BackgroundSignal-averaged electrocardiogram (SAECG) records myocardial depolarization, and can detect inhomogeneous/slow conduction in fibrotic myocardium, which promotes reentrant ventricular arrhythmias (VAs). Hypertrophic cardiomyopathy (HCM) is associated with a high prevalence of cardiac fibrosis and VAs, but abnormal SAECG has low predictive power for VAs. We hypothesized that HCM-specific structural/electrical remodeling underlies this result. MethodsWe tested our hypothesis by retrospectively studying HCM patients (n = 73) who underwent transthoracic echocardiography (TTE) and cardiac magnetic resonance (CMR) imaging within 12 months of SAECG and 12‑lead ECG. Patients were divided into 2 groups (normal-SAECG, abnormal-SAECG) based on filtered-QRS duration (fQRSd), root-mean-square-voltage (RMS40) and low-amplitude (<40 μV) signal of terminal 40 ms of filtered-QRS (late potentials). Abnormal SAECG was defined as fQRSd > 114 ms, RMS40 < 20 μV or LAS40 > 38 ms. ResultsAbnormal SAECG was seen in ∼50 % of HCM patients (37/73). In the abnormal-SAECG group, 78 % (n = 29) only had prolonged fQRSd, and 22 % (n = 8) had prolonged fQRSd plus late potentials (RMS40 < 20 μV or LAS40 > 38 ms). Mean fQRSd and LAS40 were significantly higher in the abnormal-SAECG group. The abnormal-SAECG group had significantly larger LA size, lower global-LV longitudinal systolic strain/strain rate and early-diastolic strain rate by TTE; higher LV-mass index (LVMI) and LV-scar burden by CMR; higher prevalence of repolarization abnormalities on 12‑lead ECG. LVEF and adverse outcomes (VT/VF, heart failure, death) were similar in the 2 groups. Univariate analysis showed that fQRSd is positively correlated with LVMI, LV-scar mass, and negatively correlated with global-LV early diastolic strain rate. ConclusionsIn HCM, abnormal SAECG is associated with greater structural/electrical LV-remodeling, reflecting a severe global myopathy.
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