Classification According to Tachycardia Morphology

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

Evaluation of Type and Burden of Ventricular Arrhythmias

Identifying and quantifying the types and burden of sustained and nonsustained VT are necessary. Ideally, a 12-lead ECG should be obtained. In patients with ICDs, stored device data such as electrogram morphology and CL can be used to identify the clinical VT.²

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 coronary artery disease, diagnostic evaluation for acute or persistent ischemia is warranted to improve patient outcome, especially if the severity of coronary artery disease 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.¹² 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.^1,2

PreAblation Evaluation

Patients with post-MI VT should be evaluated for comorbidities that can alter the approach to mapping and ablation. Treatment of congestive heart failure and myocardial ischemia should be optimized. Coronary revascularization should be considered in patients with reversible ischemia, because substantial ischemic burden can often be aggravated by the potential induction of prolonged periods of tachycardia or hemodynamically unstable arrhythmias during the ablation procedure. In patients with frequent or incessant VT, however, catheter ablation may be required on an urgent basis before the assessment for coronary artery disease in order to gain prompt control of the ventricular arrhythmia.^1,2

Mobile LV thrombus is an absolute contraindication to endocardial catheter ablation. In contrast, LV catheter ablation may be performed despite the presence of laminated thrombus, if the patient has been therapeutically anticoagulated with warfarin for at least 4 weeks prior to ablation. Similarly, the presence of intraatrial clots should be excluded in patients with inadequately anticoagulated persistent atrial fibrillation (AF) to reduce the risk of thromboembolism in the event of AF termination following electrical shocks for termination of unstable ventricular arrhythmias.

In patients with suspected peripheral vascular disease, evaluation of the presence of severe arterial disease is warranted, as it can affect the approach to LV access (atrial transseptal versus retrograde transaortic versus epicardial).¹⁶ Similarly, an atrial transseptal approach allowing access to the LV through the mitral valve can be considered in the presence of a mechanical aortic valve or severe aortic valve disease.²

Assessment of the risks for sedation and anesthesia must be performed prior to the procedure, because these patients are likely to require deep sedation or general anesthesia.²

Arrhythmogenic Substrate Imaging

In patients with ventricular dysfunction, tissue heterogeneity with inexcitable myocardial fibrous scar and surviving myocardium may provide a potential substrate for reentry circuits. Several noninvasive methodologies have been used to assess the substrate and identify patients at high risk for ventricular arrhythmias.

Role of Electrophysiological Testing

In patients with sustained monomorphic VT, EP testing is not recommended unless catheter ablation is planned. However, EP testing is useful in patients with coronary heart disease for the diagnostic evaluation of wide QRS complex tachycardias of unclear mechanism and in those with unexplained syncope. Additionally, EP testing can be used for risk stratification late after MI in patients with ischemic CMP and nonsustained VT (see below).¹⁹

Programmed stimulation induces VT in over 90% of patients with a history of VT. Although the rate and QRS morphology of induced VT may 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.²

LEFT VENTRICULAR Ejection Fraction

Multiple studies evaluating survival of patients with prior MI established a clear relationship between reduced LVEF and increased mortality. 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.¹⁴

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 versus nonsudden).

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. Furthermore, patients with low LVEF are not uniform with regard to other prognostic markers, and not all are at high risk for SCD. In fact, most contemporary 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 can enhance the predictive accuracy of reduced LVEF for post-MI patients with high mortality risk. The first Multicenter Automatic Defibrillator Implantation Trial (MADIT I) study demonstrated that those patients with inducible VT/VF and LVEF values less than or equal to 35% 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 the second MADIT (MADIT II) or SCD Heart Failure Trial (SCD-HeFT). Similar results were found in the Multicenter UnSustained Tachycardia Trial (MUSTT).^19,21

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%.^19,21

Furthermore, using inducible VT/VF to guide prophylactic ICD therapy is limited by low sensitivity. Patients with LVEF values not exceeding 35% after MI and no inducible VT/VF still appear to have a substantial (>25%) risk of serious events over the near term.²¹

There are also no data to support the use of invasive EP testing in post-MI patients with LVEF values more than 40% or in the early post-MI period. In fact, the Beta-blocker Strategy plus Implantable Cardioverter-Defibrillator (BEST-ICD) trial found that inducible VT/VF early after MI does not predict benefit from ICD therapy. In contrast, the Cardiac Arrhythmias and Risk Stratification after Acute Myocardial Infarction (CARISMA) study found that inducible VT identified 6 weeks following an acute MI was a strong predictor of future life-threatening arrhythmias.^19,21

Additionally, EP testing is invasive and not practical for broad application as a screening tool. Nonetheless, it 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.¹⁴

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%). Additionally, 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 and, in contrast, 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 risk stratification of SCD. 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. However, the majority of studies showed no significant difference in relative risk for SCD versus total mortality. Thus, these measures do not appear to provide a reliable measure of SCD risk and there is no evidence to support their use in guiding prophylactic ICD therapy.²²

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.²² 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/sec, 10 mm/mV), which likely signifies inhomogeneous ventricular activation due to myocardial scar, ischemia, or both in patients with coronary artery disease, has been found to potentially predict increased risk of appropriate ICD therapies in patients who received an ICD for primary and secondary prevention. The usefulness of this parameter needs further evaluation.^23,24

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.^14,20

Cardiac Magnetic Resonance Imaging

Characteristics of myocardial scar architecture and tissue heterogeneity in the periinfarct zone, as defined by contrast-enhanced cardiac MR, can potentially identify a proarrhythmic substrate and appears to be a strong predictor of ventricular arrhythmias and appropriate ICD therapies. In patients with ischemic CMP, the nontransmural, but not the transmural, hyperenhanced areas were found to predict higher risk of sustained VT.¹⁸ However, large prospective trials are still required to evaluate the reliability of these techniques for risk stratification.²⁵

Risk Stratification Early Post-Infarction

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 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 in the ICD groups. 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. 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.^21,26

Whereas the cumulative incidence of SCD is greatest in post-MI patients with an LVEF of 30% or less, the incidence of SCD is greater 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 (>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.^14,21,26

Recent data suggest a potential benefit of EP testing in risk stratification in patients with ST elevation MI and LVEF less than 40% treated with primary percutaneous coronary intervention. 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.¹¹

Pharmacological Therapy

Implantable Cardioverter-Defibrillator

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 SCD prevention and up to 45% of those who receive an ICD for secondary SCD prevention will receive an appropriate shock within 3 years of implantation. ICD therapy acting via such appropriate ICD shocks reduces the risk of SCD by approximately 60%, but the occurrence of shocks is associated with progressive heart failure symptoms, a significant decline in psychosocial quality of life, and a two- to fivefold increase in mortality. The incidence of appropriate shocks can be reduced by using antitachycardia pacing in the VT or VF detection zones, or with up-titration of medical therapies. If optimization of pharmacological therapies and device programming fails to suppress appropriate ICD shocks for VT, patients are eligible for catheter ablation. Catheter ablation reduces VT/VF recurrences and thereby ICD interventions by more than 75% in patients after multiple ICD shocks. In this patient population, the incidence of procedure-related death ranges from 0% to 3%, and the incidence of major complications from 3.6% to 10%.^19,30,31 Nonetheless, most patients with post-MI VT have multiple types of monomorphic VTs, and elimination of all VTs is often 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, it is typically used for patients with coronary artery disease as an adjunct to an implantable ICD or, less commonly, to antiarrhythmic drug therapy.²

Additionally, 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. Catheter ablation has a high acute success rate in eliminating the dominant type of VT. Accumulated evidence suggests that acute suppression of clinical VT in electrical storm can be achieved in approximately 90% of patients. However, arrhythmic recurrences are frequent during follow-up.

