Korean Circ J.  2014 Jul;44(4):210-217. 10.4070/kcj.2014.44.4.210.

Catheter Ablation of Ventricular Tachycardia in Patients with Post-Infarction Cardiomyopathy

• Nazer B
• Gerstenfeld EP

• KMID: 2223880
• DOI: http://doi.org/10.4070/kcj.2014.44.4.210

Abstract

Monomorphic ventricular tachycardia (VT) in patients with post-infarction cardiomyopathy (CMP) is caused by reentry through slowly conducting tissue with in areas of myocardial scar. The use of implantable cardioverter-defibrillators (ICDs) has helped to decrease the risk of arrhythmic death in patients with post-infarction CMP, but the symptomatic and psychological burden of ICD shocks remains significant. Experience with catheter ablation has progressed substantially in the past 20 years, and is now routinely used to treat patients with post-infarction CMP who experience VT or receive ICD therapy. Depending on the hemodynamic tolerance of VT, a variety of mapping techniques may be used to identify sites for catheter ablation, including activation and entrainment mapping for mappable VTs, or substrate mapping for unmappable VTs. In this review, we discuss the pathophysiology of VT in post-infarction CMP patients, and the contemporary practice of catheter ablation.

Keyword

Tachycardia, ventricular; Catheter ablation; Myocardial infarction; Cardiomyopathy

MeSH Terms

Cardiomyopathies*
Catheter Ablation*
Cicatrix
Defibrillators, Implantable
Hemodynamics
Humans
Myocardial Infarction
Shock
Tachycardia, Ventricular*

Figure

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  Fig. 1 Mechanism of macro reentry in scar-based VT. A: three-dimensional electroanatomic voltage map of LV with areas of normal myocardium (purple), scar (red), and border zone (other colors). The yellow arrow demonstrates a potential "isthmus" area between areas of scar that may harbor the VT circuit. B: autopsy specimen of a heart with prior myocardial infarction with a septal scar (pale area). Note that the scar is heterogeneous with areas of surviving myocardium between areas of infarcted myocardium that may serve as a potential VT isthmus (black arrow). This specimen is from a different patient than that of the electroanatomic map, and is used as an example. VT: ventricular tachycardia, LV: left ventricle, RV: right ventricle.

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  Fig. 2 Localization of VT exit site using surface ECG. A: for VTs of septal origin, aVR is typically

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  Fig. 3 Demonstration of concealed entrainment of a mappable VT. After induction of VT, pacing is performed from the suspected VT exit site (orange arrow) at a rate 20-30 ms faster than the VT rate (note pacing stimuli on the left side of the panel). Pacing is then stopped, and the post-pacing interval is compared to the VT cycle length; a difference <30 ms suggests that the pacing site is within the macroreentry circuit. The QRS morphology of the paced beat (red arrow and box) is identical to the spontaneous VT (yellow arrow and box) with a 12/12 lead match, identifying this site as a critical component of the VT circuit. VT: ventricular tachycardia.

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  Fig. 4 Three-dimensional, electroanatomic voltage map in the right anterior oblique (RAO) and left anterior oblique (LAO) projections in a patient with a prior large anteroseptal myocardial infarction. Normal voltage is represented by regions with bipolar voltage >1.5 mV (purple), dense scar by regions with bipolar voltage <0.5 mV, and scar border zone by regions with bipolar voltage ≥0.5 and ≤1.5 mV. Black dots represent abnormal "late potentials" identified on intracardiac electrograms.

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  Fig. 5 Intracardiac electrogram demonstrating a high-frequency, low-amplitude late potential (solid arrows) after the QRS in sinus rhythm. This identifies a region of slow conduction that may be involved in VT maintenance, although such sites may also represent "bystanders" that are not important for VT maintenance. VT: ventricular tachycardia.

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