risk. The risk was greater in patients with LVEF of 35% or less and in those with QRS duration exceeding 120 milliseconds. However, in the absence of a prospective study of ICD implantation, randomized on the basis of fragmented QRS, it is not clear how the tool should be applied in clinical practice.

Genetic Testing

There is compelling evidence that a genetic mechanism may increase patient susceptibility to SCD following MI, and genetic assessment may play a role in the future. However, there is presently no evidence for using genetic testing to identify post-MI patients at risk.

Cardiac Magnetic Resonance Imaging

Characteristics of myocardial scar architecture and tissue heterogeneity in the periinfarct zone, as defined by contrast-enhanced cardiovascular magnetic resonance (CMR), can potentially identify a proarrhythmic substrate, and appear to be strong predictors of ventricular arrhythmias and appropriate ICD therapies. In patients with ischemic cardiomyopathy, nontransmural (rather than transmural) hyperenhanced areas were found to predict a higher risk of sustained VT. Current evidence, however, does not support the use of CMR for SCD prognostication. Large prospective trials are still required to evaluate the reliability of these techniques for risk stratification.

Risk Stratification Early Postinfarction

The risk of SCD is greatest in the first month after MI and appears to decline in the first year after MI. Nevertheless, both prospective and retrospective studies of prophylactic ICD therapy have failed to show a reduction in all-cause mortality in early post-MI patients. The reasons for the lack of benefit of early ICD implantation after MI are unclear. The reduction in the rate of death due to arrhythmia associated with ICD therapy was offset by an increase in the rate of death from nonarrhythmic cardiac causes (e.g., LV rupture, acute mitral regurgitation) in the ICD groups (see Table 22.1 ; see eFig. 22.3 ). This discrepancy not only highlights the limitations of current risk stratification techniques, but also reflects relative differences in the risk factors for SCD at different time points after MI and the fact that nonarrhythmic death accounts for an appreciable percentage of deaths during that time period. In addition, some portion of the post-MI population will eventually recover LV function, rendering them at lower risk of SCD.

Heart rate and creatinine clearance measured at baseline are strongly associated with SCD during the in-hospital period, whereas recurrent cardiovascular events (including heart failure, MI, and rehospitalization) and a baseline LVEF of 40% or less are more strongly associated with the occurrence of SCD after discharge.

Although the cumulative incidence of SCD is greatest in post-MI patients with an LVEF of 30% or less, the incidence of SCD is higher in patients with an LVEF greater than 40% in the first 30 days after MI when compared with patients with an LVEF of 30% or less after 90 days. The strength of the association between LVEF and survival free from SCD appears to be greatest in long-term follow-up (greater than 6 months). Currently, there is no strategy (invasive or noninvasive) that can reliably predict the risk for SCD or guide empiric ICD implantation soon after an MI. Data suggest it is best to wait 2 to 3 months after acute MI before performing risk stratification.

Some evidence suggests a potential benefit of EP testing in risk stratification in patients with ST-elevation MI and LVEF less than 40% treated with primary PCI. Inducible SMVT by programmed electrical stimulation performed 6 to 10 days post MI was associated with an increased risk of spontaneous VT/VF and SCD (after a mean follow-up of 28 ± 13 months). However, further evaluation in randomized clinical trials is required before adoption of this approach.

Pharmacological Therapy

Implantable Cardioverter-Defibrillator

Secondary Prevention

ICD therapy has a proven mortality benefit among patients with structural heart disease and a history of VT or VF, with a 7% absolute reduction and a 25% relative reduction in all-cause mortality (as compared with amiodarone therapy), due entirely to a 50% reduction in arrhythmic death.

Implantation of an ICD is recommended for secondary prevention in patients with prior cardiac arrest or sustained VT, even when systolic function is normal, and even in patients undergoing successful catheter ablation of the VT or responding to antiarrhythmic therapy, because the latter two approaches do not sufficiently reduce residual risk of SCD ( Table 22.2 ; Fig. 22.2 ). Also, ICD implantation is recommended in patients with syncope and inducible SMVT even if they do not otherwise meet criteria for primary prevention. Importantly, in patients with incessant VT or VF, an ICD should not be implanted until sufficient arrhythmia is achieved to prevent repeated ICD shocks.