Catheter ablation also should be considered for patients with frequent premature ventricular complexes (PVCs), nonsustained VTs, or VT that is presumed to cause ventricular dysfunction.²

The optimal time of catheter ablation in ICD patients (after multiple ICD interventions or before any ICD intervention) remains unclear. 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 for VT should generally be considered early in the treatment of patients with recurrent VT, even before initiating antiarrhythmic drug therapy. In fact, catheter ablation was found to reduce VT/VF recurrences and thereby ICD shocks by 43% to 73% when applied prophylactically, that is, before any ICD shock has been delivered. Interestingly, in this patient population the ablation-related mortality rate was 0%, and major complications occurred in 3.8% to 4.7%. Catheter ablation also significantly reduced the rate of hospitalizations for cardiac reasons, and was associated with a trend to fewer deaths in the ablation group during follow-up. The benefit was more pronounced in patients with LVEF of 30% or less.^2,19,30,31

Table 22-1 lists the indications of ablation for ischemic VT, in accordance with the ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden death.¹⁹

TABLE 22-1 Indications for Ablation of Ischemic Ventricular Tachycardia^*

ICD = implantable cardioverter-defibrillator; LV = left ventricular; MI = myocardial infarction; VT = ventricular tachycardia.

* In accordance with the ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden death.

From Zipes DP, Camm AJ, Borggrefe M, et al: ACC/AHA/ESC 2006 guidelines 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 and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death), J Am Coll Cardiol 48:e247-e346, 2006.

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 V₂ to V₄ with the persistence of an r or R wave through lead V₆), although apical exit sites also occur (Fig. 22-7).¹⁶ 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. 22-5).³⁴

FIGURE 22-7 Scheme of regions of ventricular tachycardia exit sites in post-infarction 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 6:S86-S90, 2009, with permission.)

Left axis deviation is seen in inferior MI VTs when the exit site is near the septum. The more the VT moves from the midline toward the lateral (i.e., posterior) wall, the more right or superior the axis will become. VTs with LBBB (especially when left axis deviation is present) have a characteristic location at the inferobasal septum (see Fig. 22-6). 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.

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 V₁, R in lead V₆) with left superior axis, and RBBB pattern (R in lead V₁, QS in lead V₆) and right superior axis.^3,32

Anterior Myocardial Infarction Ventricular Tachycardias

Anterior MIs are usually associated with more extensive myocardial damage. Therefore, the accuracy of the ECG in localizing the origin of VTs associated with anterior MI is less than in those with inferior MI.³⁴

VTs with LBBB and left axis deviation usually originate from the inferoapical septum, but occasionally there is a discrepancy, with the exit site being more superior than expected for the QRS axis. LBBB VTs associated with anteroseptal MI can present with QS complexes across the precordium (i.e., negative concordance), and they are always associated with a Q wave in leads I and aVL. If an R wave is seen in lead V₁ along with the Q wave in lead aVL, the location of the exit site is more posterior on the septum, closer to the middle third (see Fig. 22-6). VTs with LBBB and right inferior axis arise on the upper half of the mid- or apical septum but occasionally can be off the septum (see Fig. 22-7).^16,32

RBBB VTs originating from the apex usually have a right and superior axis. Lead V₁ usually has a qR or, occasionally, a monophasic R wave, but there is almost always a QS or QR complex in leads V₂, V₃, and/or V₄. More commonly, when there are QS complexes in leads I, II, and III, there are also QS complexes across the precordium from lead V₂ through V₆. VTs with RBBB and right inferior axis arise on the septum but also can be seen across the apex superiorly on the free wall. In both cases, there is a negative deflection in leads aVR and aVL. VTs with LBBB or RBBB patterns and a marked inferior right axis arise superiorly on what usually is the edge of an anterior aneurysm.³²

The most difficult VTs to localize are VTs with RBBB and right superior axis associated with anterior MI. QS complexes in the lateral leads (V₄ to V₆) reflect an origin near the apex, regardless of whether it is septal or lateral. It is almost impossible to distinguish VTs arising from the apical septum and the apical free wall based on the ECG alone. It is only when the VT location moves more posterolaterally that a difference can be appreciated as the R wave in lead aVR becomes dominant over the R wave in lead aVF. This is usually associated with a large apical aneurysm, but occasionally can also be seen with a posterolateral MI.³²

High Posterolateral Myocardial Infarction Ventricular Tachycardias

VTs associated with high posterior MI (left circumflex artery territory) are characterized by a prominent R wave in leads V₁ to V₄ and right inferior axis.³²

Recommended Stimulation Protocols

For evaluation of ventricular arrhythmias, multipolar catheters are typically positioned in the high RA, the HB position, and the RV apex. Recording the His potential during VT is important to differential BBR VT from myocardial VT. The most commonly used stimulation protocol applies pacing output at twice the diastolic threshold current and a pulse width of 1 to 2 milliseconds. Single VESs during NSR and at pacing drive CLs of 600 and 400 milliseconds are delivered, first from the RV apex and then from the RV outflow tract (RVOT). The prematurity of extrastimuli is increased until refractoriness or induction of sustained VT is achieved. Long-short cycle sequences may be tested. If these measures fail to induce VT, double and then triple VESs are used in the same manner. Because a VES with a very short coupling interval is more likely to induce VF as opposed to monomorphic VT, it may be reasonable to limit the prematurity of the VESs to a minimum of 180 milliseconds when studying patients for whom only inducible SMVT would be considered a positive endpoint. If VT still cannot be induced, rapid ventricular pacing is started at a CL of 400 milliseconds, gradually decreasing the pacing CL until 1:1 ventricular capture is lost or a pacing CL of 220 milliseconds is reached. Repeating the protocol at other pacing drive CLs, at other RV or LV stimulation sites, and/or after administration of isoproterenol or procainamide is then attempted.^3,19

An alternative stimulation protocol uses a shorter pacing drive CL (350 milliseconds) and a reverse order of the pacing drive CL (i.e., starting the stimulation protocol at 350, then 400, and then 600 milliseconds). This accelerated protocol has been shown in one report to reduce the number of protocol steps and duration of time required to induce monomorphic VT by an average of more than 50% and improves the specificity of programmed electrical stimulation without impairing the yield of monomorphic VT.

