Left ventricular thrombus formation after acute myocardial infarction
- 1Department of Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands
- 2Department of Cardiology, Erasmus Medical Center, Rotterdam, the Netherlands
- Correspondence to Professor Dr Jan J Piek, Department of Cardiology, Academic Medical Center, University of Amsterdam, PO Box 22660, 1100 DD Amsterdam, The Netherlands;
Contributors RD: drafting the manuscript; FZ: critical revision; JP: interpretation of the data.
- Acute myocardial infarction
- LV thrombus formation
- cardiac remodelling
- coronary intervention (PCI)
- acute coronary syndrome
Cardiovascular disease remains the leading cause of death in western society. Mortality from acute myocardial infarction (AMI) has decreased since the introduction of primary percutaneous coronary intervention (PCI), which has proved to be superior to thrombolytic therapy by demonstrating lower mortality rates and reduced clinical adverse events. Nevertheless, postinfarct complications still lead to morbidity and mortality in a large number of patients.
One of the most feared complications is the occurrence of thromboembolic events (mostly cerebrovascular accidents) due to left ventricular (LV) thrombus formation. The risk of LV thrombus formation is highest during the first 3 months following acute myocardial infarction, but the potential for cerebral emboli persists in the large population of patients with chronic LV dysfunction. Since these thromboembolic events are usually unheralded by warning signs of transient cerebral ischaemia, the only truly satisfactory medical approach is adequate management of these high risk groups. This article discusses the incidence, diagnosis and management of LV thrombus formation after an AMI.
Pathogenesis of LV thrombus
The combination of blood stasis, endothelial injury and hypercoagulability, often referred to as Virchow's triad, is a prerequisite for in vivo thrombus formation. In the presence of LV thrombus formation after AMI, the three components of this triad can also be recognised (figure 1). LV regional wall akinesia and dyskinesia result in blood stasis, often recognised on two dimensional echocardiography by the occurrence of spontaneous LV contrast. Prolonged ischaemia leads to subendocardial tissue injury with inflammatory changes. Finally, patients with an acute coronary syndrome display a hypercoagulable state with, for example, increased concentrations of prothrombin, fibrinopeptide A, and von Willebrand factor, and decreased concentrations of the enzyme responsible for cleaving von Willebrand factor (ADAMTS13).w1 w2 This triad can result in the formation of LV thrombus composed …