Catheter ablation of ventricular tachycardia in patients with postinfarction left ventricular aneurysm

Abstract

Background: While ventricular tachycardia (VT) in the setting of postmyocardial infarction left ventricular aneurysms (LVA) is not uncommonly encountered, there is a scarcity of data regarding the safety, efficacy, and outcomes of ablation of VT in this subset of patients.Methods: Our study included consecutive patients aged 18 years or older with postmyocardial infarction LVA who presented to Mayo Clinic for catheter ablation of VT between 2002 and 2018.Results: Of 34 patients, the mean age was 70.4 ± 9.1 years; 91% were male. Mean LVEF was 29 ± 9.7% and left ventricular end-diastolic dimension was 64.9 ± 6.6 mm.The site of the LVA was apical in 21 patients (62%). Fifteen patients (44%) presented with electrical storm or incessant VT. Nine patients (26%) had a history of intracardiac thrombus. All except for one patient had at least one VT originating from the aneurysm. The mean number of VTs was 2.9 ± 1.7. All patients underwent ablation at the site of the aneurysm. Ablation outside the aneurysm was performed in 13 patients (38%). Low-voltage fractionated potentials and/or late potentials at the aneurysmal site were present in all cases. Complete elimination of all VTs was achieved in 18 (53%), while the elimination of the clinical VT with continued inducibility of nonclinical VTs was achieved in a further 11 patients (32%). Two patients developed cardiac tamponade requiring pericardiocentesis. During a mean follow-up period of 2.3 ± 2.4 years, 11 patients (32%) experienced VT recurrence.Freedom from all-cause mortality at 1-year follow-up was 94%. Conclusion:Radiofrequency catheter ablation targeting the aneurysmal site is a feasible and reasonably effective management strategy for clinical VTs in patients with postinfarction LVA.

Microelectrode voltage mapping for substrate assessment in catheter ablation of ventricular tachycardia: A dual‐center experience

“…Ventricular aneurysms are commonly associated with recurrent VT due to reentry involving surviving myocites inside the aneurysm or at its edge. 7,[20][21][22] In the subset of patients with LV aneurysms in our study (n = 10), standard bipolar voltage mapping in sinus rhythm showed dense scar electrograms in 59.7% of mapping locations inside the aneurysm (Figure 2, panel C). However, microelectrode mapping allowed the detection of significantly higher voltages in the same locations.…”

Man with chest tightness and diaphoresis

“…It may be the site of origin for ventricular tachycardia 2 . Antiarrhythmic drugs and radiofrequency catheter ablation are frequently used to reduce ventricular tachycardia frequency and shocks in patients with implantable cardioverter‐defibrillators 3 …”

Epicardial Ablation as a Treatment of Recurrent Ventricular Tachycardia Originating From a Left Ventricular Aneurysm: A Case Report and Review of the Literature

“…Most cardiomyopathies are predisposed to developing VT and include, among others, arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy, and hypertrophic cardiomyopathy [ 3 ]. In addition, left ventricular aneurysms (LVAs) and pseudoaneurysms are two complications of MI that can lead to serious morbidity and even death [ 4 ]. LVA formation involves the dilation of the ventricular wall that leads to a well-delineated outward bulging of the affected LV wall due to myocardial thinning and scar formation.…”

“…LVA formation involves the dilation of the ventricular wall that leads to a well-delineated outward bulging of the affected LV wall due to myocardial thinning and scar formation. LVA that develops after myocardial infarction may lead to VT, among other complications including thrombus formation [ 4 ]. LVAs themselves are potential arrhythmogenic substrates and, given their complex and often apical anatomy, may be difficult to target from the endocardium [ 4 ].…”

“…LVA that develops after myocardial infarction may lead to VT, among other complications including thrombus formation [ 4 ]. LVAs themselves are potential arrhythmogenic substrates and, given their complex and often apical anatomy, may be difficult to target from the endocardium [ 4 ].…”