ASSOCIATION OF BODY MASS INDEX WITH CLOPIDOGREL RESISTANCE

Authors

  • Usman Nawaz PhD Scholar, Pharmacology Department, Amry Medical College, National University of Medical sciences (NUMS) Rawalpindi
  • Mudassar Noor Assistant Professor, Pharmacology Department Army Medical College, National University of Medical sciences (NUMS) Rawalpindi 
  • Chaudhry Altaf Consultant Hematologist, Armed Focres Institute of Pathology (AFIP), National University of Medical sciences (NUMS) Rawalpindi
  • Akbar Waheed Professor of Pharmacology and PhD supervisor, Pharmacology Department, Amry Medical College, National University of Medical sciences (NUMS) Rawalpindi
  • Saleem Ahmad Khan Principal & Dean Army Medical College, Professor of Pathology, National University of Medical Sciences (NUMS) Rawalpindi

DOI:

https://doi.org/10.69656/pjp.v14i3.305

Keywords:

BMI, clopidogrel responders, clopidogrel resistance, Pakistan

Abstract

Background: Clopidogrel is an essential component of dual antiplatelet treatment for ischemic heart disease. We planned to explore the association of body mass index with clopidogrel resistance in ischemic heart disease patients. Methods: Three hundred and ninety patients of ischemic heart disease who were taking clopidogrel 75mg/day, were included in the study. Patients were categorized according to their body mass index (BMI) into underweight (BMI<18.50 Kg/m2), normal weight (BMI 18.50–22.99 Kg/m2), overweight (BMI 23.00–24.99 Kg/m2), and obese (BMI>25 Kg/m2). Their blood samples were taken and platelet aggregation studies were performed using Chronolog light transmission aggregometer to confirm clopidogrel resistant status. Results: None of the underweight, 19.50% of the normal weight, 24.20% of the overweight and 33.60% of the obese patients were found to be clopidogrel resistant. Clopidogrel resistance was significantly higher in obese patients as compared to normal weight patients, p=0.019. No significant difference in clopidogrel response was found between normal weight and overweight patients, as well as overweight and obese patients. Mean BMI of clopidogrel resistant patients was significantly higher than mean BMI of clopidogrel responders (26.46±3.82 vs 24.15±3.39 Kg/m2), p<0.001. Correlation between BMI and platelet aggregation was significant (p<0.001, r=0.20). Conclusion: BMI is inversely related to the platelet inhibition by clopidogrel. Higher BMI is related to clopidogrel resistance in ischemic heart disease patients.

