Purpose of review: While chronic risk factors for stroke are reasonably well understood, the acute precipitants, or triggers, of stroke, remain relatively understudied.
Recent findings: Several converging lines of evidence indicate that transient perturbations in systemic metabolism may provoke the onset of cardiovascular events, including stroke. Epidemiologic data, including studies utilizing novel designs that consider intraindividual differences across different time periods, have been used to clarify triggers for myocardial ischemia, and these methods are beginning to be employed in stroke research. Acute infections, particularly upper respiratory infections, and other inflammatory stimuli have emerged as important triggers of acute ischemic stroke. The mechanisms involved include immunologically mediated activation of platelets and endothelial dysfunction. There also appears to be a period of time, or 'stroke-prone state', characterized by diffuse activation of the vasculature during which patients may be at increased risk of initial and recurrent ischemic events.
Summary: Confirmation of these findings in further studies may help elucidate the mechanisms behind this short-term increase in stroke risk. Improved methods of assessment of this period of heightened susceptibility could lead to more temporally focused preventive interventions.