Monomorphic VT has a single stable QRS morphology from beat to beat, indicating repetitive ventricular depolarization in the same sequence (Fig. 22-1). Multiple monomorphic VTs refers to more than one morphologically distinct monomorphic VT, occurring as different episodes or induced at different times. Polymorphic VT has a continuously changing 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 (see Fig. 22-1).³ 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 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 beats/min) VT that has a sinusoidal QRS configuration that prevents identification of the QRS morphology (see Fig. 22-1). Ventricular fibrillation (VF) is a rapid (usually >350 beats/min), grossly irregular ventricular rhythm with marked variability in QRS amplitude and cycle length (CL), and a changing morphology (see Fig. 22-1).^1,²

FIGURE 22-1 Surface ECG of different types of ventricular tachycardias. VT = ventricular tachycardia.

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.³ However, 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 a ventricular extrastimulation (VES) and have no relevance to clinical nonsustained VT. Repetitive polymorphic responses are also common (up to 50%), 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.³ Incessant VT is a continuous sustained VT that recurs promptly over several hours despite repeated interventions (e.g., electrical cardioversion) for termination.⁴ 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).^1,²

Classification According to QRS Morphology in V₁

VT with a left bundle branch block (LBBB)-like pattern has a predominantly negative QRS polarity in lead V₁ (QS, rS, qrS), whereas VT with a right bundle branch block (RBBB)-like pattern has a predominantly positive QRS polarity in lead V₁ (rsR′, qR, RR, R, RS). However, the VT may not show features characteristic of the same bundle branch block (BBB)-like morphology in other leads.^1,³

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 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.^1,²

Mechanism of Post-Infarction Ventricular Tachycardia

The majority of sustained monomorphic VTs (SMVTs) are caused by reentry involving a region of ventricular scar. The scar is most commonly caused by an old myocardial infarction (MI), but right ventricular (RV) dysplasia, sarcoidosis, Chagas disease, other nonischemic cardiomyopathies, surgical ventricular incisions for repair of tetralogy of Fallot, other congenital heart diseases, or ventricular volume reduction surgery (Batista procedure) can also cause scar-related reentry. Dense fibrotic scar creates areas of anatomical conduction block, and fibrosis between surviving myocyte bundles decreases cell-cell coupling and distorts the path of propagation, causing areas of slow conduction and block, which promotes reentry. In post-MI VT, a variety of different circuit configurations are possible. Generally, the reentrant circuit arises in areas of fibrosis interspersed with bundles of viable myocytes, producing a zigzag course of activation of and transverse conduction along a pathway lengthened by branching and merging bundles of surviving myocytes, leading to inhomogeneous anisotropy (see Fig. 3-18). Heterogeneity in tissue composition and autonomic innervations in these regions may create areas of aberrant conduction that generate the substrate for reentrant arrhythmias. Buried in the arrhythmogenic area is the common central pathway, the critical isthmus, causing slowing of impulse conduction, 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 (bystander).^4,⁵

Although previous data suggested that most isthmuses are anatomically determined by heterogeneous scar geometry, a recent study found that the diastolic pathway critical to post-MI VT reentrant circuits is typically protected by a boundary of fixed and functional block. In the majority of cases, development of functional unidirectional block was a prerequisite for initiation of VT, by protecting a region of myocardium that subsequently forms at least one border of the diastolic pathway. Evidence indicates that formation of functional block leading to reentry is associated with large dispersion in refractory periods over short anatomical distances.⁶

The critical isthmus contained in these reentry circuits often is a narrow path of tissue with abnormal conduction properties. Depolarization of the small mass of tissue in the isthmus is usually not detectable on the surface electrocardiogram (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 back to the entrance of the isthmus through an outer loop or an inner loop (see Fig. 5-14).⁴ An outer loop is a broad sheet of myocardium along the border of the infarct. Depolarization of the outer loop can be detectable on the surface ECG. Reentrant circuits can have one or more outer loops. An inner loop is contained within the scar. Inner loop pathways can serve as potential components of a new reentrant circuit should the central common pathway be ablated. If multiple loops exist, the loop with the shortest conduction time generally determines the VT CL and is therefore the dominant loop. Any loop with a longer conduction time behaves as a bystander. Those bystander loops can serve as a potential component of a new reentrant circuit if the dominant loop is ablated.

