ABSTRACT
One of the potential complications of acute myocardial infarction is left ventricular thrombus (LVT). The incidence of LVT following acute myocardial infarction has decreased dramatically with early invasive reperfusion techniques or fibrinolysis. However, the risk of LVT formation remains significant and is associated with an increased risk of systemic embolism, stroke, cardiovascular events, and even death. Current guidelines indicate that dual antiplatelet therapy and anticoagulation therapy for at least 3 months can reduce the risk of these events. While vitamin K antagonist is the preferred oral anticoagulant, there is growing evidence to support the use of direct-acting oral anticoagulants in LVT management. Cardiac magnetic resonance has shown the highest diagnostic accuracy for LVT assessment, followed by echocardiography with contrast agents. This article serves as a general review of the pathophysiology, diagnosis, and management of LVT.
Subject(s)
Myocardial Infarction , Thrombosis , Anticoagulants/therapeutic use , Contrast Media , Factor Xa Inhibitors , Humans , Myocardial Infarction/complications , Myocardial Infarction/therapy , Platelet Aggregation Inhibitors/adverse effects , Thrombosis/diagnostic imaging , Thrombosis/etiology , Vitamin KABSTRACT
Our previous work showed the presence of endothelin-1 (ET-1) receptors, ETA and ETB, in human vascular endothelial cells (hVECs). In this study, we wanted to verify whether ET-1 plays a role in the survival of hVECs via the activation of its receptors ETA and (or) ETB (ETAR and ETBR, respectively). Our results showed that treatment of hVECs with ET-1 prevented apoptosis induced by genistein, an effect that was mimicked by treatment with ETBR-specific agonist IRL1620. Furthermore, blockade of ETBR with the selective ETBR antagonist A-192621 prevented the anti-apoptotic effect of ET-1 in hVECs. However, activation of ETA receptor alone did not seem to contribute to the anti-apoptotic effect of ET-1. In addition, the anti-apoptotic effect of ETBR was found to be associated with caspase 3 inhibition and does not depend on the density of this type of receptor. In conclusion, our results showed that ET-1 possesses an anti-apoptotic effect in hVECs and that this effect is mediated, to a great extent, via the activation of ETBR. This study revealed a new role for ETBR in the survival of hVECs.