Another proposed stimulation protocol exclusively uses four VESs; at no point are one, two, or three VESs used. At each basic drive train pacing CL, programmed electrical stimulation is initiated with coupling intervals of 290, 280, 270, and 260 milliseconds for the first through fourth VES. The coupling intervals of the VESs are then shortened simultaneously in 10-millisecond steps until S₂ (the first VES) falls during the refractory period or a 200-millisecond coupling interval is reached. If S₂ is refractory at 290 milliseconds, all extrastimuli are lengthened by 30 milliseconds, and programmed electrical stimulation is then initiated. This six-step protocol was tested in a single report and was shown to improve the specificity and efficiency of programmed electrical stimulation without compromising the yield of inducibility of monomorphic VT in patients with coronary artery disease.

Reproducibility of Ventricular Tachycardia Initiation

More than 90% of patients with clinical SMVT will have inducible VT, regardless of the underlying pathology, with the exception of exercise-induced VT. Patients with cardiac arrest or nonsustained VT have a lower incidence of inducibility; inducibility is higher in patients with coronary artery disease.

SMVT can be reproducibly initiated from day to day and year to year, especially in patients with coronary artery disease. However, the exact mode of initiation is not necessarily reproducible. Once SMVT is initiated, it is easier to reinitiate by repeating the same stimulation protocol that was initially successful, either longitudinally (by repeating the entire protocol) or horizontally (by repeating each coupling interval).³

While reproducibility of sustained VT can be variable when comparing induction during the initial month post-MI with subsequent months, induction of any sustained VT in the more chronic phase of MI is highly reproducible over both short-term and extended time intervals. However, a change in the number of extrastimuli required for VT reinduction is reported in 30% to 70% of patients, and is more common as the time interval between studies increases. Similar inconsistencies are reported in the exact QRS morphology and CL of induced VTs during repeated testing. These data confirm that the substrate for chronic post-MI inducible VT per se can be highly stable for up to several years in the absence of major changes in clinical status. However, the mode of induction and VT characteristics demonstrate substantial variability; therefore, it is improbable that such features would predict long-term outcome.³⁵

Relationship of Ventricular Extrastimulus Coupling Interval and Pacing Cycle Length to the Onset of Ventricular Tachycardia

Conduction delay is required for the initiation of reentrant rhythms; thus, an inverse relationship between the coupling interval of the VES initiating the VT or the pacing train CL and the interval from the VES to the first VT complex favors reentry. In contrast, a linear relationship of the pacing CL or VES coupling interval to the interval to the first VT complex and initial CL of the VT favors triggered activity. In reentrant VT, the initial CL reflects conduction through the VT circuit, which in the absence of exit block should demonstrate the same or longer CL as the remaining VT cycles, depending on whether any conduction delay is produced in the circuit on initiation.³

Endpoints of Programmed Electrical Stimulation

His Bundle Activation

No Visible His Potential During Ventricular Tachycardia

The His potential cannot 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. Additionally, when complete ventricular–His bundle (VH) block is present, dissociated His potentials will be observed.³

Visible His Potential During Ventricular Tachycardia

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 HV interval than the one noted during VT, usually helps clarify the situation.³

In patients with coronary artery disease, the relative timing of the retrograde His potential in the QRS depends on how quickly the His-Purkinje system (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 a His bundle–ventricular [HV] interval during VT shorter than that during NSR; Fig. 22-9) and can also occur just after the onset of ventricular activation (with a VH interval; Fig. 22-10). 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; it further implies that retrograde conduction from the exit of VT (defined by the onset of the QRS) to the HB is less than the anterograde conduction time over the HPS to activate the ventricle.¹ Engagement of the HPS, when present, can allow for more rapid activation of the myocardium, which in turn results in a narrower QRS. Some have suggested that the site of origin of such VTs is within the HPS (i.e., fascicular VTs), although proof that such VTs originate from the fascicles and differ from other forms of VT is often lacking. The retrograde His potential appears to reflect passive activation of the HPS, rather than involvement of the HPS in the reentrant circuit. This concept is supported by several observations. HB deflections can appear intermittently (typically in a 2:1 or 3:2 fashion, and occasionally in a Wenckebach periodicity), and changes in the VH interval can occur without changes in the tachycardia CL (Fig. 22-11). In fact, marked changes in the tachycardia CL can be present with no changes in the VH interval. Furthermore, AES or atrial pacing can result in anterograde capture of the HB in the presence or absence of ventricular capture or fusion beats. Such an event, linking atrial activation to the HB deflection, proves that HB deflections are caused by anterograde activation and are unrelated to maintenance of the VT in the vast majority of cases.³

FIGURE 22-9 Ventricular tachycardia with short constant His bundle (HB)–ventricular (HV) interval, consistent with early retrograde activation of the HB.

FIGURE 22-10 Ventricular tachycardia with a constant ventricular–His bundle (VH) interval, consistent with retrograde activation of the His bundle (HB). HB activation is recorded by the ablation catheter positioned in the left ventricular outflow tract.

FIGURE 22-11 Ventricular tachycardia (VT) with variable relationship between ventricular and His bundle (HB) activation. HB catheter position is verified by observation of His potentials during normal sinus rhythm (NSR) at left. His potentials are observed intermittently during VT, with variable relationship to the QRS complexes, suggesting that the His-Purkinje system is not an essential part of the VT circuit.

The mere presence of a His potential before the QRS with a normal HV interval is not absolutely reliable evidence that the tachycardia is a supraventricular tachycardia (SVT). The HV interval during VT is usually less than that during NSR; hence, if infranodal conduction delay is present during NSR, the VT can exist in the presence of an apparently normal HV interval (i.e., 35 to 55 milliseconds), but will be less than that during NSR. In post-MI VT, because ventricular activation is occurring in diastole (albeit slow enough not to be apparent on the surface ECG), the HPS could be activated during this time, giving rise to a short or possibly normal HV interval during the VT. The time to conduct retrogradely to the HB can theoretically be less than the time required to exit from the VT circuit and produce the onset of the QRS, thereby producing an HV interval. Such VTs, which are rare, have a narrow QRS. BBR VT can also give rise to an HV interval that is longer than that during NSR.

For wide complex tachycardias with the His potential preceding the QRS, an HV interval that is shorter during tachycardia than during NSR suggests VT or preexcited SVT (see Fig. 18-3), whereas an HV interval during tachycardia that is equal to or longer than that during NSR suggests SVT with aberrancy (see Fig. 18-24), BBR VT (see Fig. 26-3), or, rarely, other VTs. A changing AH interval, failure to observe anterograde His potential during VT with AV dissociation, or both suggests the presence of retrograde conduction with concealment in the AVN.

