QRS prolongation is associated with associated with adverse cardiac remodeling in hypertrophic cardiomyopathy
Hernan L Vera-Sarmiento1, Talha Tanriverdi2, David Hurtado-de-Mendoza3
1Hypertrophic Cardiomyopathy Center of Excellence, Division of Cardiology, University of California San Francisco, San Francisco, CA, United States of America.
Insights
Abnormal signal-averaged electrocardiogram (SAECG) in hypertrophic cardiomyopathy (HCM) patients indicates significant structural and electrical remodeling. This finding highlights a more severe global myopathy in affected individuals.
Area of Science:
- Cardiology
- Electrophysiology
- Cardiovascular Imaging
Background:
- Signal-averaged electrocardiogram (SAECG) detects myocardial depolarization and identifies slow conduction in fibrotic tissue, a precursor to ventricular arrhythmias (VAs).
- Hypertrophic cardiomyopathy (HCM) presents a high incidence of cardiac fibrosis and VAs, yet SAECG shows limited predictive value for VAs.
- HCM-specific structural and electrical remodeling is hypothesized to explain the low predictive power of SAECG.
Purpose of the Study:
- To investigate the relationship between abnormal SAECG findings and underlying structural/electrical remodeling in hypertrophic cardiomyopathy (HCM) patients.
- To determine if HCM-specific remodeling contributes to the low predictive power of SAECG for ventricular arrhythmias (VAs).
Main Methods:
- Retrospective study of 73 HCM patients with SAECG, transthoracic echocardiography (TTE), and cardiac magnetic resonance (CMR) imaging.
- Patients classified into normal and abnormal SAECG groups based on filtered-QRS duration (fQRSd), root-mean-square-voltage (RMS40), and late potentials (LAS40).
- Abnormal SAECG defined by fQRSd > 114 ms, RMS40 < 20 μV, or LAS40 > 38 ms.
Main Results:
- Approximately 50% of HCM patients (37/73) exhibited abnormal SAECG.
- The abnormal SAECG group showed significantly higher fQRSd and LAS40, larger left atrial size, reduced global LV longitudinal strain/strain rate, and impaired early diastolic strain rate.
- CMR revealed higher LV-mass index (LVMI) and LV scar burden in the abnormal SAECG group; fQRSd correlated positively with LVMI and scar mass.
Conclusions:
- Abnormal SAECG in HCM patients is associated with more extensive structural and electrical left ventricular (LV) remodeling.
- These findings suggest that abnormal SAECG reflects a more severe global myopathy in HCM.
- The study underscores the link between SAECG abnormalities and advanced cardiac remodeling in HCM.
Background:
Signal-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.
Methods:
We 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.
Results:
Abnormal 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.
Conclusions:
In HCM, abnormal SAECG is associated with greater structural/electrical LV-remodeling, reflecting a severe global myopathy.
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