Perivalvular Fibrosis and Monomorphic Ventricular Tachycardia

Abstract

T he basis for arrhythmogenesis in patients with nonischemic cardiomyopathy and ventricular tachycardia (VT) needs further elucidation. Cardiac arrest and/or nonsustained VT are common arrhythmia presentations in the setting of nonischemic cardiomyopathy, with sustained monomorphic VT being relatively uncommon. 1,2 Importantly, bundlebranch reentrant VT is identified as the VT mechanism in a significant percentage of patients with monomorphic VT in the setting of nonischemic cardiomyopathy. 3,4 However, even in patients with nonischemic left ventricular (LV) or right ventricular (RV) cardiomyopathy, the majority of VT appears to originate from the myocardium and is not due to bundlebranch reentry. 4 -11 Detailed substrate, activation, and entrainment mapping has begun to provide some valuable clues related to the mechanism and pathophysiology of scar-based VT in the setting of nonischemic cardiomyopathy resulting from a variety of causes. 4 -11 Although not focusing on VT after valve surgery, these data have been helpful in identifying likely regions of origin for VT and facilitating ablative therapy in other nonischemic settings. Article p 2005 Lessons Learned From Ablation of VT After Valve SurgeryWhen dealing with uncommon disease processes, one looks to centers with sizable clinical experience to review their results and provide important insight. In this issue of Circulation, the report by Eckart and colleagues 12 answers that charge. Six years of clinical experience with VT ablation resulted in the identification of 20 patients who developed VT after prior cardiac valve surgery and underwent catheter ablative therapy. Importantly, most of the patients demonstrated mildly to moderately depressed LV function with a median LV ejection fraction of 45%. Characterization of the substrate, mechanism, and outcome of ablative therapy provides important insight in terms of pathogenesis. Such detailed information should be compared with findings at the time of VT ablation in a variety of other nonischemic cardiomyopathies to attempt to identify common and potentially important pathophysiological links. 4 -11 Indeed, the study by Eckart and colleagues is modestly handicapped by its retrospective study design. Details of the preoperative status of LV function and the surgical intervention were unavailable, making it difficult to determine whether some abnormalities preceded or were created by surgical incisions, venting, or the like. The timing of the "late" onset of VT as it relates to the surgery also is probably much shorter than the described 12 years for the second mode of presentation timing. Of note, 12 of the 16 patients who underwent ablation late after surgery because of VT in the present report already had an implantable cardioverterdefibrillator in place for a median of 4.5 years, presumably for a documented arrhythmia episode in most. 12 Nevertheless, a distinction between early, Ͻ1 month, and late, Ͼ1 to 20 years, is valid and somewhat similar to the bimodal distribution of VT after myocardial infarct...

Loss of Cardiomyocyte Integrin-Linked Kinase Produces an Arrhythmogenic Cardiomyopathy in Mice

“…However, it is characteristic of patients demonstrating monomorphic VTs associated with nonischemic cardiomyopathies. 21,22 A similar distribution of fibrosis has recently been described with the use of late gadolinium enhancement MRI in patients with lamin A/C (LMNA) mutation cardiomyopathy. 23 This regional localization may be related to the effects of local mechanical stresses, which might have particularly important effects when part of the mechanosensor apparatus, like ILK, is deleted.…”

ECG Criteria to Identify Epicardial Ventricular Tachycardia in Nonischemic Cardiomyopathy

“…We centered our attention on the basal anterior or superior and lateral region of the LV because the gross anatomic changes in those regions most commonly serve as the substrate for VT in this setting. 7,8 Furthermore, the focus on this important anatomic region permitted a sufficient number of VTs to be identified and detailed pace mapping to be performed so that a meaningful comparison of ENDO versus EPI QRS morphologies could be made. The results unequivocally show that the morphological criteria (presence of a q wave in lead I and absence of q waves in the inferior leads) appear to be the most specific criteria and in the case of presence of a QWL1 also a very sensitive criterion for identifying an EPI site of origin of all prior published criteria.…”

“…5,6 Furthermore, it has also been previously noted that up to 90% of VTs in NICM originate from substrate-based abnormalities that are located near the superior and lateral perivalvular aortic and mitral valve region. 7,8 It would appear, therefore, that the value of published ECG criteria for identifying an EPI origin must be rigorously assessed in patients with NICM, focusing on this perivalvular region to establish their true accuracy in this important setting. To attempt to accomplish this charge, we studied patients with NICM to (1) assess the value of published interval and morphological criteria for identifying an EPI origin from the basal superior and lateral left ventricle (LV) using a comparison of pace maps and VT-generated QRS complexes from endocardial (ENDO) versus EPI origin and (2) to determine whether a more effective algorithm using modified criteria for identifying an EPI origin in this setting could be established.…”

Ventricular tachycardia mapping and ablation in arrhythmogenic right ventricular cardiomyopathy/dysplasia: Lessons Learned

“…A detailed RV endocardial voltage map is created in sinus rhythm using the standard 0.5-1.5 mV voltage cutoffs to define the endocardial substrate as previously discussed [13,22] . Special attention is focused on the periannular area and any identified low-voltage areas to ensure adequate sampling has occurred [23][24][25] . Occasionally, it can be technically challenging to perform catheter manipulation in the periannular tricuspid valve region.…”