Right Ventricular Apical Local Activation Time

In the setting of apical MI, VT with an RBBB pattern and R/S ratio in lead V₁ more than 1 is common, but lateral versus septal surface ECG QRS morphologies significantly overlap, with variable early R wave progression and a similar frontal plane axis. Assessing the activation time to a fixed reference endocardial recording at the RV apex can help regionalize a septal versus lateral origin for such VTs. For RBBB-type VT in the setting of an apical infarct, the QRS-to-RV apical activation time is consistently less than 100 milliseconds for an apical LV septal origin and more than 125 milliseconds for a lateral apical origin. The same values for the QRS-to-RV apical activation time will also help identify a septal versus lateral wall origin in the setting of prior nonapical infarcts.

Ventricular Extrastimulation During Ventricular Tachycardia

Initially, a single VES is delivered at a coupling interval 10 to 20 milliseconds shorter than the tachycardia CL. The coupling interval is then gradually decreased by 5- to 10-millisecond decrements, until the local effective refractory period (ERP) is reached. The RV apex is used as the initial site of stimulation. Stimulation from other sites (RVOT and LV) also can be used to gain information regarding the site specificity of a given response. The return CL is analyzed to evaluate whether the VES has influenced the VT in terms of resetting, ability and pattern of termination, and site specificity for stimulation affecting the VT.³

If resetting or termination of VT is not observed with single VESs, stimulation is repeated using double VESs. The first VES is delivered at a coupling interval 20 milliseconds greater than the longest coupling interval at which a single VES resets the VT, or 20 milliseconds above the local ERP if a single VES fails to interact with the VT. The second VES is delivered at a coupling interval equal to the tachycardia CL, and then this coupling interval is progressively decreased in 5- to 10-millisecond decrements until the local ERP is reached. The use of double VESs allows comparable coupling intervals to reach the circuit at a greater relative degree of prematurity and ability to influence the VT than if the same coupling interval were used for a single VES. By this methodology, only a single VES interacts with the circuit; if the two VESs are delivered such that each VES interacts with the site of impulse formation, interpretation of the response would then be difficult. Thus, the first VES is delivered so that it would not interact with the circuit but would help the second VES to do so.³

The response of VT to VES is evaluated for manifest or concealed perpetuation, resetting with or without fusion, and termination.

Manifest Perpetuation

Manifest perpetuation is said to be present when the VES fails to influence the VT, resulting in a full compensatory pause surrounding the VES. Factors influencing the ability of the VES to interact with the VT include tachycardia CL, local ventricular ERP at the stimulation site, and distance between the stimulation site and VT circuit. The tachycardia CL and duration of the excitable gap are the most important factors; the faster the VT (especially with CLs less than 300 milliseconds) and the shorter the duration of the reentrant circuit excitable gap, the more difficult it is for the VES to enter the VT circuit. Local ERP at the stimulation site and at the site of impulse formation also can limit the prematurity with which the VES can be introduced. Also, the farther the stimulation site is from the VT circuit, the more difficult it is for the VES to reach the circuit with adequate prematurity.

Failure of a VES to affect the VT circuit helps demonstrate the extent of the ventricular myocardium that is not required for the VT. Thus, the ability to capture significant portions of the ventricle by the VES without affecting the VT suggests that those captured areas are not required for the VT circuit. Similarly, intermittent capture of the HPS during VT suggests that it also is not necessary to maintain the VT, regardless of where the His potential is located relative to the QRS during the VT. In an analogous fashion, sinus captures (occurring spontaneously or in response to atrial stimulation) may occur without influencing the VT. The demonstration that neither the proximal HPS nor the majority of the ventricles are required to sustain the VT suggests that the VT circuit must occupy a relatively small and electrocardiographically silent area of the heart.³

Concealed Perpetuation

Concealed perpetuation implies that the VES not only fails to influence the VT circuit, but also is followed by a pause that exceeds the tachycardia CL or that is occasionally interrupted by a sinus capture before the next VT beat. Such pauses are a form of functional exit block, because the VT impulse is unable to exit the circuit and depolarize the ventricles that have just been activated by the VES (Fig. 22-12).³

FIGURE 22-12 Concealed perpetuation in ventricular tachycardia (VT). For reentrant slow VT (cycle length = 690 milliseconds), a single ventricular extrastimulus (VES) is introduced (S) that seems to terminate the VT; a conducted sinus complex (*) follows and then VT recurs. However, inspection of the distal ablation (Abl_1-2) electrogram shows that VT never actually terminated, because the mid-diastolic electrogram continues unperturbed by the VES.

Resetting

Resetting is the advancement (acceleration) of VT by a timed VES with a pause that is less than fully compensatory before resumption of the VT (Fig. 22-13). The first return VT complexes should have the same morphology and CL as the VT before the VES, regardless of whether a single or multiple extrastimuli are used.

FIGURE 22-13 Resetting of ventricular tachycardia (VT). A single ventricular extrastimulus from the right ventricular outflow tract (RVOT) captures the ventricle during VT and causes the subsequent QRS to occur earlier than anticipated (dashed line), indicating resetting.

The introduction of a single VES (S₂) during VT yields a return cycle (S₂-V₃) if the VT is not terminated. If S₂ does not affect the VT circuit, the coupling interval (V₁-S₂) plus the return cycle (S₂-V₃) will be equal to twice the VT cycle (2 × V₁V₁)—that is, a fully compensatory pause will occur (see Fig. 3-14). Resetting of VT occurs when a less than fully compensatory pause occurs (by at least 20 milliseconds). In this situation, V₁-S₂ + S₂-V₃ will be less than 2 × V₁V₁, as measured from the surface ECG. Tachycardia CL oscillation should be taken into account when the return cycle is evaluated. To account for any tachycardia CL oscillation, at least a 20-millisecond shortening of the return cycle is required to demonstrate resetting. When more than a single VES is used, the relative prematurity should be corrected by subtracting the coupling interval(s) from the spontaneous tachycardia cycles when the VESs are delivered.³

To reset a reentrant VT, the stimulated wavefront must reach the reentrant circuit, encounter excitable tissue within the circuit (i.e., enter the excitable gap of the reentrant circuit), collide in the antidromic (retrograde) direction with the previous tachycardia beat, and continue in the orthodromic (anterograde) direction to exit at an earlier than expected time and perpetuate the tachycardia (see Fig. 3-15). If the VES encounters a fully excitable tissue, which commonly occurs in reentrant tachycardias with large excitable gaps, the tachycardia is advanced (i.e., made to occur earlier) by the extent to which the stimulated wavefront arrives at the entrance site prematurely. If the tissue is partially excitable, which can occur in reentrant tachycardias with small or partially excitable gaps, or even in circuits with large excitable gaps when the VES is very premature, the stimulated wavefront will encounter some conduction delay in the orthodromic direction within the circuit. As a consequence, the degree of advancement of the next tachycardia beat will depend on both the degree of prematurity of the VES and the degree of slowing of its conduction within the circuit. Therefore, the reset tachycardia beat can be early, on time, or later than expected.