TABLE 22.2

AHA/ACC/HRS Recommendations for Prevention of Sudden Cardiac Death in Patients With Ischemic Heart Disease

Secondary Prevention
• In patients with ischemic heart disease, who either survive SCA due to VT/VF or experience hemodynamically unstable VT or stable VT not due to reversible causes, an ICD is recommended if meaningful survival greater than 1 year is expected.	Class I
• In patients with ischemic heart disease and unexplained syncope who have inducible sustained monomorphic VT on EP study, an ICD is recommended if meaningful survival of greater than 1 year is expected.	Class I
Primary Prevention
• In patients with LVEF of 35% or less that is due to ischemic heart disease who are at least 40 days post MI and at least 90 days postrevascularization, and with NYHA class II or III HF despite GDMT, an ICD is recommended if meaningful survival of greater than 1 year is expected.	Class I
• In patients with LVEF of 30% or less that is due to ischemic heart disease who are at least 40 days post MI and at least 90 days postrevascularization, and with NYHA class I HF despite GDMT, an ICD is recommended if meaningful survival of greater than 1 year is expected.	Class I
• In patients with NSVT due to prior MI, LVEF of 40% or less and inducible sustained VT or VF at EP study, an ICD is recommended if meaningful survival of greater than 1 year is expected.	Class I
• In nonhospitalized patients with NYHA class IV symptoms who are candidates for cardiac transplantation or an LVAD, an ICD is reasonable if meaningful survival of greater than 1 year is expected.	Class IIa
• An ICD is not indicated for NYHA class IV patients with medication-refractory HF who are not also candidates for cardiac transplantation, an LVAD, or a CRT defibrillator that incorporates both pacing and defibrillation capabilities.	Class III

 

AHA, American Heart Association; ACC, American College of Cardiology; CRT, cardiac resynchronization therapy; EP, electrophysiological; GDMT, guideline-directed management and therapy; HF, heart failure; HRS, Heart Rhythm Society; ICD, implantable cardioverter-defibrillator; LVAD, left ventricular assist device; LVEF, left ventricular ejection fraction; MI, myocardial infarction; NSVT, nonsustained ventricular tachycardia; NYHA, New York Heart Association; SCA, sudden cardiac arrest; VF, ventricular fibrillation; VT, ventricular tachycardia.

From Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart Rhythm . 2017 Oct 26. [Epub ahead of print]

AHA/ACC/HRS Recommendations for Secondary Prevention of Sudden Cardiac Death (SCD) in Patients With Ischemic Heart Disease (IHD) .

^a Exclude reversible causes. ^b History consistent with an arrhythmic etiology for syncope. ^c ICD candidacy as determined by functional status, life expectancy, or patient preference. EP, Electrophysiological; GDMT, guideline-directed management and therapy; ICD, implantable cardioverter-defibrillator; LVEF, left ventricular ejection fraction; SCA, sudden cardiac arrest; VA, ventriculoatrial; VT, ventricular tachycardia.

(From Al-Khatib, SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart Rhythm. 2017 Oct 26. [Epub ahead of print])

Although one report has questioned the benefit from an ICD compared with pharmacological therapy in patients with VT and LVEF exceeding 40%, the guidelines did not stratify recommendations based on the LVEF. This seems appropriate for two reasons: the prognostic importance of the LVEF was based on subset analysis and, given the current ease of ICD implantation, the potential adverse consequences of choosing a possibly less effective therapy are too great.

