Antiplatelet and anticoagulation therapy in acute cerebral infarction

Abstract

Effective treatments have recently been developed for acute cerebral infarction based on the pathophysiology. In atherothrombosis, artery-to-artery thrombosis plays a pivotal role in artery territory infarction and even in watershed infarction. In the latter, hemodynamic insufficiency is thought to prompt microembolism from the plaque in the area of borderzone of pial arteries. To suppress development of platelet thrombus on the ruptured plaque, strong antiplatelet therapy is required until the plaque stabilizes. Clinically dual antiplatelet therapy (DAPT) was reported to be more effective than mono therapy in suppressing microembolic signal in the middle cerebral artery. In addition, recent CHANCE trial reported that DAPT with aspirin and clopidogrel for the first 21 days is more effective in suppressing stroke recurrence than aspirin alone. Risk of cerebral hemorrhage was not enhanced in the DAPT group. Short term DAPT in the acute phase may soon be a standard treatment for acute atherothrombosis. For prevention of cardioembolism in patients with atrial fibrillation, new oral anticoagulants (NOAC) have recently been introduced. In cases where risk of hemorrhagic transformation is minimal, immediate anticoagulation with NOAC may provide clinical benefit including prompt anticoagulant effect, no need for drug dosing, and low risk of intracerebral hemorrhage.