Effect of Number of Ventricular Extrastimuli

Approximately 60% of VTs can be reset with a single VES and 85% with double VESs using RV pacing. All VTs reset by a single VES can also be reset by double VESs. Double VESs produce resetting over a longer range of coupling intervals and should therefore be used to characterize the excitable gap of the VT more fully. The resetting zone is approximately 70 milliseconds for most VTs, but is usually longer in those VTs reset by both single and double VESs than those requiring double VESs. Resetting zones in response to single VESs usually occupy 10% to 20% of the VT cycle. This is increased to approximately 25% in response to double VESs, but occasionally can exceed 30%, even in response to a single VES. VTs with LBBB morphology are less likely to require double VESs for resetting than VTs with RBBB morphology, regardless of the frontal plane axis, because VTs with LBBB arise in or adjacent to the septum, closer to the RV stimulation site.³

Effect of Site of Stimulation

Resetting does not require that the pacing site be located in the reentrant circuit. The closer the pacing site to the circuit, however, the less premature a single VES can be and reach the circuit without being extinguished by collision with the tachycardia wavefront emerging from the VT circuit. The longest coupling interval for a VES to be able to reset a reentrant tachycardia will depend on the tachycardia CL, the duration of the excitable gap of the tachycardia, local refractoriness at the pacing site, and conduction time from the stimulation site to the reentrant circuit. Neither local ventricular ERP nor local activation time influences the number of VESs required for resetting. Approximately 10% to 20% of VTs demonstrate site specificity in response to VES. Using double VESs reduces this site specificity. Approximately 70% of VTs can be reset with a single VES delivered to the RV apex or RVOT. Resetting of VT by a single VES can always be achieved from some site in the LV, even when resetting cannot be achieved from RV sites.³

Return Cycle

The return cycle is the time interval from the resetting VES to the next excitation of the pacing site by the new orthodromic VT wavefront. This corresponds to the time required for the stimulated impulse to reach the circuit, conduct through the circuit, and exit. The noncompensatory pause following the VES and the return cycle are typically measured at the pacing site; however, they can also be measured to the onset of the surface ECG complex. Conduction time between the pacing site and the VT circuit may or may not be equal to that from the VT circuit to the pacing site. Differences in the VT circuit entrance and exit can result in differences in conduction time to and from the pacing site. These differences depend on the site of stimulation and VT site of origin. In VTs reset by both single and double VESs, the shortest return cycle seen by both methods is usually the same. If the return cycle is measured from the VES producing resetting to the onset of the first return VT QRS complex on the surface ECG, the shortest return cycle will be less than the tachycardia CL in more than 40% of VTs. Because stimulation is usually performed from the RV, conduction time into the VT circuit is incorporated into that measurement. If one considers conduction time between the pacing site and the circuit to be equal to that from the circuit to the pacing site (i.e., local activation time) and subtracts this value from the return cycle as measured to the surface ECG QRS, the resultant value for the return cycle is less than the tachycardia CL in 80% of VTs.³

Resetting Response Curves

Flat or mixed (flat, and then increasing) response curves characterize reentrant VTs. A flat curve is noted in approximately two-thirds of VTs, suggesting that a fully excitable gap is present. It also signifies anatomically separate entrance and exit sites of the circuit (see Fig. 3-16). In approximately 40% of VTs, the types of resetting curves can vary, depending on the site of ventricular stimulation. VESs from different pacing sites likely engage different sites in the VT circuit that are in different states of excitability or refractoriness and, therefore, result in different conduction velocities and resetting patterns.³

Resetting with Fusion

The ability to reset a tachycardia after it has begun activating the myocardium (i.e., resetting with fusion) excludes automatic and triggered mechanisms and is diagnostic of reentry. Resetting with ECG fusion requires wide separation (in time, distance, or both) of entry and exit sites of the VT circuit, with the stimulus wavefront preferentially engaging the entrance. For resetting with fusion to occur, the premature paced wavefront has to reach the entrance of the reentrant circuit before it reaches the exit, and, at the same time, allow for the VT wavefront to exit the reentrant circuit, while the VT wavefront is unable to reach the entrance of the circuit before the paced wavefront (Fig. 22-14). Fusion of the stimulated impulse can be observed on the surface ECG and/or intracardiac recordings if the stimulated impulse is intermediate in morphology between a fully paced complex and the tachycardia complex. The ability to recognize surface ECG fusion requires a significant mass of myocardium to be depolarized by both the VES and VT. If presystolic activity in the reentrant circuit is present before delivery of the VES that resets the VT, this must be considered to represent local fusion. Thus, a VES delivered after the onset of the tachycardia QRS on the surface ECG that enters and resets the VT circuit will always demonstrate local fusion. Resetting with local fusion and a totally paced surface QRS complex suggests that the reentrant circuit is physically small. The farther the stimulation site is from the reentrant circuit, the less likely resetting with ECG fusion will occur. In this setting, the VES should be delivered at a shorter coupling interval to enable the paced wavefront to reach the VT circuit with sufficient prematurity; hence, the stimulated impulse will reflect a purely paced QRS without ECG fusion.

FIGURE 22-14 Schematic representation of the relationship of the return cycle during resetting of ventricular tachycardia (VT) to the absence or presence of surface ECG fusion. A, Stylized VT circuit, with direction of propagation as shown; electrogram is from a remote site. B, Single ventricular extrastimulus (VES) is introduced during VT at a coupling interval of 250 milliseconds. Left panel, The VES occurs early enough that the circuit’s exit site is captured; thus, there is no fusion. Meanwhile, the paced wavefront (blue arrows) enters the entrance of the diastolic corridor before the approaching wavefront of the prior VT cycle (red arrow), allowing resetting. Right panel, Resetting is demonstrated in that the first VT cycle after the VES occurs at less than twice the tachycardia cycle length (TCL). C, A slightly later VES is introduced, with a paced wavefront (blue arrows) approaching the diastolic pathway’s exit after the VT wavefront (red arrows) has already left; this results in ECG fusion. Meanwhile, as before, the paced wavefront arrives at the entrance site before the VT wavefront, allowing resetting. The right panel again shows resetting, this time with fusion. Asterisks = pacing site; CI = coupling interval; Egm = intracardiac electrogram.

