17β-Estradiol Does Not Designate Non-Sex-Specific Early Ventricular Arrhythmia in Acute Myocardial Infarction, in Contrast to C-Reactive Protein

Despite the evidence from experimental studies that endogenous hormones have sex-related effects on action potential duration, the relationship between gonadal steroids and ventricular repolarization in acute myocardial infarction (AMI) is not clear. We tested the hypothesis that endogenous 17β-estradiol (E2) and 17β-estradiol-to-testosterone ratio (E2/T) are associated with inflammation, influencing the occurrence of early ventricular arrhythmia (VA) in AMI. Electrocardiographic (ECG) repolarization indices, including resting heart rate (HR), corrected QT (QTc) interval, QTc minimum (QTcmin), QTc maximum (QTcmax), and QTc dispersion (QTcd), along with E2, total T, and the ratio of E2 to T (E2/T), were measured and analyzed after percutaneous coronary intervention in 86 patients (36 women, 41.9%). In a non-specific sex analysis, the incidence of early VA in the course of AMI was determined by the ejection fraction of the left ventricle (OR 0.876, <i>p</i> = 0.054), and by the peak levels of plasma C-reactive protein (OR 1.026, <i>p</i> = 0.077). Endogenous plasma 17β-estradiol tended to be higher in cases with early ventricular arrhythmia (124.5 ± 79 vs. 181 ± 192.8, <i>p</i> = 0.089). 17β-estradiol levels were significantly predicted by C-reactive protein (OR 1.050, <i>p</i> = 0.042). This study found that reduced systolic function of the left ventricle and higher peak CRP levels are associated with endogenous plasma 17β-estradiol in the acute phase of MI, and predicted the risk of early in-hospital ventricular arrhythmia.