Abstract
Background
Resistance to antiplatelet therapy, especially aspirin or clopidogrel, triggers other therapies for patients with coronary heart disease (CHD). Enhanced external counterpulsation (EECP) is a noninvasive, pneumatic technique that provides beneficial effects for patients with CHD. However, the physiological effects of EECP have not been fully studied, and the role of EECP on platelet function remains poorly understood.
Methods
A total of 168 patients with CHD were finally selected from the Second Xiangya Hospital and randomly assigned to either a control group or EECP group. The control group accepted only standard medical treatment, while the EECP group accepted standard medical treatment and EECP treatment. Blood samples were collected from patients at baseline and after EECP, and platelet aggregation was assessed. Changes in platelet aggregation were compared before and after treatment.
Results
There was no difference in the basal levels of arachidonic acid (AA) induced platelet maximum aggregation ratio (MAR) between the two groups. The AA-induced platelet MAR was significantly decreased after EECP therapy. The logistic analysis showed that low HDL-C was not favorable for the decrease in platelet aggregation.
Conclusion
EECP therapy is favorable for lowering platelet aggregation in patients with CHD, especially the AA-induced platelet aggregation ratio.
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Change history
05 February 2021
A Correction to this paper has been published: https://doi.org/10.1007/s10557-021-07152-8
Abbreviations
- CHD:
-
Coronary heart disease
- LDL-C:
-
Low-density lipoprotein cholesterol
- HDL-C:
-
High-density lipoprotein cholesterol
- MAR:
-
Maximum aggregation ratio
- BMI:
-
Body mass index
- ACS:
-
Acute coronary syndromes
References
Antithrombotic Trialists’ Collaboration. Collaborative meta-analysis of randomized trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ. 2002;324:71–86.
Krasopoulos G, Brister SJ, Beattie WS, et al. Aspirin “resistance” and risk of cardiovascular morbidity: systematic review and meta-analysis. BMJ. 2008;336:195–8.
Snoep JD, Hovens MM, Eikenboom JC, et al. Association of laboratory-defined aspirin resistance with a higher risk of recurrent cardiovascular events: a systematic review and meta-analysis. Arch Intern Med. 2007;167:1593–9.
Baigent C, Blackwell L, Collins R, et al. Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomized trials. Lancet. 2009;373:1849–60.
Gasparyan AY, Watson T, Lip GY. The role of aspirin in cardiovascular prevention: implications of aspirin resistance. J Am Coll Cardiol. 2008;51:1829–43.
Bhatt DL, Fox KA, Hacke W, et al. Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events. N Engl J Med. 2006;354:1706–17.
Antithrombotic Trialists’ (ATT) Collaboration, Baigent C, Blackwell L, et al. Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomized trials. Lancet. 2009;373:1849–60.
Antithrombotic Trialists’ Collaboration. Collaboration meta-analysis of randomized trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high-risk patients. BMJ. 2002;324:71–86.
Hovens MM, Snoep JD, Eikenboom JC, et al. Prevalence of persistent platelet reactivity despite use of aspirin: a systematic review. Am Heart J. 2007;153(2):175–81.
Gurbel PA, Bliden KP, Hiatt BL, et al. Clopidogrel for coronary stenting: response variability, drug resistance, and the effect of pretreatment platelet reactivity. Circulation. 2003;107:2908–13.
Hennekens CH, Schror K, Weisman S, et al. Terms and conditions: semantic complexity and aspirin resistance. Circulation. 2004;110:1706–8.
Serebruany VL, Steinhubl SR, Berger PB, et al. Variability in platelet responsiveness to clopidogrel among 544 individuals. J Am Coll Cardiol. 2005;45:246–51.
Michaels AD, Accad M, Ports TA, et al. Left ventricular systolic unloading and augmentation of intracoronary pressure and Doppler flow during enhanced external counterpulsation. Circulation. 2002;106:1237–42.
Manchanda A, Soran O. Enhanced external counterpulsation and future directions: step beyond medical management for patients with angina and heart failure. J Am Coll Cardiol. 2007;50:1523–31.
Arora RR, Chou TM, Jain D, et al. The multicenter study of enhanced external counterpulsation (MUST-EECP): effect of EECP on exercise-induced myocardial ischemia and anginal episodes. J Am Coll Cardiol. 1999;33:1833–40.
Guan J, Cong Y, Ren J, et al. Comparison between a new platelet count drop method PL-11, light transmission aggregometry, VerifyNow aspirin system and thromboelastography for monitoring short-term aspirin effects in healthy individuals. Platelets. 2015;26(1):25–30.
Bonetti PO, Barsness GW, Keelan PC, et al. Enhanced external counterpulsation inproves endothelial function in patients with symptomatic coronary artery disease. J Am Coll Cardiol. 2003;41:1761–8.
Casey DP, Conti CR, Nichols WW, et al. Effect of enhanced external counterpulsation on inflammatory cytokines and adhesion molecules in patients with angina pectoris and angiographic coronary artery disease. Am J Cardiol. 2008;101:300–2.
Rubenstein DA, Yin W. Quantifying the effects of shear stress and shear exposure duration regulation on flow induced platelet activation and aggregation. J Thromb Thrombolysis. 2002;30:36–45.
Sheriff J, Bluestein D, Girdhar G, et al. High-shear stress sensitizes platelets to subsequent low-shear conditions. Ann Biomed Eng. 2010;38:1442–50.
Yin W, Shanmugavelayudam SK, Rubenstein DA. The effect of physiologically relevant dynamic shear stress on platelet and endothelial cell activation. Thromb Res. 2011 Mar;127(3):235–41.
Jastrzebska M, Chelstowski K, Wodecka A, et al. Factors influencing multiplate whole blood impedance platelet aggregometry measurements, during aspirin treatment in acute ischemic stroke: a pilot study. Blood Coagul Fibrinolysis. 2013;24(8):830–8.
Yeung J, Tourdot BE, Fernandez-Perez P, et al. Platelet 12-LOX is essential for FcγRIIa-mediated platelet activation. Blood. 2014;124(14):2271–9.
Acknowledgements
We thank all patients who participated in this study, Xiaoxiu Wang for platelet aggregation ratio measurement, and the Department of Clinical Laboratory, Second Xiangya Hospital, for their assistance.
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This work was supported by National Nature Scientific Funding of China (No. 81672264), and the Fundamental Research Funds for the Central Universities of Central South University (No.2018zzts260).
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Yating Wang and Danyan Xu designed the study, analyzed the data, and prepared the manuscript.
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Wang, Y., Xu, D. The Effect of Enhanced External Counterpulsation on Platelet Aggregation in Patients with Coronary Heart Disease. Cardiovasc Drugs Ther 36, 263–269 (2022). https://doi.org/10.1007/s10557-020-07140-4
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DOI: https://doi.org/10.1007/s10557-020-07140-4