Resetting with surface ECG fusion of the QRS during RV stimulation is observed in 60% of VTs, 40% of which are usually reset with a VES delivered after the onset of the VT QRS. VTs reset with fusion have a higher incidence of flat resetting curves, longer resetting zones, and significantly shorter return cycle, measured from the stimulus to the onset of the VT QRS, than VTs not reset with fusion. The return cycle corrected to the tachycardia CL is shorter with VTs reset with fusion (0.89 versus 1.12). In 80% of VTs reset with fusion, the return cycle is shorter than the tachycardia CL measured at the onset of the QRS (versus only 4% of VTs reset without fusion). The return cycle minus local activation time is equal to the time for the wavefront to traverse the distance from the entrance to the exit of the circuit. This interval is less than the tachycardia CL in 100% of VTs reset with fusion. These findings are consistent with widely separate entrance and exit sites of the VT circuit.³

Termination

Termination of VT by a VES occurs when the VES collides with the preceding tachycardia impulse antidromically and blocks in the reentrant circuit orthodromically (see Fig. 3-15). This occurs when the VES enters the reentrant circuit early enough in the relative refractory period, because it fails to propagate in the anterograde direction and encounters absolutely refractory tissue. In the retrograde direction, it confronts increasingly recovered tissue and is able to propagate until it collides with the circulating wavefront and terminates the arrhythmia.

Termination of VT by a single VES is uncommon, occurring in 10% to 46% of VTs. The closer the stimulation site to the circuit, the more prematurely a VES can engage the VT circuit, because the refractoriness and conduction delay in intervening myocardial tissue are avoided. The success of termination, however, is directly related to the number of VESs used. Occasionally, when stimulation is performed at the critical isthmus of the VT circuit, termination can occur with a nonpropagated VES that fails to depolarize the bulk of the myocardium but is adequate to depolarize the isthmus and make it refractory to the incoming VT wavefront, resulting in termination of the VT (Fig. 22-15).³

FIGURE 22-15 Ventricular tachycardia (VT) termination by a subthreshold ventricular extrastimulus (VES). VT is shown with the ablation electrode recording a small mid-diastolic potential (arrows). A single VES (S) is delivered during VT that does not appear to capture myocardium, yet terminates the tachycardia.

Ventricular Pacing During Ventricular Tachycardia

Rapid ventricular pacing is performed during VT at a pacing CL 10 to 20 milliseconds shorter than the tachycardia CL. The pacing CL is then decreased in 10-millisecond decrements in a stepwise fashion until the VT is terminated. Pacing is stopped after each pacing CL and the response of VT to pacing is assessed. It is important to ensure that termination and reinitiation of the VT have not occurred during the pacing train, which would then affect the interpretation of the VT response.

It is critical to synchronize the initiation of pacing to the electrogram at the pacing site, because absence of synchronization will lead to a variable coupling interval of the first paced impulse to the VT. It is also important to perform overdrive ventricular pacing at each pacing CL for sufficiently long duration to allow the pacing drive to penetrate and affect the VT circuit. Pacing for a short period is a common mistake; it results in erroneous evaluation of the VT response. For VTs that are not stable enough to allow completion of an entire stimulation protocol, synchronized bursts of pacing at variable pacing CLs for a specified but variable number of beats, can usually be performed and can provide information about resetting or entrainment, overdrive suppression, and termination.

The response of VT to overdrive pacing is evaluated for overdrive suppression, acceleration, transformation into distinct uniform VT morphologies, entrainment, ability and pattern of termination, and site specificity for stimulation affecting the VT.

Overdrive Suppression

Overdrive suppression analogous to that seen with automatic rhythms has not been observed in post-MI VTs, although prolonged return cycles can be seen at rapid pacing rates.

Acceleration

Acceleration by overdrive pacing refers to sustained shortening of the tachycardia CL following cessation of pacing. Acceleration occurs in 25% of VTs, and is more common with ventricular pacing than with VES (35% versus 5%). However, overdrive acceleration of VT analogous to that seen in triggered rhythms (i.e., linear relation of pacing CL to early acceleration of the tachycardia CL) is uncommon in post-MI VT. Because rapid ventricular pacing is usually required to terminate faster VTs, these VTs have a higher incidence of acceleration (40% of VTs with CL < 300 milliseconds with rapid ventricular pacing). Approximately 50% of the accelerated VTs can be terminated with even faster ventricular pacing; the other 50% (which can be polymorphic VT or ventricular flutter) require electrical cardioversion.

Acceleration is classified according to the morphology of the accelerated tachycardia: VT morphology identical to or different from the original VT, or polymorphic VT. An accelerated VT with a QRS morphology identical to the original VT suggests that the accelerated VT is using the same exit of the original VT circuit. The most likely mechanism underlying this form of VT acceleration is an area of block that determines the size of the reentrant circuit, which is determined to some extent by refractoriness. Rapid pacing can shorten the refractoriness in a proximal region of the arc of block, which would in turn shorten the length of the reentrant pathway. If the distal component of the arc of block remains unchanged, acceleration of the VT will occur with the same exit site and hence the same QRS morphology. Alternatively, rapid pacing can remove block in a shorter potential pathway, creating a smaller circuit.³

On the other hand, a VT morphology different from the original VT can be secondary to a change in the exit site from the same circuit, a reversal of the reentrant circuit, or the termination of the initial VT and initiation of a different VT elsewhere. Polymorphic VT with or without degeneration to VF can occur because of the inability of the myocardium to respond to the pacing CL with the development of changing activation wavefronts, leading to multiple reentrant wavelets that can degenerate into VF. There is no way to predict which type of acceleration will occur. However, in the presence of antiarrhythmic drugs, acceleration to different morphologically distinct VTs is common.

Transformation

Transformation of the index VT into multiple distinct uniform VT morphologies can occur in response to overdrive pacing. It is not infrequent for stimulation during one VT to induce another VT of different morphology and CL, only to be changed to a third or fourth one by continued stimulation. The significance of all these multiple morphologically distinct VTs induced during overdrive pacing of the spontaneous VT is uncertain if they were never seen before spontaneously or induced by programmed stimulation. Usually, however, these VTs can also be induced by programmed electrical stimulation. Nevertheless, any VT (even if not seen before) that is uniform and has a CL longer than 250 milliseconds is clinically important. Those VTs may not have been observed previously because the original VT dominates because it is more readily inducible. Induction of rapid unstable VTs (CL <250 milliseconds) in patients who presented with only stable VT does not have prognostic value.³

The ability to change from one VT to another with a different CL using single or double VESs is infrequent during triggered rhythms (other than those because of digitalis), and is another observation that is most compatible with a reentrant mechanism.

Entrainment

Overdrive ventricular pacing at long CLs (i.e., 10 to 30 milliseconds shorter than the tachycardia CL) can almost always entrain reentrant VTs. The slower the pacing rate and the farther the pacing site from the reentrant circuit, the longer the pacing drive required to penetrate and entrain the tachycardia.