Sustained VT or VF occurring within the first 24 to 48 hours of an uncomplicated acute MI are usually considered to be a result of a transient, reversible arrhythmogenic event caused by acute ischemia rather than a permanent arrhythmogenic substrate; hence, they are thought to be relatively benign and do not predict an increased risk for recurrent arrhythmic events in patients who are successfully revascularized. Early ICD implantation is not recommended in those patients unless coronary revascularization is not possible and there is evidence of significant preexisting LV dysfunction. On the other hand, ICD implantation is recommended for all patients who develop sustained VT or VF beyond the first 48 hours following acute MI or in the context of a complicated MI, which are considered indicators of worse long-term prognosis and high risk of SCD, even after successful revascularization. Early ICD implantation (or the temporary use of a wearable cardioverter-defibrillator) is usually recommended in those patients However, it is worth noting that the temporal cutoff between “early” and “late” is not clear. Many investigators prefer a 24-hour (rather than 48-hour) cutoff.

Importantly, prolonged episodes of sustained monomorphic VT or VF may be associated with a rise of cardiac enzymes related to myocardial supply-demand mismatch rather than a primary coronary event. Therefore, in patients with CAD who present with sustained VT or VF and modest elevations of cardiac enzymes, it should not be assumed that a new MI was the cause of the VT or VF. If clinical evaluation for ischemia does not support the occurrence of a new MI, these patients should be treated similarly to patients who have sustained VT and no documented rise in cardiac enzymes, including ICD implantation for secondary prevention.

Although ICDs improve overall survival, they do not eliminate the substrate responsible for sustained arrhythmias and therefore do not prevent arrhythmias. Furthermore, ICD shocks, both appropriate and inappropriate, are associated with increased mortality and reduced quality of life. To reduce the risk of these events, ICD detection criteria and therapies should be programmed to minimize inappropriate shocks, prevent shocks for potentially self-terminating VTs, and favor antitachycardia pacing therapies when feasible. Long VT detection intervals prior to the delivery of ICD therapies and rapid VF detection rates reduce shocks and improve mortality in patients receiving an ICD for primary prophylaxis. The value of programming a long VT detection time in patients with a history of sustained VT or VF is less certain. Furthermore, although device programming can reduce the frequency of ICD shocks, it does not reduce the risk of VT recurrence or eliminate the symptoms associated with the arrhythmia, such as palpitations, dizziness, and syncope.

Primary Prevention

Current guidelines recommend prophylactic ICD implantation in patients with prior MI and reduced LVEF (less than 35%) who are on optimal medical management (see Table 22.2 ; Fig. 22.3 ). These recommendations are based on the fundamental relationship that exists between reduced LVEF and cardiovascular mortality and the findings of MADIT II and SCD-HeFT. Both MADIT II and SCD-HeFT clearly demonstrated a mortality benefit from prophylactic ICD therapy in patients with a history of MI and severely reduced LVEF (≤30% and ≤35%, respectively). However, the absolute mortality reduction in these trials was modest: 5.6% over 27 months in MADIT II and 7.3% over 60 months in SCD-HeFT. Fewer than one in five ICD recipients in MADIT II and SCD-HeFT received appropriate ICD therapies over average follow-up periods of 20 and 60 months, respectively. Because appropriate ICD therapies overestimate the mortality benefit of ICD therapy by at least twofold, fewer than 1 in 10 patients who receive a prophylactic ICD for an LVEF of 35% or less post MI are likely to receive a survival benefit in the near term. In two meta-analyses of these trials, ICD therapy in high-risk CAD patients resulted in a net risk reduction for total mortality of 20% to 30%.

AHA/ACC/HRS Recommendations for Primary Prevention of SCD in Patients With Ischemic Heart Disease.

^a Scenarios exist for early ICD placement in select circumstances such as patients with a pacing indication or syncope. ^b Advanced HF therapy includes CRT, cardiac transplant, and left ventricular assist device. CRT, Cardiac resynchronization therapy; EP, electrophysiological; GDMT, guideline-directed management and therapy; HF, heart failure; ICD, implantable cardioverter-defibrillator; IHD, ischemic heart disease; LVEF, left ventricular ejection fraction; MI, myocardial infarction; NSVT, nonsustained ventricular tachycardia; NYHA, New York Heart Association; pts, patients; SCD, sudden cardiac death; VT, ventricular tachycardia; WCD, wearable cardioverter-defibrillator.

