Sex hormones and arrhythmia in myocardial ischemia

Abstract

The mechanisms by which gender affects cardiac electrophysiological parameters and alters the predisposition to certain arrhythmias are not well understood, although differences in the expression and function of ion channels and in the activation of the autonomic nervous system may contribute. In their study Philp and coworkers address the issue of the effect of 17b-estradiol on ventricular vulnerability in a rat model of ischemia. Their data show that there is a dose-dependent antiarrhythmic activity of 17b-estradiol administration with suppression ventricular premature beats, ventricular tachycardia and ventricular fibrillation during ischemia. Furthermore they show a dose-dependent blockage of I CaL by 17b-estradiol which is again stronger in female than in male mice. They postulate that the shown gender-selective, concentration-dependent inhibition of I CaL is sufficient to account for the reduction in ischaemia-induced arrhythmia. With this data they have added important information on the influence of sex hormones on cardiac electrophysiology under pathophysiological conditions. (2006) Keywords: cardiac arrhythmia; myocardial infarction; gender; sex hormones; ion channels Coronary artery disease, the most common cause of ventricular tachyarrhythmias, is the leading cause of death in both men and women (Cahndra et al., 1998;Marrugat et al., 1998). However, the incidence of sudden cardiac death at all age groups is significantly lower in women (Kannel et al., 1998;Kim et al., 2001) and traditional risk factors do not seem to predict sudden death to the same extent in women as they do in men (Lerner and Kannel, 1986;Kannel et al., 1998). British Journal of PharmacologyThe mechanisms by which gender affects cardiac electrophysiological parameters and alters the predisposition to certain arrhythmias are not well understood, although differences in the expression and function of ion channels (Katsube et al., 1998;Leblanc et al., 1998;Trepanier-Boulay et al., 2001) and in the activation of the autonomic nervous system (Burke et al., 1997;Airaksinen et al., 1998;Cahndler and DiCarlo, 1998; Umetani et al., 1998) may contribute. Furthermore, gender has an influence on certain electrophysiological parameters, such as the corrected quantitative transmission (QT) interval, ventricular refractoriness and action potential duration (Burke et al., 1997; TrepanierBoulay et al., 2001;Saba et al., 2002). However, to date the exact mechanisms that underlie sex hormone-based differences in cardiac electrophysiology after myocardial infarction have not been established. Female sex hormones, in particular estrogen, may play a role in this process. The myocardium contains both functional estrogen receptor a (ERa) and estrogen receptor b (ERb) (Grohé et al., 1998). These transcription factors can activate downstream target genes such as the endothelial/inducible isoforms of the nitric oxide (NO) synthase as well as connexin 43 in the heart (Strehlow et al., 2003).In their study, Philp et al. (2006) address the issue of the effect ...

Angiographic Correlation and Synergistic Effect of Coronary Artery Stenosis and Cerebral Artery Stenosis: A Retrospective Study

“…There was no significant difference in the rate of myocardial infarction between groups B1 and B2 ( p =0.169, OR=2.889, 95% CI=0.618–13.496), whereas the morbidity rates for ischemic stroke between groups B1 and A1 showed a weak trend toward a significant difference ( p =0.060, OR=3.682, 95% CI=0.911–14.876), suggesting that the synergistic effect of CoAS and CeAS might increase the risk of ischemic stroke but not myocardial infarction. The reason might be associated with the cardiogenic etiologies of myocardial ischemia, such as arrhythmia, cardiogenic embolism, and decreased cardiac function [ 23 – 25 ]. Because the different therapeutic strategies after angiography, such as angioplasty, bypass surgery and drug treatment, might interfere with the synergistic effect of CoAS and CeAS [ 26 – 28 ], this study retrospectively analyzed the morbidity rates for myocardial infarction and ischemic stroke before angiography.…”