Following the first beat of the pacing train that penetrates and resets the reentrant circuit, the subsequent stimuli will interact with the reset circuit, which has an abbreviated excitable gap. Depending on the degree that the excitable gap is preexcited by that first resetting stimulus, subsequent stimuli fall on fully or partially excitable tissue. Entrainment is said to be present when two consecutive extrastimuli conduct orthodromically through the circuit with the same conduction time while colliding antidromically with the preceding paced wavefront. During entrainment, the paced stimuli enter the reentrant circuit, block with the existing tachycardia wavefront in the antidromic direction, and conduct through the circuit in the orthodromic direction to produce the return cycle beat.

Entrainment Criteria

Classic criteria for recognition of entrainment are the following: (1) fixed fusion of the paced complexes at any single pacing CL; (2) progressive fusion as the pacing CL decreases (i.e., the surface ECG progressively looks more like the purely paced QRS complex than a pure tachycardia QRS complex); and (3) resumption of the same VT morphology following pacing with a nonfused tachycardia QRS complex at a return cycle equal to the pacing CL (see Figs. 5-15 and 5-16). The return cycle is defined as the interval from the last paced beat to the first VT beat, and is measured from the surface QRS or RV electrograms.^36,37

Entrainment with Fusion

As noted, fusion of the stimulated impulse can be observed on the surface ECG, intracardiac recordings, or both. The stimulated impulse will have hybrid morphology between the fully paced QRS and the tachycardia QRS (Fig. 22-16; and see Figs. 5-15 and 5-16). The ability to demonstrate surface ECG fusion requires a significant mass of myocardium to be depolarized by both the extrastimulus and the tachycardia. The farther the stimulation site from the reentrant circuit, the less likely entrainment with ECG fusion will occur. Overdrive pacing of a tachycardia of any mechanism can result in a certain degree of fusion, especially when the pacing CL is only slightly shorter than the tachycardia CL. Such fusion, however, is unstable during the same pacing drive at the same pacing CL, because pacing stimuli fall on a progressively earlier portion of the tachycardia cycle, producing progressively less fusion and more fully paced morphology. Such phenomena should be distinguished from entrainment, and sometimes this requires pacing for long intervals to demonstrate variable degrees of fusion. Focal tachycardias (automatic, triggered activity, or microreentrant) cannot manifest fixed or progressive fusion during overdrive pacing (Fig. 22-17). Moreover, overdrive pacing frequently results in suppression (automatic) or acceleration (triggered activity) of focal VTs rather than resumption of the original tachycardia with an unchanged tachycardia CL.^36,37

FIGURE 22-16 Fusion with ventricular pacing during macroreentrant post-infarction ventricular tachycardia (VT). VT with a right bundle branch block pattern and right superior axis is shown at left (cycle length [CL], 405 milliseconds, in blue shading). In the panels at right, pacing during VT over a range of CLs from the right ventricular (RV) apex (with a left bundle branch block pattern and left superior axis) is shown. Pure RV pacing during sinus rhythm at CL of 600 milliseconds is shown at far right (yellow shading). It is evident that while pacing during VT, QRS complexes at each paced CL are different from both VT and pure pacing, indicating contribution of both the VT and paced wavefronts to the QRS complexes (fusion, most evident in leads III, aVL, aVF, and V₁ and V₂).

FIGURE 22-17 Lack of fusion with ventricular pacing during focal ventricular tachycardia (VT) in a patient with cardiomyopathy. VT with a right bundle branch block pattern and left superior axis is shown at left in blue shading (cycle length [CL], 470 milliseconds). In the panels at right, pacing during VT over a range of CLs from the right ventricular outflow tract (RVOT, with a left bundle branch block pattern and right inferior axis) is shown. It is clear that while pacing during VT, all QRS complexes are identical, indicating no contribution of the VT to the QRS complexes (thus no fusion).

Entrainment with Manifest Fusion

Entrainment of reentrant tachycardias commonly produces manifest fusion that is stable (fixed) during the pacing drive at a given pacing CL; repeated entrainment at pacing CLs progressively shorter than the tachycardia CL results in different degrees of QRS fusion, with the resultant QRS configuration looking more like a fully paced configuration (see Figs. 5-15 and 5-16).

Entrainment with Inapparent Fusion

Entrainment with inapparent fusion (also referred to as local or intracardiac fusion) is said to be present when a fully paced QRS morphology (with no ECG fusion) is observed during entrainment, even when the tachycardia impulse exits the reentrant circuit (orthodromic activation of the presystolic electrogram is present). In this setting, fusion is limited to a small area and does not produce surface ECG fusion, and only intracardiac (local) fusion can be recognized (see Fig. 5-18). Local fusion can only occur when the presystolic electrogram is activated orthodromically. Collision with the last paced impulse must occur distal to the presystolic electrogram, either at the exit from the circuit or outside the circuit. In such cases, the return cycle measured at this local electrogram will equal the pacing CL. Therefore, a stimulus delivered after the onset of the surface ECG QRS during entrainment will always demonstrate local fusion. This is to be distinguished from entrainment with antidromic capture. When pacing is performed at a CL significantly shorter than the tachycardia CL, the paced impulse can penetrate the circuit antidromically and retrogradely (antidromically) capture the presystolic electrogram so that no exit from the tachycardia circuit is possible. Consequently, the surface QRS appears fully paced. When pacing is stopped, the impulse that conducts antidromically also conducts orthodromically to reset the reentrant circuit with orthodromic activation of the presystolic electrogram. When antidromic (retrograde) capture of the local presystolic electrogram occurs, the return cycle, even when measured at the site of the presystolic electrogram, will exceed the pacing CL by the difference in time between when the electrogram is activated retrogradely (i.e., preexcited antidromically) and when it would have been activated orthodromically (see Fig. 5-15).³⁶

Entrainment with Concealed Fusion

Entrainment with concealed fusion (sometimes also referred to as “concealed entrainment”) is defined as entrainment with orthodromic capture and a surface ECG complex identical to that of the tachycardia (Fig. 22-18). Entrainment with concealed fusion suggests that the pacing site is within a protected isthmus inside or outside the reentrant circuit, but attached to the circuit (i.e., the pacing site can be in, attached to, or at the entrance to a protected isthmus that forms the diastolic pathway of the circuit). In this setting, transient entrainment is achieved when the orthodromically directed stimulated wavefront resets the tachycardia, but an antidromically stimulated wavefront collides with the tachycardia wavefront in or near the reentry circuit and fails to exit the slow conduction zone. Only tissue near the pacing site within the critical isthmus is antidromically activated; hence, there is no evidence of fusion. Compared with the intrinsic tachycardia, this antidromic capture may result in earlier intracardiac recordings from bipole sites located adjacent to the pacing region. The morphological appearance of the ECG, however, is the same during entrainment as during the tachycardia. Entrainment with concealed fusion can occur by pacing from bystander pathways, such as a blind alley, alternate pathway, or inner loop, that are not critical to the maintenance of reentry. In this situation, activation propagates from the main circuit loop but is constrained by block lines having the shape of a cul-de-sac; ablation at these sites does not terminate reentry.³⁶