(From Al-Khatib, SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart Rhythm. 2017 Oct 26. [Epub ahead of print])

EP testing appears most useful as an adjunct study in patients having equivocal results after noninvasive testing and in whom the potential benefit of ICD therapy is uncertain. Examples include patients with remote MI, nonsustained VT, and an LVEF between 30% and 40%, as suggested by the most recent guidelines, or in combination with other clinical risk factors or symptoms suggestive of VTs including palpitations, presyncope, and syncope. Patients with CAD who are found to have inducible monomorphic VT during programmed stimulation should be treated for the prevention of SCD. The mode of stimulation (burst pacing, single, or double VESs vs. triple VESs) of sustained VT does not influence prognosis and should not influence treatment decisions.

In the acute to subacute period after MI, the arrhythmia substrate is dynamic. LV function can improve in up to 70% of patients. Although the risk of SCD is highest in the first month after MI, there is currently no reliable risk stratification strategy that can guide early prophylactic ICD implantation. In fact, primary prevention trials with ICD have failed to show a reduction in all-cause mortality (despite a decrease in arrhythmic mortality) in early post-MI patients identified on the basis of the current risk stratifiers. SCD in this period may occur from not only arrhythmic, but also nonarrhythmic (mechanical) causes, limiting ICD benefits. Accordingly, the current published guidelines recommend avoiding ICD implantations in the early post-MI phase. Therefore, in the early post-MI period, medical therapy and coronary revascularization, when feasible, should be optimized. The LVEF should then be measured at least 40 days after the MI and, if the LVEF remains at 35% or less, the patient should be considered for ICD implantation. Whether the 40-day waiting period still applies in patients with acute MI who have known LV dysfunction and who have previously satisfied criteria for implantation of a primary prevention ICD is still controversial. Because those patients have an increased rate of nonarrhythmic mortality that is unlikely to be significantly impacted by early ICD implantation, some investigators recommend implementing the 40-day waiting period in these patients.

It is important to understand, however, that the mere presence of elevated cardiac enzymes does not establish a diagnosis of acute MI. If clinical evaluation for ischemia does not support the occurrence of a new MI, early implantation of an ICD is recommended in patients who otherwise would be candidates for implantation on the basis of primary prevention or secondary prevention criteria. The requirement to delay ICD implantation for 40 days after presentation is not applicable if a clear diagnosis of acute MI is not established. This mandatory waiting period should not be imposed on patients who would otherwise qualify for an ICD for either primary or secondary prevention.

Similarly, the waiting period may not be mandated in patients who, within 40 days of an MI, require a nonelective permanent pacemaker implantation or present with syncope that is thought to be due to ventricular tachyarrhythmia (by clinical history, documented nonsustained ventricular tachycardia [NSVT], or EP study), who would also meet primary prevention criteria for implantation of an ICD, and recovery of LV function is uncertain or not expected. Early ICD implantation with appropriately selected pacing capabilities is recommended in these patients.

In addition, improvement of LVEF of 5% to 6% or more can be observed in 15% to 65% of patients following coronary revascularization. Therefore LVEF should be reevaluated 6 to 12 weeks after coronary revascularization to assess potential indications for primary prevention ICD implantation. As noted previously, the waiting period may not be mandatory for patients in whom recovery of LV function is uncertain or not expected and either require a nonelective permanent pacemaker implantation or present with syncope that is thought to be due to ventricular tachyarrhythmia (by clinical history, documented NSVT, or EP study).

Wearable cardioverter-defibrillators effectively terminate VT and VF and are a potential therapeutic option to bridge patients from hospital discharge until follow-up evaluation of LV function to assess the value of ICD for primary prevention of SCD. The wearable external defibrillator vest can provide protection from SCD during the early period after MI until arrhythmic risk may be reduced after improvement in LVEF or until ICD implantation can be performed for those with persistently reduced LVEF. In one report, the risk of VT/VF was highest in the first month of wearable cardioverter-defibrillator use, with a median time until first treatment of 9 days, and 1.4% of patients were resuscitated by the external defibrillator in the early weeks post MI. Of treated patients, 75% received therapy in the first month of use, and 96% in the first 3 months of use. However, whether wearable external defibrillators improve total mortality is uncertain. No randomized study has validated the role of wearable cardioverter-defibrillators in preventing early SCD compared to optimal medical therapy alone. A wearable cardioverter-defibrillator would not be expected to offer a mortality benefit where an ICD does not except by avoiding early deaths related to ICD implantation (estimated at only 0.2%). Total mortality rate is expected to remain high (based on the previous ICD trial results) because both ICDs and wearable external defibrillators will favorably impact arrhythmic causes of death, but will not treat nonarrhythmic causes of mortality.

