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  • br Specific concerns of each VT substrate

    2019-04-25


    Specific concerns of each VT substrate
    Complications Potential complications associated with epicardial catheter ablation of VTs are very rare and the procedures are generally safe [4–6,11,13–16,17,25,33–35]. However, transthoracic epicardial access and ablation could result in uncommon complications [36]. The electrophysiologists should be aware of the relevant complications, and know how to minimize their occurrence, and how to rapidly recognize and treat the complications that they encounter. Therefore, these procedures should be performed at well-experienced AG-14361 rhythm centers.
    Conclusions
    Conflict of interest
    Introduction Ventricular tachycardia (VT) most frequently occurs in the presence of structural heart disease, and it is an important cause of mortality and morbidity. The vast majority of cases of structural heat disease are associated with some degree of scarring that serves as the substrate for sustained VT. Implantable cardioverter defibrillators (ICDs) or cardiac resynchronization therapy defibrillators are used in patients at high risk of sudden death due to malignant ventricular arrhythmias. However, despite effective VT termination, recurrent VT, which gives rise to frequent ICD discharges, is associated with increased rates of mortality and congestive heart failure hospitalization as well as reduced patient quality of life [1–8]. Pharmacological therapies such as beta-blockers, amiodarone, and sotalol are used to reduce recurrent VT. The combined use of amiodarone and beta-blockers is more effective than sotalol or beta-blocker therapy alone [9]. However, it is important to recognize that these pharmacological therapies may have adverse effects on clinical outcomes. Amiodarone causes multiple organ toxicities that are associated with increased mortality in patients with New York Heart Association class III heart failure and no ICD [10]. The side effects of amiodarone restrict its long-term use in more than 20% of patients [9]. Catheter ablation is an effective therapeutic option in the management of scar-related VT [11,12]. Ablation targets a critical isthmus to interrupt the re-entrant circuit [11–14]. Ideally, VT will be reliably inducible, hemodynamically well tolerated, and of a single morphology, allowing for activation and entrainment mapping. However, this is the exception rather than the rule. Hemodynamic instability and non-inducibility throughout the procedure can render the VT unmappable [13,14]. Furthermore, most patients with scar-related VT have multiple VT circuits with multiple QRS morphologies on surface electrocardiograms. VT frequently changes QRS morphology (often with entrainment attempts). A previous multicenter study showed that 31% of patients had only unmappable VT and 38% patients had both mappable and unmappable VT morphologies targeted [13]. In these situations, a substrate-based approach is attractive. A substrate mapping and ablation strategy in sinus rhythm allows us to offer ablation therapy to patients with unmappable VT. Various ablation strategies such as targeting late potentials, endo- and epicardial scar homogenization, and eliminating local abnormal ventricular activities (LAVA) have been described previously [15–23]. In this article, we review substrate-based approaches and tips for mapping and ablation of VT substrate in patients with structural heart disease.
    Substrate mapping in sinus rhythm In previous studies using explanted human hearts, de Bakker et al. demonstrated that AG-14361 there are bridges of surviving myocardial cells within the post-infarction VT scar that connect opposite borders of the scar [24–26]. The surviving fibers surrounded by electrically unexcitable fibrosis serve as a slow-conducting pathway of VT re-entrant circuits. In non-ischemic dilated cardiomyopathy, replacement of muscle by fibrosis creates conducting channels that similarly facilitate a re-entrant circuit. Cassidy et al. noted that local electrograms at the sites of VT origin displayed lower amplitudes and longer electrogram durations than those at other sites, as obtained from intra-operative mapping in sinus rhythm [27]. Endocardial abnormal and fractionated electrograms can be eradicated by surgical subendocardial resection, with long-term arrhythmia-free rates of 60–80% in patients with a previous myocardial infarction [28].