FIGURE 22-18 Entrainment mapping of ventricular tachycardia (VT). A, Entrainment of VT from a distant site. Diagrammatic representation of a figure-of-8 VT circuit at left, with an electrogram recorded at a site remote from critical circuit elements. At center, during entrainment pacing, the paced wavefront from this remote site (^*) interacts with the circuit by colliding with a VT wavefront that has exited the diastolic corridor while also entering the diastolic corridor at the opposite end. This results in fusion (part of the ventricle depolarized by the VT wavefront, part by the paced wavefront). For as long as pacing continues, this fusion of ventricular activation remains stable. With cessation of pacing (right figure), the last paced wavefront enters the diastolic corridor as on other cycles but there is no subsequent paced wavefront to collide with the wavefront that is exiting the corridor; thus the first return cycle complex is entrained, but not fused. The post-pacing interval (PPI) measured at the site of pacing reflects the time it takes to make one complete revolution around the circuit plus any time required to get from the pacing site to the circuit and back from the circuit to the pacing site. B, Entrainment of VT from a site within the circuit. The pacing site (^*) is within the circuit but outside the diastolic corridor. As a result, the entrained QRS complex shows fusion and the PPI equals the VT cycle length (CL). C, Entrainment of VT from a site within the critical isthmus. The pacing site (*) is within the circuit and inside the diastolic corridor, recording the mid-diastolic electrogram. As a result, the entrained QRS complex shows no fusion and the PPI equals the VT CL. The S-QRS interval equals the electrogram-to-QRS interval during VT. This is the ideal ablation site. Egm = intracardiac electrogram; PCL = pacing cycle length; TCL = tachycardia cycle length.

Occasionally, one of the first few stimuli of a drive train intended to entrain VT terminates VT without propagation. Subsequent stimuli often result in QRS complexes that do not resemble VT, leading the operator to conclude that the site is far from the isthmus. Review of the first few stimuli of pacing may show that the site actually was very attractive for ablation (Fig. 22-19).

FIGURE 22-19 Nonpropagated ventricular tachycardia (VT) termination during attempted entrainment. VT is shown with a diastolic potential (blue arrow); during attempted stimulation at this site during VT, the first several stimuli (S) have no effect but the fifth stimulus (red arrow) results in VT termination without propagation of the impulse (no subsequent QRS). Subsequent stimuli capture the site but result in a very different QRS configuration.

Post-Pacing Interval

The post-pacing interval (PPI) is the interval from the last pacing stimulus that entrained the tachycardia to the next recorded electrogram at the pacing site (see Fig. 22-18). The PPI should be measured to the near-field potential that indicates depolarization of tissue at the pacing site. The PPI remains relatively stable when entrainment of VT is performed at the same site, regardless of the length of the pacing drive. This is in contrast to overdrive suppression seen in automatic arrhythmias, which would be associated with progressive delay of the first tachycardia beat return cycle with progressively longer overdrive pacing drives.^36–38

Termination

The ability to terminate SMVT by rapid ventricular pacing, VES, or both is influenced most importantly by the tachycardia CL (50% of VTs with CLs <300 milliseconds will require electrical cardioversion), but also by the local ERP at the pacing site, conduction time from the stimulation site to the site of origin of the VT, duration of the excitable gap, and presence of antiarrhythmic agents.

Failure of rapid ventricular pacing or VES to terminate VT has several potential explanations: the reentrant circuit being a protected focus; inability of VES to access the reentrant circuit because of local myocardial refractoriness; absence of an accessible excitable gap; termination of VT followed by reinitiation by a subsequent pacing impulse in the same pacing drive; and/or failure of conduction block to occur within the reentrant circuit, despite accelerating the VT to the faster pacing rate.

Factors influencing termination of VT can be modified. Refractoriness at the site of stimulation can be modified by the use of multiple VESs or a higher pacing current. The distance, conduction time, or both from the site of stimulation to the VT site can be modified by changing the site of stimulation. The tachycardia CL can be increased by antiarrhythmic agents, but the response is unpredictable. However, two problems are frequently encountered in attempts to terminate VT—acceleration of the VT by overdrive pacing and the appearance of multiple distinct uniform VT morphologies.³

Regardless of the mode of stimulation used, termination is usually abrupt, which distinguishes reentrant VTs from triggered VTs. In reentrant VTs, termination must occur when an impulse penetrates the circuit and blocks in both directions. Rapid ventricular pacing is the most efficacious way of VT termination, regardless of the tachycardia CL. Approximately 80% of VTs terminated by a single VES have a tachycardia CL longer than 400 milliseconds. All VTs terminated by single or double VESs can also be terminated by ventricular pacing. Termination is less likely to occur when the VT cannot be reset with very premature VES (i.e., the VES coupling interval is more than 75% of the tachycardia CL).³

A single VES delivered during entrainment of VT can facilitate termination of VT by allowing easier access to the excitable gap. Even when a single VES or overdrive pacing alone fails to terminate the VT, the combination of both may be successful. Overdrive pacing ensures stable resetting of the VT circuit, allowing a single VES to interact with the circuit much more prematurely than it could in the absence of entrainment. Overdrive pacing also shortens the excitable gap of tissue in the reset circuit, making it possible for a single VES to terminate the VT. This technique avoids the need for multiple VESs, which can increase the heterogeneity of conduction and refractoriness in the intervening tissue and produce polymorphic VT, and the need for rapid pacing, which might induce acceleration of the VT. This method is especially helpful in VTs that were accelerated by rapid pacing and especially in those VTs for which antiarrhythmic agents have made the tachycardia more difficult to terminate.³

Effects of Drugs on Ventricular Tachycardia

Class I agents are the most uniformly successful drugs for slowing the rate of or terminating SMVT. These drugs can also facilitate the induction of SMVT in patients in whom SMVT cannot be induced by the standard programmed electrical stimulation protocol and in patients with coronary artery disease and nonsustained VT. These drugs can also occasionally produce incessant SMVT in patients who, before therapy, only had paroxysmal events. This phenomenon, almost always associated with a slower VT and prolongation of conduction by the agent, would not be expected if the mechanism were triggered activity or abnormal automaticity. Adenosine, beta blockers, and calcium channel blockers are ineffective for termination of post-MI VT.³

Exclusion of Triggered Activity Ventricular Tachycardia

Exclusion of Bundle Branch Reentrant Ventricular Tachycardia

Exclusion of Supraventricular Tachycardia