Catheter Ablation

Catheter ablation of post-MI VT is generally indicated as a palliative and adjunctive therapy in post-MI patients with ICD who experience frequent recurrences of VT or ICD therapies. Recurrences of VT/VF causing frequent ICD therapies (including ICD shocks) are relatively common; approximately 20% to 35% of ICD recipients for primary prevention and up to 45% of those who receive an ICD for secondary prevention will receive an appropriate shock within 3 years of implantation.

Although ICD shocks for rapid VT or VF reduces the risk of SCD by approximately 60%, the occurrence of shocks can have deleterious consequences. ICD shocks are associated with progressive heart failure symptoms, a significant decline in psychosocial quality of life, and a two- to fivefold increase in nonarrhythmic mortality, despite termination of the acute arrhythmic event. The incidence of appropriate shocks can be reduced by using antitachycardia pacing in the VT or VF detection zones, or with up-titration of effective medical therapies. If optimization of pharmacological therapies and device programming fails to suppress appropriate ICD shocks for VT, or when ventricular arrhythmias precipitate significant symptoms, such as angina, presyncope, syncope, or worsening heart failure, catheter ablation is recommended.

Compared to antiarrhythmic drug therapy, catheter ablation is significantly more effective in reducing the risk of VT recurrences in patients with ischemic cardiomyopathy, and has emerged to become a standard of care to prevent medically refractory ICD shocks. Successful VT ablation can minimize long-term exposure to antiarrhythmic drugs or substantially reduce their dose requirement, which can potentially improve long-term outcomes. However, a reduction in overall mortality has yet to be demonstrated.

Catheter ablation reduces VT recurrences and thereby ICD interventions by more than 75% in patients after multiple ICD shocks. However, most patients with post-MI VT have multiple types of monomorphic VTs, and elimination of all VTs often is not feasible, and because the recurrence of an ablated VT or the onset of a new VT can be fatal, RF ablation is rarely used as the sole therapy for VT. Instead, VT ablation is typically used for patients with CAD as an adjunct to an ICD. In this patient population, the incidence of ablation procedure-related death ranges from 0% to 3%, and the incidence of major complications ranges from 3.6% to 10%.

Catheter ablation is necessary and can be life saving in patients with electrical storm and incessant VT without any apparent correctable cause and despite adequate medical treatment. Repeated ICD shocks within a short time interval, known as an ICD “storm,” occur in 10% to 25% of patients. Accumulated evidence suggests that acute suppression of VT in an electrical storm can be achieved in up to 90% of patients. However, arrhythmic recurrences are frequent during follow-up. In the setting of incessant VT, catheter ablation is preferred over antiarrhythmic drug therapy. Catheter ablation may also be considered for patients with recurrent polymorphic VT or VF when those arrhythmias are triggered by PVCs of consistent QRS morphology. In this setting, ablation targets the arrhythmia trigger rather than the substrate.

