Patients who survive a stroke have an increased risk for recurrent vascular events. The mechanisms underlying the events are barely understood. A recent study suggests that stroke-enhanced atherosclerosis is induced through brain-released alarmins, which lead to systemic vascular inflammation and plaque formation. Interfering with these processes may lead to novel therapeutic approaches. Patients who survive a stroke have an increased risk for recurrent vascular events. The mechanisms underlying the events are barely understood. A recent study suggests that stroke-enhanced atherosclerosis is induced through brain-released alarmins, which lead to systemic vascular inflammation and plaque formation. Interfering with these processes may lead to novel therapeutic approaches.
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