Elad Anter and Mark E. Josephson

Chapter Outline

Anatomy and Pathophysiology

The most common anatomical substrate for monomorphic ventricular tachycardia (VT) is extensive healed myocardial infarction with resultant left ventricular (LV) dysfunction. The extent of myocardial scar and the degree of LV dysfunction are the most important determinants of arrhythmia risk after infarction.1,2 Patients with tolerated VT have more extensive scar, more frequent incidence of discrete LV aneurysm, and more pronounced LV dysfunction than patients with nonsustained VT or sudden cardiac death.

The electrophysiological substrate for monomorphic VT gradually develops over the first 2 weeks after myocardial infarction and once established appears to remain indefinitely.³ The incidence of sustained monomorphic VT after myocardial infarction had traditionally been 3%; however, contemporary therapy with an early revascularization strategy has led to smaller infarcts with less frequent aneurysm formation and thus has reduced the incidence of VT to less than 1%.⁴ Nonetheless, this lower incidence of VT is balanced by increased prevalence owing to an aging population with a greater number of surviving patients at risk. It is unclear whether aggressive revascularization coupled with improved pharmacotherapies aimed at limiting cardiac remodeling has fundamentally changed the pathophysiology of ventricular arrhythmias. It is, however, perceivable that the resultant smaller and often patchy infarcts are associated with more limited conduction abnormalities, and thus result in faster and less well tolerated ventricular arrhythmias.

The time interval from infarct to first episode of VT is highly variable, ranging from weeks to years. Approximately 30% of patients will experience the first episode of sustained monomorphic VT within the first year after myocardial infarction with a predictable incidence of 2% to 5% per year thereafter. Late occurring sustained monomorphic VTs are more commonly encountered after inferior myocardial infarction. It is interesting to note that clinical characteristics including infarct size, LV function, and presence of aneurysm do not distinguish those patients developing VT early from those who develop it late.

During the infarct healing process, necrotic myocardium is replaced with fibrous tissue that surrounds surviving myocytes. In addition, the reduced number of gap junctions coupled with altered cellular distribution results in a slow, nonuniform anisotropic conduction that may promote reentry. Other electrophysiological consequences of infarction include abnormalities in refractoriness, inexcitability, and enhanced automaticity, all of which may contribute to arrhythmogenicity. However, abnormalities of conduction are most prominent and provide the electrophysiological substrate for VT.⁵ Abnormalities of conduction can be described in terms of electrogram characteristics and endocardial activation in sinus rhythm. Endocardial recordings from sites of VT origin during sinus rhythm consistently demonstrate low amplitude, prolonged duration, and multicomponent potentials frequently occurring after the end of the QRS (Figures 84-1 and 84-2). Furthermore, the degree of abnormal signals and conduction delay can distinguish patients with sustained VT from those with prior myocardial infarction and no tachycardia. In general, patients with prior myocardial infarction and sustained monomorphic VT have more profound electrogram abnormalities and endocardial conduction delay compared with those with coronary disease and no VT or nonsustained VT (Figure 84-3).

The relationship between abnormal electrograms and VT was studied in tissues removed from sites of VT origin and sites distant from VT. These studies showed that abnormal electrograms are associated with viable bundles of muscle fibers embedded in and separated by connective tissue.5–7 Studies using confocal microscopy and immunofluorescent staining of gap junctions showed alterations in the number, the distribution, and possibly the function of connexin43—a major cardiac gap junction in the ventricle.^8–10 The amplitude of the electrograms seems to be closely related to the number of viable muscle fibers under the recording electrode. Detailed mapping studies with microelectrodes in human tissue and in canine infarct models of VT demonstrated that slow propagation of an impulse through areas from which abnormal fractionated electrograms are recorded is associated with relatively normal sodium-dependent action potentials, implicating poor intercellular coupling in slow propagation of the cardiac impulse.^5,11

The relationship between abnormal electrograms and the VT substrate was also validated in the surgical experience to treat ventricular arrhythmias. Miller et al. analyzed the mechanism by which subendocardial resection successfully treats postinfarct-related VT. The origin of VT was mapped and showed extensive areas of abnormal electrograms (especially late and split potentials) that were completely eradicated following subendocardial resection (Figure 84-4). These data suggest that subendocardial resection removes the critical areas of slow conduction that are required from reentry. Whether or not it removes the whole reentrant circuit is unknown, but certainly absence of late potentials and normalization of electrograms suggest improved conduction. These findings are supported by more recent data demonstrating reduced recurrence of arrhythmiafollowing catheter-based ablation of abnormal electrograms.^12,13 In addition, data have shown that scars of myocardial infarction patients with no clinical arrhythmias not only are smaller than those of matched patients with spontaneous VT but also have much lower prevalence of isolated and late potentials within the scar.¹⁴

In attempts to replicate the surgical experience with catheter mapping, the development of three-dimensional mapping systems has allowed characterization of the anatomical substrate with detailed spatial relationships between substrate and voltage. Initial work by Cassidy and coworkers validated this concept using bipolar electrogram characteristics (voltage and duration) to identify the underlying substrate at individual endocardial sites.¹⁵ With the use of a 4-mm-tip electrode attached to a second pole 2 mm proximally (filtered at 10 and 400 Hz), normal bipolar voltage is approximately 1.6 mV in the left ventricle and 1.3 mV in the right ventricle. These data were further validated in human and porcine models of infarction and in isolated human autopsy studies.^16–18 Statistical analysis showed that 95% of endocardial recordings from individuals with normal, nonhypertrophied left ventricle had a bipolar voltage greater than 1.55 mV. A bipolar electrogram amplitude of 0.5 mV or less represented dense scar, and areas with bipolar amplitude between 0.5 and 1.0 mV represented the border zone (Figure 84-5). In addition, an increasing body of literature is validating these voltage definitions in humans. Bello and coworkers were able to image scar with both computed tomography and positron emission tomography.¹⁹ Fahmy and associates extended this approach to allow image integration with bipolar voltage maps.²⁰ However, the highest-resolution imaging of scar geometry is currently obtained by examination of the zone of delayed gadolinium enhancement (DGE) on magnetic resonance imaging. Codreanu and colleagues showed excellent correlation of DGE with a zone of bipolar voltage less than 1.54 mV.²¹ The ability to “visualize” electroanatomical information during both sinus rhythm and ventricular tachycardia reinforced several observations regarding the nature of the VT circuit. The “protected isthmus” of the reentrant VT circuits is contained within the dense scar (bipolar electrogram amplitude <0.5 mV), and the exit site of the arrhythmia to normal endocardium is consistently located at the border zone (bipolar electrogram amplitude between 0.5 and 1.5 mV). Voltage mapping may also facilitate identification of “channels” within the infarct. Channels are corridors of preferential conduction through dense scar that can serve as an isthmus during VT. They are indicated by relatively preserved voltage within the dense scar, the presence of late potentials, or a long stimulus to QRS time with pacing during sinus rhythm. They may be visualized on the electroanatomical map by adjustment of the voltage representation on the color isopotential map (Figure 84-6).^22,23 In addition, data suggest that the endocardial unipolar voltage map, with its larger field of view, may reveal epicardial abnormalities; however, this requires further investigation.²⁴

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