The optimal time of catheter ablation in ICD patients (after multiple ICD interventions or before any ICD intervention) remains unclear. Current guidelines recommend considering catheter ablation for VT that recurs despite antiarrhythmic drug therapy or when antiarrhythmic drugs are not tolerated or desired ( Box 22.1 ). In clinical practice, VT ablation is often not considered until pharmacological options have been exhausted, often after the patient has suffered substantial morbidity from recurrent episodes of VT and ICD shocks. However, recent studies suggest that catheter ablation should generally be considered early in the course treatment of post-MI VT, before escalating medication therapy, or even before initiating antiarrhythmic drug therapy in select patients. In fact, small randomized studies of treatment after the first VT episode in post-MI patients have demonstrated significantly reduced VT recurrences following ablation compared with conventional medical therapy. Interestingly, in this patient population the ablation-related mortality rate was 0%, and major complications occurred in 3.8% to 4.7%. In contrast, acute and long-term ablation success is more limited when VT ablation is performed in patients with previous MI selected after failure of prior antiarrhythmic drug therapy. Whether earlier ablation can alter the prognosis of post-MI VT and improve survival compared with comprehensive medical therapy over extended follow-up remains uncertain.

Catheter ablation also should be considered for patients with frequent PVCs or nonsustained or sustained VT that is presumed to cause ventricular dysfunction.

Alternative Interventional Treatment

Several interventional approaches, such as transcoronary ethanol ablation, surgical cryoablation, or percutaneous catheter ablation facilitated by a surgically created epicardial window, can be considered for selected patients with recurrent or incessant VT in whom antiarrhythmic drug therapy and percutaneous endocardial and epicardial catheter ablation have failed or are not feasible (e.g., due to presence of pericardial adhesion or mechanical aortic and mitral valves, or proximity to coronary arteries). However, experience with these approaches is limited, and they are considered last-resort options.

Transcoronary ethanol ablation can be of value for intramural circuits that are refractory to endocardial-epicardial ablation techniques. This technique requires subselective cannulation of the coronary arterial branches supplying the target region. Before ethanol injection, the appropriate target can be confirmed by infusion of iced saline through the arterial lumen. Alcohol injection is performed only if iced saline successfully terminates the VT or renders it noninducible by programmed electrical stimulation.

An epicardial window can allow access to epicardial substrates when percutaneous epicardial access is not feasible. Surgical creation of a subxiphoid pericardial window and manual dissection with lysis of pericardial adhesions can allow catheter mapping and ablation. Surgical treatment of ventricular arrhythmias is rarely required today, but remains a viable therapeutic option for VT refractory to conventional therapies, especially patients requiring surgical coronary revascularization or aneurysm resection and LV reconstruction for refractory heart failure, or known LV thrombus.

Electrocardiographic Clues to the Underlying Substrate

VTs arising from normal myocardium typically have rapid initial forces, whereas slurring of the initial forces is frequently seen when the VT arises from an area of scar or from the epicardium. In addition, VTs originating from very diseased hearts usually have lower amplitude complexes than those arising in normal hearts, and the presence of notching and fractionation of the QRS can be a sign of scar tissue with resultant disrupted wavefront propagation.

Although QS complexes can be seen in a variety of disorders, the presence of qR, QR, or Qr complexes in related leads is highly suggestive of the presence of an infarct. Sometimes it is easier to recognize the presence of MI during VT than during NSR (i.e., LBBB in NSR masking an infarct).

Electrocardiographic Localization of Postinfarction Ventricular Tachycardia

Bundle Branch Block Pattern

Post-MI VTs with RBBB patterns always arise in the LV, and VTs with LBBB patterns almost always arise in or adjacent to the LV septum. Therefore LBBB patterns, which all cluster on or adjacent to the septum, have a higher predictive accuracy (regardless of the presence of anterior vs. inferior MI) than RBBB patterns, which could be septal or located on the free wall. Most VTs with RBBB patterns associated with inferior MI are clustered in a small region, but are more widely disparate with anterior MI ( Figs. 22.7–22.9 ).

Surface Electrocardiogram of Sustained Monomorphic Ventricular Tachycardia With Right Bundle Branch Block (RBBB) Pattern.

Left panel, Ventricular tachycardia (VT) with RBBB pattern and normal axis in a patient with prior anterior myocardial infarction (MI). The site of origin was mapped to the midanterior left ventricular (LV) wall. Note the qR pattern in leads V ₁ to V ₃ , consistent with anterior infarct. Middle panel, VT with RBBB pattern and left superior axis in a patient with prior inferior MI. The site of origin was mapped to the posterobasal LV free wall. Right panel, VT with RBBB pattern and left superior axis in a patient with prior inferior MI. The site of origin was mapped to the midinferior LV wall.

