Abstract 16794: Early Detection of Myocardial Fibrosis by Electrocardiographic Abnormalities in Sickle Cell Patients

Abstract

Introduction: Advances in screening and treatment of sickle cell disease (SCD) continue to increase life expectancy of this population. As a result, mortality from cardiopulmonary causes has become the most prevalent cause of death. While the specific etiology of cardiac death remains unclear, multiple studies have shown that diastolic dysfunction and prolonged QT are associated with early mortality in SCD. Recently, the physiopathology of a novel cardiomyopathy with both restrictive and hyperdynamic features was described in the SCD population. In addition, a high incidence of repolarization nonspecific abnormalities has been reported in SCD patients. Although these serve as surrogates for repolarization heterogeneity, because of difficulty in reproducibility and measurability they are rarely considered of clinical significance. Hypothesis: Repolarization abnormalities are the earliest manifestation of microvascular changes and fibrosis in the myocardium of SCD patients. Methods: We performed a retrospective electrocardiographic and echocardiographic analysis of 88 patients from our SCD clinic. We used commercially available QT guard plus (QTgp) software to analyze repolarization heterogeneity parameters, and performed echocardiographic measurements of previously validated diastolic markers. In addition, data from 77 individuals - matched demographically with our SCD population- with structurally normal hearts and with normal ECGs was analyzed with QTgp. Results: Our statistical analysis showed correlation between Left ventricular mass index (LVMI), and mitral E/a ratio with T wave morphology changes (T peak, T offset, t wave morphology dispersion, and QRST vector) (table 1). In addition we found that T wave morphology was significatively different between our healthy controls and our SCD population (table 2). Conclusion: T wave morphology changes could be used as an early marker of diastolic dysfunction and increased LVM in the SCD population.