The higher cardiovascular risk in men and post-menopausal women implies a protective action of estrogen. A large number of experimental studies have provided strong evidence indicating that estrogen has protective effect in the process of myocardial infarction (MI). Estrogen may prevent deterioration of cardiac function post-MI through improving heart failure of cadiocyte biology and also through mediating arrhythmia. The alternations by estrogen in immune function, apoptosis and endothelial progenitor cells after MI may be the most important mechanisms for cadiocyte survival. For the control of cardiac hypertrophy, estrogen acts as both a potent vasodilator and a direct mediator for cadiocyte. The major mechanisms underlying arrhythmia effect may involve affecting neural remodeling, electrical remodeling and structural remodeling.
In this new book, the authors mainly focus on the current mechanisms underlying the estrogen effects after MI through genomic pathway and non-genomic pathway. A further understanding of estrogen and estrogen receptors function and regulation may lead to the development of highly specific prevention and treatment of cardiovascular diseases.