Current and future concepts in stroke prevention

Abstract

Stroke is a major cause of morbidity and mortality in an aging population. The current understanding of the pathophysiology of atherosclerotic diseases, the most common cause of stroke, and the evidence for existing therapeutic interventions for the prevention of stroke are presented. Specifically, we review the evidence for antiplatelet agents, anticoagulants, antihypertensive medications, lipid-lowering agents and carotid endarterectomy for stroke prevention.

Fig. 1: The role of inflammatory processes in thrombus formation and plaque rupture. Leukocytes localize in the earliest atherosclerotic lesions, binding to vascular cell adhesion molecules (VCAM-1) on the vascular endothelium and migrating into the intima. This initiates and perpetuates a local inflammatory response. Monocytes mature into lipid-scavenging macrophages and subsequently foam cells. T-lymphocytes express inflammatory cytokines, which continue to stimulate macrophages and endothelial cells and further proliferation of smooth muscle cells. Later, macrophages produce proteolytic enzymes that degrade the collagen of the plaque's fibrous cap, making it susceptible to rupture, and produce procoagulant tissue factor, which triggers plaque thrombosis. Photo: Christine Kenney

Fig. 2: Platelet aggregation and subsequent thrombosis may be prevented by several mechanisms and agents. ASA blocks platelet cyclooxygenase and the formation of thromboxane A₂, while the thienopyridines block adenosine-diphosphate–mediated aggregation. Photo: Christine Kenney