Surface Electrocardiogram of Sustained Monomorphic Ventricular Tachycardia With Left Bundle Branch Block (LBBB) Pattern.

Left panel, Ventricular tachycardia (VT) with LBBB pattern and right inferior axis in a patient with prior anterior myocardial infarction (MI). The site of origin was mapped to the midanterior left ventricular (LV) septum. Middle panel, VT with LBBB pattern and left superior axis in a patient with prior inferior MI. The site of origin was mapped to the inferobasal LV septum. Right panel, VT with LBBB pattern and left inferior axis in a patient with prior anterior MI. The site of origin was mapped to the anteroapical LV septum.

Electrocardiographic Location of Ventricular Tachycardia (VT) Origin.

(A) Location should be assessed based on three axes: septal/lateral, superior/inferior, and basal/ apical. (B) Examples of VTs from different locations arising from scars of anterior or inferior myocardial infarction (MI) . Although complete electrocardiographic assessment requires analysis of all three axes, only some representative leads essential for the diagnosis in each case are shown in the colored squares. LAO , Left anterior oblique; RAO , right anterior oblique.

(From Benito B, Josephson ME. Ventricular tachycardia in coronary artery disease. Rev Española Cardiol. [English ed.] . 2012;65:939–955.)

Inferior Myocardial Infarction Ventricular Tachycardias

With inferior MI, most VTs have basal exit sites and thus have relatively preserved precordial R waves (that usually are present in leads V ₂ to V ₄ with the persistence of an r or R wave through lead V ₆ ). However, more extensive inferior MIs can result in apical exits ( Fig. 22.10 ).

Scheme of Regions of Ventricular Tachycardia Exit Sites in Postinfarction Patients.

INF, inferior axis; L, left; LBBB, left bundle branch block; R, right; RBBB, right bundle branch block; RWP, precordial R-wave progression pattern (diagrammed in table at bottom); SUP, superior axis.

(From Miller JM, Scherschel JA. Catheter ablation of ventricular tachycardia: skill versus technology. Heart Rhythm . 2009;6:S86–S90, with permission.)

VT with LBBB morphology.

VTs with LBBB (especially when left axis deviation is present) have a characteristic location at the inferobasal septum (see Fig. 22.8 ). As the VT axis shifts to a more normal axis, the exit site moves higher up along the septum. Rarely, inferior MI VTs can have exit sites as high as the aortic valve along the septum. Very rarely, the VT can only be ablated from the RV.

VT with RBBB morphology.

In VTs with RBBB, the R waves can persist across the precordium (positive concordance). When the VT originates near the posterior basal septum and when it arises more laterally (or posteriorly), there can be a decrease in the R wave amplitude across the precordium because the infarct can extend to the posterolateral areas (see Fig. 22.7 ). Left axis deviation is seen in inferior MI VTs when the exit site is near the septum. As the VT exit moves from the midline toward the lateral (i.e., posterior) wall, the QRS axis becomes directed more rightward or superior.

The mitral isthmus (between the mitral annulus and inferior infarct scar) contains a critical region of slow conduction in some patients with VT following inferior MI, providing a vulnerable and anatomically localized target for catheter ablation. This critical zone of slow conduction is activated parallel to the mitral annulus in either direction, resulting in two distinct QRS configurations not seen in VTs arising from other sites: LBBB pattern (rS in lead V ₁ , R in lead V ₆ ) with left superior axis, and RBBB pattern (R in lead V ₁ , QS in lead V ₆ ) and right superior axis.

Epicardial Ventricular Tachycardias

Epicardial VT exits are uncommon in post-MI VT because of the subendocardial nature of the underlying substrate. With all other factors being equal, an epicardial origin of ventricular activation widens the initial part of the QRS complex (pseudo-delta wave). When the initial activation starts in the endocardium, rapid depolarization of the ventricles occurs along the specialized conducting system, resulting in a relatively narrower QRS on the surface ECG and the absence of a pseudo-delta wave. In contrast, when the initial ventricular activation occurs in the epicardium, the intramyocardial conduction delay produces a slurred initial part of the QRS complex.

