Abstract
Diabetes mellitus, particularly type 2 diabetes mellitus (T2DM), significantly elevates the risk of ischemic stroke through mechanisms involving chronic hyperglycemia, endothelial dysfunction, and a prothrombotic state. This review explores the interplay between T2DM and ischemic stroke, focusing on pathophysiological mechanisms, synergistic effects of comorbid conditions, and the implications of acute hyperglycemia in stroke outcomes. Chronic hyperglycemia in T2DM leads to oxidative stress, inflammation, and vascular changes that contribute to endothelial dysfunction, promoting atherosclerosis and increasing stroke risk. Furthermore, T2DM-associated prothrombotic states involve heightened platelet reactivity, altered coagulation factors, and impaired fibrinolysis, compounding the risk of thrombus formation and ischemic events. The coexistence of hypertension, dyslipidemia, and obesity further amplifies this risk, creating a cluster of interrelated metabolic abnormalities that exacerbate cerebrovascular damage. Acute hyperglycemia during ischemic stroke worsens outcomes by increasing infarct size, disrupting the blood-brain barrier, and exacerbating inflammation and oxidative stress. Management of hyperglycemia in acute stroke remains challenging, as intensive glucose control may lead to hypoglycemia without significantly improving outcomes. Emerging therapeutic strategies, including the use of GLP-1 receptor agonists and SGLT2 inhibitors, show promise in reducing cardiovascular complications and stroke risk while addressing glucose regulation and comorbid conditions. This review underscores the importance of integrated management strategies that address the multifactorial nature of T2DM and its complications to mitigate ischemic stroke risk and improve outcomes. Future research should focus on optimizing glycemic control strategies and exploring novel therapeutic interventions to target the complex interplay between T2DM and cerebrovascular disease.
Published Version
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