Abstract 15921: Correlation Between Repolarization Changes in Signal Averaged Electrocardiography and Myocardial Fibrosis in Adults With Hypertrophic Cardiomyopathy

Abstract

Introduction: Hypertrophic Cardiomyopathy (HCM) is known as one of the most common causes of sudden cardiac death. Its propensity to lethal arrhythmias is a result of myocardial remodeling leading to aberrant conduction and increased reentrant electrical activity. Previous studies suggest an association between the amount of myocardial fibrosis found on Cardiac Magnetic Resonance (CMR) and the risk of these ventricular arrhythmias. Signal Average Electrocardiography ( SAECG) is a noninvasive technique used to detect subtle conduction abnormalities that can be missed on standard Electrocardiography ( ECG ). Hypothesis: Non-uniform conduction through fibrotic tissue seen in CMR leads to unsynchronized myocardial depolarization which correlates with further repolarization abnormalities that can be detected by SAECG. Method: In this retrospective study, results of SAECG were used to classify 73 HCM patients into Normal or Abnormal groups based on the presence of two or more of three predetermined criteria (fQRS, RMS40, LAS40). Replacement fibrosis was assessed by measuring late gadolinium enhancement (LGE) . Interstitial fibrosis was assessed by measuring T1 relaxation times, using the Look-Locker sequence. Results: A statistically significant association between the presence of myocardial fibrosis on CMR and abnormal SAECG was found with a difference of proportions of 41.3% between the subgroups. Left ventricular mass index was found to be significantly higher in the abnormal subgroup (Normal: 61.2 ± 19.6; Abnormal: 82.4 ± 37.1; p = <0.003, CI 95% [2.93; 39.47]). The presence of T wave inversions on standard ECG was only seen in those who had an abnormal SAECG exam. Conclusion: Abnormal SAECG in patients with HCM is associated with the presence of LGE on CMR. This study showed a subset of patients with absence of LGE despite having abnormal SAECG, which implies that there are other complex mechanisms besides replacement fibrosis, that predisposes this population to ventricular arrhythmias. This can also be highlighted by the fact that there was no difference between the two groups in the T1 mapping time. We believe that SAECG could be an objective assessment of the arrhythmogenic substrate present in patients with HCM.