Current Antiplatelet Treatment Strategy in Patients with Diabetes Mellitus

Abstract

Patients with diabetes mellitus (DM) have accelerated atherosclerosis with an increased risk for atherothrombotic cardiovascular complications. A state of high platelet reactivity and activation, hypercoagulability (prothrombotic state) and a subdued response to standard antiplatelet agents may explain high rate of adverse cardiovascular events in patients with DM. Several antithrombotic treatment strategies have been developed to control the prothrombotic state in patients with DM: dose modification of commonly used agents; use of potent agents; and addition of a third antithrombotic drug (triple therapy) to commonly prescribed dual antiplatelet therapy of aspirin and a P2Y12 inhibitor. The present review aims to provide an overview of the current knowledge on platelet abnormalities in patients with DM, focusing on the challenges and perspectives of antiplatelet treatment strategies in this population.

Aortic thrombosis in dogs

“…In people, DM is associated with an increased risk of thrombosis, most commonly coronary artery disease and cerebrovascular events . In addition to the increased incidence of atherosclerosis, platelets in patients with DM appear to be hyperreactive, leading to increased adhesion, activation, and aggregation . Multiple mechanisms are theorized to contribute to increased platelet activity, including excess fatty acid synthesis, increased P‐selectin expression, osmotic effects secondary to hyperglycemia, increased protein kinase C activity, and glycosylation of platelet surface proteins .…”

“…In addition to the increased incidence of atherosclerosis, platelets in patients with DM appear to be hyperreactive, leading to increased adhesion, activation, and aggregation . Multiple mechanisms are theorized to contribute to increased platelet activity, including excess fatty acid synthesis, increased P‐selectin expression, osmotic effects secondary to hyperglycemia, increased protein kinase C activity, and glycosylation of platelet surface proteins . Decreased insulin activity is associated with depressed response to antithrombotic molecules, including prostacyclin and nitric oxide as well as increased intraplatelet calcium concentration, leading to heightened degranulation activity .…”

“…Multiple mechanisms are theorized to contribute to increased platelet activity, including excess fatty acid synthesis, increased P‐selectin expression, osmotic effects secondary to hyperglycemia, increased protein kinase C activity, and glycosylation of platelet surface proteins . Decreased insulin activity is associated with depressed response to antithrombotic molecules, including prostacyclin and nitric oxide as well as increased intraplatelet calcium concentration, leading to heightened degranulation activity . Upregulation of glycoprotein IIb/IIIa expression and signaling has also been documented …”

“…Decreased insulin activity is associated with depressed response to antithrombotic molecules, including prostacyclin and nitric oxide as well as increased intraplatelet calcium concentration, leading to heightened degranulation activity . Upregulation of glycoprotein IIb/IIIa expression and signaling has also been documented …”

Resistance to Antiplatelet Drugs in Patients With Cerebrovascular Disease

“…In our cohort, patients with diabetes had a higher propensity towards biochemical clopidogrel resistance whereas association with aspirin resistance was not found. Diabetes, elevated Hb1Ac were previously found to be associated with increased prevalence of clopidogrel resistance (Sakr et al, 2016;Jung, Tantry, Gurbel, &Jeong, 2015). However, data of association between diabetes and aspirin resistance are controversial.…”