Aspirin resistance in stable angina patients with type 2 diabetes mellitus: Clinical and hemostatic determinants
Republican specialized scientific practical medical center of therapy and medical rehabilitation, Tashkent, Uzbekistan.
Review
World Journal of Advanced Pharmaceutical and Life Sciences, 2026, 10(02), 001-010.
Article DOI: 10.53346/wjapls.2026.10.2.0012
Publication history:
Received on 10 February 2026; revised on 24 March 2026; accepted on 27 March 2026
Abstract:
Background: Aspirin remains a cornerstone of secondary prevention in patients with stable angina; however, a substantial proportion of patients with type 2 diabetes mellitus (T2DM) exhibit reduced responsiveness to aspirin therapy. This phenomenon, commonly referred to as aspirin resistance or aspirin hyporesponsiveness, is associated with persistent platelet activation, impaired primary hemostasis control, and increased residual ischemic risk. In patients with stable coronary artery disease and T2DM, the problem is particularly relevant because diabetes promotes a prothrombotic milieu through platelet hyperreactivity, endothelial dysfunction, oxidative stress, chronic inflammation, and altered blood rheology.
Objective: To review current evidence on the clinical and hemostatic determinants of aspirin resistance in patients with stable angina and T2DM, with particular emphasis on mechanisms of primary hemostatic dysfunction, laboratory assessment, and therapeutic implications.
Main body: This review analyzes the pathophysiological basis of impaired aspirin response in T2DM, including enhanced platelet turnover, increased thromboxane-dependent and thromboxane-independent platelet activation, metabolic dysregulation, and inflammatory signaling. Special attention is given to hemostatic determinants such as platelet aggregation abnormalities, erythrocyte aggregation, coagulation disturbances, and endothelial dysfunction, all of which may contribute to reduced antiplatelet efficacy. Clinical factors including poor glycemic control, obesity, hypertension, dyslipidemia, chronic kidney disease, and treatment-related variables are also examined. The review further summarizes current laboratory methods for assessing aspirin responsiveness and discusses their strengths and limitations in routine clinical practice.
Conclusion: Aspirin resistance in stable angina patients with T2DM is a multifactorial clinical and biological phenomenon reflecting the complex interaction between cardiometabolic abnormalities and hemostatic dysregulation. Better recognition of its determinants may improve risk stratification and support more individualized antiplatelet strategies in this high-risk population.
Keywords:
Aspirin resistance; Aspirin hyporesponsiveness; Stable angina; Type 2 diabetes mellitus; Platelet aggregation; Primary hemostasis; Erythrocyte aggregation; Antiplatelet therapy; Chronic coronary syndrome; Thrombosis
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