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References

1. Bashir S, Poornima R. Pharmacogenetic variations related to clopidogrel resistance and its clinical implications: An issue which remains largely unaddressed. . Asian J Pharm Clin Res 2016;9(5):194–6.
2. Gallotta A, Marengoni A, Pasina L, Cortesi L, Nobili A. Prevalence of older in-patients at risk of clopidogrel resistance according to the STIB score. Results from REPOSI registry. Eur J Intern Med 2017;41:e17–8.
3. Wu ZK, Wang JJ, Wang T, Zhu SS, Chen XL, Liu C, et al. Clopidogrel resistance response in patients with coronary artery disease and metabolic syndrome: the role of hyperglycemia and obesity. J Geriatr Cardiol 2015;12(4):378–82.
4. Wang ZJ, Zhou YJ, Liu YY, Yu M, Shi DM, Zhao YX, et al. Impact of clopidogrel resistance on thrombotic events after percutaneous coronary intervention with drug-eluting stent. Thromb Res 2009;124(1):46–51.
5. Cui G, Zhang S, Zou J, Chen Y, Chen H. P2Y12 receptor gene polymorphism and the risk of resistance to clopidogrel: A meta-analysis and review of the literature. Adv Clin Exp Med 2017;26(2):343–9.
6. Bonello-Palot N, Armero S, Paganelli F, Mancini J, De Labriolle A, Bonello C, et al. Relation of body mass index to high on-treatment platelet reactivity and of failed clopidogrel dose adjustment according to platelet reactivity monitoring in patients undergoing percutaneous coronary intervention. Am J Cardiol 2009;104:1511–5.
7. Al-Azzam SI, Alzoubi KH, Khabour OF, Nusair MB, Al-Hadidi H, Awidi A, et al. Factors that contribute to clopidogrel resistance in cardiovascular disease patients: environmental and genetic approach. Int J Clin Pharmacol Ther 2013;51(3):179–86.
8. Shetkar SS, Ramakrishnan S, Seth S, Chandna P, Verma SK, Bhargava B, et al. CYP 450 2C19 polymorphisms in Indian patients with coronary artery disease. Indian Heart J 2014;66(1):16–24.
9. Shalia KK, Shah VK, Pawar P, Divekar SS, Payannavar S. Polymorphisms of MDR1, CYP2C19 and P2Y12 genes in Indian population: Effects on clopidogrel response. Indian Heart J 2013;65(2):158–67.
10. Humayun A, Shah AS, Alam S, Hussein H. Relationship of body mass index and dyslipidemia in different age groups of male and female population of Peshawar. J Ayub Med Coll Abbottabad 2009;21(2):141–4.
11. Angiolillo DJ, Fernandez-Ortiz A, Bernardo E, Ramírez C, Sabaté M, Jimenez-Quevedo P, et al. Platelet function profiles in patients with type 2 diabetes and coronary artery disease on combined aspirin and clopidogrel treatment. Diabetes 2005;54:2430–5.
12. Gurbel PA, Tantry US. Clopidogrel resistance? Thromb Res 2007;120(3):311–21.
13. Kumar S, Saran RK, Puri A, Gupta N, Sethi R, Surin WR, et al. Profile and prevalence of clopidogrel resistance in patients of acute coronary syndrome. Indian Heart J 2006;59(2):152–6.
14. Bliden KP, DiChiara J, Tantry US, Bassi AK, Chaganti SK, Gurbel PA. Increased risk in patients with high platelet aggregation receiving chronic clopidogrel therapy undergoing percutaneous coronary intervention. J Am Coll Cardiol 2007;49(6):657–66.
15. Peng Fei, Xing Yan-hui MS. Analysis of clopidogrel resistance and its influencing factors in patients with ischemic stroke and transient ischemic attack. Chinese J Clin Neurosci 2017;3:10.
16. Feher G, Koltai K, Alkonyi B, Papp E, Keszthelyi Z, Kesmarky G, et al. Clopidogrel resistance: role of body mass and concomitant medications. Int J Cardiol 2007;120(2):188–92.
17. Wang L, Wang X, Chen F. Clopidogrel resistance is associated with long-term thrombotic events in patients implanted with drug-eluting stents. Drugs in R & D 2010;10(4):219–24.
18. Dentali F, Squizzato A, Ageno W. The metabolic syndrome as a risk factor for venous and arterial thrombosis. Semin Thromb Hemost 2009;35(5):451–7.
19. Nieuwdorp M, Stroes ES, Meijers JC, Büller H. Hypercoagulability in the metabolic syndrome. Curr Opin Pharmacol 2005;5(2):155–9.
20. Anfossi G, Russo I, Trovati M. Platelet dysfunction in central obesity. Nutr Metab Cardiovasc Dis 2009;19(6):440–9.
21. Konstantinides S, Schäfer K, Koschnick S, Loskutoff DJ. Leptin-dependent platelet aggregation and arterial thrombosis suggests a mechanism for atherothrombotic disease in obesity. J Clin Invest 2001;108(10):1533–40.
22. Davì G, Guagnano MT, Ciabattoni G, Basili S, Falco A, Marinopiccoli M, et al. Platelet activation in obese women: role of inflammation and oxidant stress. JAMA 2002;288:2008–14.
Pak J Physiol 2018;14(3)

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Published

09-08-2018

How to Cite

1.
Nawaz U, Noor M, Altaf C, Waheed A, Khan SA. ASSOCIATION OF BODY MASS INDEX WITH CLOPIDOGREL RESISTANCE. Pak J Phsyiol [Internet]. 2018 Aug. 9 [cited 2024 Nov. 24];14(3):50-3. Available from: https://pjp.pps.org.pk/index.php/PJP/article/view/305

Issue

Vol. 14 No. 3 (2018): Pakistan Journal of Physiology

Section

Original Article

License

Pakistan Journal of Physiology, Pak J Physiol, PJP is FREE for research and academic purposes. It can be freely downloaded and stored, printed, presented, projected, cited and quoted with full reference of, and acknowledgement to the author(s) and the PJP. The contents are published with an international CC-BY-ND-4.0 License.