The critical isthmus in post-MI VT is typically bounded by two approximately parallel conduction barriers that consist of a line of double potentials, a scar area, or the mitral annulus. The endocardial reentrant VT rotates around the isthmus boundaries and propagates slowly through the critical isthmus, which harbors diastolic potentials and measures, on average, approximately 30 mm long by 16 mm wide. The axis of a critical isthmus is typically oriented parallel to the mitral annulus plane in perimitral circuits and perpendicular to the mitral annulus plane in other circuits.⁴ Ablation lesions produced with standard radiofrequency (RF) ablation catheters are usually less than 8 mm in diameter, relatively small in relation to the entire reentry circuit, and can be smaller than the width of the reentry path at different points in the circuit. Successful ablation of a large circuit is achieved by targeting an isthmus where the circuit can be interrupted with one or a small number of RF lesions, or by creating a line of RF lesions through a region containing the reentry circuit.

A recent study using electroanatomical substrate mapping found that 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 similar ischemic cardiomyopathy patients with spontaneous SMVT, despite equally severe left ventricular (LV) dysfunction as well as similar infarct age and distribution. These differences in the endocardial 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 <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.⁷

It is not uncommon 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 may be induced in the EP laboratory, especially during antiarrhythmic therapy. The induction of multiple VT morphologies during an ablation procedure suggests that the arrhythmogenic substrate has the capability to support multiple reentrant circuits or different exit sites from a single circuit. Distinct VT morphologies (as defined by the 12-lead ECG and tachycardia CL) often share a common isthmus but differ in propagation direction, location, or both 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 settings of acute ischemia. Focal VT may also occur in the absence of an acute ischemic event in patients with chronic ischemic heart disease. A recent study found that a focal mechanism was present in up to 9% of VTs that were induced in patients with ischemic heart disease during EP study for RF ablation.⁸

Cardiac arrest and sudden cardiac death (SCD) in post-MI patients are predominantly caused by VT or VF. Bradyarrhythmias, including heart block, as well as electromechanical dissociation contribute to SCD, although they seem to account for a minority of events.

Clinical Considerations

Epidemiology

Coronary heart disease is the most frequent cause of clinically documented VT and VF (76% to 82% of patients). The incidence of SMVT in patients with an acute MI varies with the type of MI. Among almost 41,000 patients with an ST elevation (Q wave) MI treated with thrombolysis in the GUSTO-1 trial, 3.5% developed VT alone and 2.7% developed both VT and VF. A pooled analysis of four major trials of almost 25,000 patients with a non–ST elevation acute coronary syndrome (non–ST elevation MI and unstable angina) noted a lower incidence of VT—0.8% developed VT alone and 0.3% developed both VT and VF.^1,⁹

SMVT within the first 2 days of acute MI is uncommon, occurring in up to 3% of patients as a primary arrhythmia and with VF in up to 2%, and is associated with an increase in in-hospital mortality compared with those without this arrhythmia. However, among 21- to 30-day survivors, mortality at 1 year is not increased, suggesting that the arrhythmogenic mechanisms can be transient in early post-MI SMVT. 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 LV ejection fraction (LVEF), and such VT is a predictor of a worse prognosis.⁹ 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 are anterior wall MI; frequent episodes of sustained VT, nonsustained VT, or both; 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 CLs) persists.^2,¹⁰ In patients with ST elevation MI treated with primary percutaneous coronary intervention, delayed reperfusion (>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.¹¹

Most episodes of SMVT associated with MI occur during the chronic phase. VT occurs in 1% to 2% of patients late after MI. 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 VF 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 implantable cardioverter-defibrillator (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, and, hence, improve quality of life and reduce mortality.¹²

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.

SCD accounts for up to 15% of total mortality in industrialized countries and claims the lives of more than 300,000 people per year in the United States. 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 coronary artery disease 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 arrest victims.¹³

The risk for total and arrhythmic 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 may result from delayed ventricular remodeling resulting in the creation or activation of reentrant VT circuits on the infarct border as well as from heart failure developing late after MI.¹⁴

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. Although the cause of this change is unknown, 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.¹⁵