Key result
Surviving myocardial islands within fibrofatty tissue drive VT substrate in ARVC.
Case Report (n=1)
In ARVC, surviving myocardium within fibrofatty tissue generates low-voltage, long-duration electrograms that serve as the substrate for ventricular tachycardia, which can be distinguished from pure fat during electroanatomic mapping.
May inform substrate mapping in ARVC; hypothesis-generating from single case and requires prospective validation before practice change.
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is characterized by ventricular arrhythmias and fibrofatty replacement of the right ventricular (RV) myocardium. Although the RV is the predominant chamber involved, left ventricular (LV) involvement has also been documented.1–4 Electrophysiological correlations of histopathologic findings in nonischemic cardiomyopathy, and especially in ARVC, are limited.5 We report a case of ARVC that presented with ventricular tachycardia (VT) and diffuse fibrofatty involvement of both the RV and LV.
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Watanabe et al. (2015) conducted a case report in Arrhythmogenic right ventricular cardiomyopathy (n=1). Electroanatomic mapping and catheter ablation was evaluated on Correlation of electroanatomic mapping with histopathologic findings. Electroanatomic mapping and histopathology in a patient with ARVC demonstrated that islands of surviving myocardium within fibrofatty tissue are electrically active, exhibit low-voltage, long-duration electrograms, and serve as the substrate for ventricular tachycardia.
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