Abstract

Objective: Clopidogrel therapy is the standard of care in patients with unstable angina. However, a percentage of subjects are nonresponders to clopidogrel and this leads to increased adverse outcome. On the other way round, some responsive patients are exposed to bleeding complications. Detection of both in daily practice is important in order to tailor the treatment protocol. In this study we aimed to estimate the cutoff value of mean platelet volume (MPV) for both platelet responsiveness and bleeding risks. Methods: The study was planned as a prospective cohort study. A total number of 230 patients admitted to our CCU with unstable angina over a period of one year (from June 2013 to May 2014) were enrolled. Exclusion criteria were: severe anemia, throm-bocytopenia, myelodysplastic syndrome, coagulopathy and recent blood transfusion. In all patients clopidogrel was initially started and maintained during the hospital stay. Blood (2 ml) was collected in dipotassium EDTA tubes from all patients on the first day of admission by a clean puncture. Samples for MPV analysis were drawn on admission, and analyzed within 1 hour of admission after sampling by Beckman Caulter LH 780 Analyzer. Grouping was then done according to MPV of the patients into group (I) who had a low MPV less than or equal to 7.00 fl, and group (II) with MPV equal to or higher than 9.00 fl. Demographical and clinical variables of the patients were recorded. Routine laboratory parameters were also recorded. Clinical manifestations during the admission period were meticulously reported. Major complications as bleeding or, urgent need for percutaneous coronary intervention (PCI) were also studied. Results: Among the 230 patients analyzed, 175 patients (76%) were found to have MPV ≤7.00 fl (group (I)) and 55 patients (24%) had MPV ≥9.00 fl (group (II)) with mean ± SD MPV (8.4 ± 1.5 fl, vs 11.7 ± 1.2 fl respectively) (p < 0.001). Observation of clinical course during admission period revealed a statistically more significant clinical deterioration in group (II) than group (I) and the presence of more frequent AMI cases in group (II) having a high MPV. A high cutoff value of 9.7 fl for MPV was detected in prediction of clopidogrel nonresponsiveness (group (II)) with a sensitivity of 78.2% and specificity of 66.8%, and a low cutoff value for bleeding tendency lower than 6.3 fl was detected in group (I) with a sensitivity of 71.4% and specificity of 62.5%. Conclusion: This study showed that MPV can be used as a simple bedside predictor for detection of clopidogrel response in patients with unstable angina. And a cutoff value for both platelet responsiveness and risk of bleeding is now reached. This may lead to enhancement in our decision for early intervention and attention for bleeding risk during clopidogrel therapy.

Highlights

  • Platelets are non-nucleated blood cells which play a crucial role in the process of coagulation. Their function is strongly associated with atherogenesis and atherothrombosis which are important in pathogenesis of cardiovascular diseases [1]

  • Platelets have been implicated in the pathogenesis of cardiovascular disorders, including atherosclerosis and its complications, such as acute myocardial infarction (AMI), unstable angina (UA), and sudden cardiac death

  • Study design: This study was designed as a prospective cohort study for estimating the diagnostic accuracy of mean platelet volume (MPV) in determining the course and prognosis of patients with unstable angina

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Summary

Introduction

Platelets are non-nucleated blood cells which play a crucial role in the process of coagulation. Their function is strongly associated with atherogenesis and atherothrombosis which are important in pathogenesis of cardiovascular diseases [1]. Coronary artery disease (CAD) is looming large as the new epidemic disease. Both endogenous and exogenous risk factors such as smoking, diabetes mellitus, hypertension, hypercholesterolaemia, mental stress, and obesity, acting either singly or in combination, significantly increase the chances of developing coronary atherosclerosis [2]. Platelet hyper-reactivity and local platelet activation have been suggested to play a causal role in acute coronary events [2]

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