Abstract 12158: Electrophysiological Substrate of Hypertrophic Cardiomyopathy.

Introduction: Mechanisms of arrhythmogenicity in hypertrophic cardiomyopathy (HCM) are not well understood. Hypothesis: We hypothesized that HCM is characterized by specific electrophysiological (EP) substrate as compared to patients with the well-understood arrhythmogenic substrate (ischemic cardiomyopathy), as well as to individuals free from the arrhythmogenic substrate. Methods: We conducted a prospective case-control study. HCM patients (n=10; age 61±9 y; left ventricular ejection fraction (LVEF) 60±9%) were included if had either (1) documented history of sustained ventricular tachyarrhythmia (VT/VF) or resuscitated sudden cardiac arrest (SCA), or (2) LV wall thickness of > 30mm, or (3) extensive fibrosis on cardiac MRI (>15% of total myocardial volume), or (4) >7.5%/5-year risk of SCA. Three groups of controls included: (1) Healthy individuals (n=10; age 28±6 y; LVEF>70%), (2) Post-infarction (MI) patients with LV hypertrophy (LVH) and arrhythmogenic substrate as proven by the history of SCA or sustained VT/VF with appropriate ICD shock, (n=10; age 64±9 y; LVEF 31±15%), (3) Post-MI patients with LVH, presumably free from arrhythmogenic substrate (n=10; age 70±7y; LVEF 46±16%). All participants underwent 12-lead ECG, cardiac CT or MRI, and 128-electrodes body surface mapping (BioSemi ActiveTwo, Netherlands). Non-invasive epicardial activation maps were reconstructed using inverse solutions approach. Spatial ventricular gradient (SVG) magnitude and direction, vector magnitude QT integral (VMQTi), and spatial QRS-T angle were measured. Results: HCM patients had the widest QRS-T angle [130°±48° vs. 126°±50° (post-MI with VT/VF) vs. 108°±46° (post-MI no arrhythmia) vs. 60±23 (Healthy); P=0.003], and the largest VMQTi (166±81 vs. 84±34 mV*ms (post-MI with VT/VF) vs. 120±42 mV*ms (post-MI no arrhythmia) vs. 115±19 mV*ms (Healthy); P=0.008). SVG vector pointed higher up in HCM (SVG elevation 92°±33° vs. 80°±17° (post-MI with VT/VF) vs. 71°±21° (post-MI no arrhythmia) vs. 59°±9° (Healthy); P=0.011). Activation map in HCM was characterized by increased heterogeneity (Figure). Conclusions: HCM is characterized by increased global electrical heterogeneity, representing HCM-specific arrhythmogenic EP substrate. [ABSTRACT FROM AUTHOR]