Several ECG findings suggest an epicardial origin of the LV VT with an RBBB pattern, and all generally rely on the late engagement of rapidly conducting His-Purkinje fibers by tachycardia circuit exits on the epicardium, including the presence of a pseudo-delta wave, very wide QRS complex (duration ≥200 milliseconds), long R wave peak time in lead V ₂ , and shortest RS complex duration in any precordial lead longer than 120 milliseconds ( Fig. 22.11 ). However, the proposed 12-lead ECG features for differentiation of epicardial versus endocardial VT exit sites were assessed in patients without MI, and their utility for localization of post-MI VTs has not been validated. ECG criteria for identifying an epicardial origin of VT appear to be region and substrate specific. In fact, in a more recent study, these ECG characteristics failed to reliably identify post-MI VTs requiring epicardial ablation. Slow initial forces can be present during tachycardia at the MI scar region and, hence, not specific for epicardial origins. Furthermore, the presence of typical Q waves in the VT ECGs of patients with previous MI precludes the use of morphological ECG criteria, and when present in the precordial leads, Q waves can interfere with the measurement of all interval criteria. It is also important to note that the VT 12-lead ECG provides information about the VT exit site from the scar border, which is generally not the ablation target. In post-MI VT, the critical isthmus constitutes the target for ablation; this isthmus can be complex, and can have an endocardial and epicardial trajectory permitting successful ablation from the endocardium (especially in the presence of wall thinning) even in a VT with an epicardial exit. Therefore endocardial mapping should be the first approach to catheter ablation for VTs in patients with ischemic heart disease, even when the surface ECG suggests an epicardial origin of the tachycardia.

Electrocardiogram of Post-Myocardial Infarction Ventricular Tachycardia That Required Epicardial Ablation.

Note delayed QRS upstroke in V ₂ and delayed S wave downstroke (pseudo-delta wave) and long RS interval in V ₃ and V ₄ .

Induction of Tachycardia

Tachycardia Features

His Bundle Activation

No visible His potential during VT.

The His potential may not be observed during VT in many patients, likely because the retrograde His potential is masked by ventricular activation or because of suboptimal catheter position. A proper HB catheter position can be verified by observation of the immediate appearance of the His potential on termination of the VT, the disappearance of the His potential on initiation of VT, or the sudden appearance of the His potential when spontaneous or induced supraventricular beats capture the HB (with or without ventricular capture) during VT. In addition, when complete ventricular–His bundle (VH) block is present, dissociated His potentials will be observed (an extremely rare phenomenon).

Visible His potential during VT.

His potentials can be recorded during VT in approximately 80% of patients. When the His potential is visible during VT, it is often difficult to determine whether the recorded His potential is anterograde or retrograde, and whether an apparent His potential is actually a right bundle branch (RB) potential. Recording the RB or left bundle branch (LB) potentials to demonstrate that their activation precedes HB activation during VT, and HB pacing producing a longer His bundle–ventricular (HV) interval than the one noted during VT, usually helps clarify the situation.

In post-MI VT, the relative timing of the retrograde His potential in the QRS depends on how quickly the HPS is engaged and how slowly the impulse reaches the ventricle to produce the QRS. Thus depending on the relative conduction time up the HPS versus through the slowly conducting muscle to give rise to the QRS, the His potential can occur before, during, or after the QRS. The His potential can occasionally occur before ventricular activation (with an HV interval during VT shorter than that during NSR; eFig. 22.4 ) and can also occur just after the onset of ventricular activation ( eFig. 22.5 ). The occurrence of an HV interval (i.e., with the His potential preceding the QRS onset) shorter than that during NSR (in the absence of preexcitation) or a VH interval (i.e., with the His potential following the QRS onset) implies the presence of retrograde HB activation.

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1. Typical Atrial Flutter
2. Atrial Fibrillation
3. Conventional Intracardiac Mapping Techniques
4. Wide Complex Tachycardias

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