Post-infarct left ventricular thrombosis is mechanistically related to ventricular wall rupture.

Left ventricular thrombus (LVT) after acute myocardial infarction (AMI) remains to be a common complication bearing adverse prognostic implication. Majority of LVT occurs within the first week after AMI. Over decades, the regional stasis of blood flow is regarded as the main reason for LVT formation. Here we hypothesize that LVT developed within the first week after AMI is the consequence of an incomplete wall rupture. Endocardial rupture with exposure of infarcted tissues triggers platelet thrombosis within the rupture site and then the thrombus grows towards the ventricular chamber forming LVT. This hypothesis is implicated by the comparable clinical features of patients with LVT or with cardiac rupture, and supported by experimental findings in murine model of AMI revealing the mechanistic link between rupture and LVT. This hypothesis, if confirmed, would improve our understanding on the pathophysiology of both rupture and LVT as two pivotal mechanical complications after AMI, and the role of platelets in the setting of AMI and hence the use of anti-platelet therapies. Future studies are warranted to test this hypothesis by serial cardiac imaging on AMI patients with high risk of LVT.