Antithrombotic Therapy for Cerebrovascular Disorders: Acute Myocardial Infarction

The predictive value of left ventricular thrombi (LVT) for embolism has received considerable recent attention. LVT virtually always overlie ventricular wall motion abnormalities and are consequently much more frequently associated with anterior AMI than with inferior AMI. Of all patients with anterior AMI, about two thirds have substantial ventricular wall motion abnormalities, and about half of these patients will have associated LVT. Overall, about one third of all anterior AMIs have associated LVT. read only
LVT are usually absent if echocardiography is performed within the first 24 h following onset of AMI, but the large majority appear during the first 2-7 days and the bulk of the remainder during the second week post-AMI. While anticoagulation reduces the incidence of LVT in the weeks following AMI, LVT can persist despite anticoagulation in many patients (Table 3). The efficacy of anticoagulation may be related to the time of initiation and the intensity. When oral anticoagulation is initiated after detection of LVT, especially if remote from AMI, LVT often persist. In summary, the formation, persistence, and embolic potential of LVT following AMI is a dynamic process dependent primarily on underlying myocardial contractility. The occasional late appearance of LVT, the evolving morphology, the time-related decline in embolic potential, and the frequent persistence despite anticoagulation suggest interaction of complex mechanisms, as yet not fully elucidated.
It is clear that patients with AMI who have LVT have a higher risk of embolism than those without LVT. The risk of embolism is greatest during the initial weeks following AMI and falls sharply in the subsequent months, despite persistence of most LVT. Protruding and/or mobile LVT have been particularly associated with embolism. While aggregate data confirm that administration of heparin in the hours following AMI reduces the prevalence of LVT, existing data are inadequate to determine whether such therapy results in clinically important reduction in emboli (Table 3). It is clear that anticoagulation does not completely protect against either LVT or embolism. Whether anticoagulation alters the size of emboli and thus influences stroke severity is unknown.

Category: Antithrombotic Therapy

Tags: antithrombotic therapy, cardioembolic source, cerebrovascular disorders