Acute myocardial infarction and thyroid function: new pathophysiological and therapeutic perspectives.

In the post-reperfusion era, molecular and genetic mechanisms of cardioprotection and regeneration represent new therapeutic challenges to limit infarct size and minimize post-ischemic remodeling after acute myocardial infarction (AMI). Activation of cell survival mechanisms can be promoted by the administration of external drugs, stimulation of internal mechanisms, and genetic manipulation to delete or replace pathological genes or enhance gene expression. Among internal cardiovascular regulatory mechanisms, thyroid hormones (THs) may play a fundamental role. TH has a critical role in cardiovascular development and homeostasis in both physiological and pathological conditions. In experimental AMI, TH has been shown to affect cardiac contractility, left ventricular (LV) function, and remodeling. Several experimental studies have clearly shown that THs participate in the regulation of molecular mechanisms of angiogenesis, cardioprotection, cardiac metabolism, and ultimately myocyte regeneration, changes that can reverse left ventricular remodeling by favorably improving myocyte shape and geometry of LV cavity, thus improving systolic and diastolic performance. This review is focused on the role of thyroid on AMI evolution and on the potential novel option of thyroid-related treatment of AMI.