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Volume 123, Issue 2, Pages 184-187 (February 2010)


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Detrimental Effects of Energy Drink Consumption on Platelet and Endothelial Function

Matthew I. Worthley, MBBS, PhD, Anisha Prabhu, BSc(Hons), Paolo De Sciscio, BHSci(Hons), Carlee Schultz, BHSci, Prashanthan Sanders, MBBS, PhD, Scott R. Willoughby, PhDCorresponding Author Informationemail address

Abstract 

Background

Energy drink consumption has been anecdotally linked with sudden cardiac death and, more recently, myocardial infarction. As myocardial infarction is strongly associated with both platelet and endothelial dysfunction, we tested the hypothesis that energy drink consumption alters platelet and endothelial function.

Methods

Fifty healthy volunteers (34 male, aged 22±2 years) participated in the study. Platelet aggregation and endothelial function were tested before, and 1 hour after, the consumption of 250 mL (1 can) of a sugar-free energy drink. Platelet function was assessed by adenosine diphosphate-induced (1 μmol/L) optical aggregometry in platelet-rich plasma. Endothelial function was assessed via changes in peripheral arterial tonometry and expressed as the reactive hyperemia index (RHI).

Results

Compared with baseline values, there was a significant increase in platelet aggregation following energy drink consumption, while no change was observed with control (13.7±3.7% vs 0.3±0.8% aggregation, respectively, P <.01). Similarly, RHI decreased following energy drink consumption (−0.33±0.13 vs 0.07±0.12 RHI [control], P <.05). Mean arterial pressure significantly increased following energy drink consumption, compared with control (P <.05). Heart rate was unaffected by energy drink consumption.

Conclusion

Energy drink consumption acutely increases platelet aggregation and decreases endothelial function in healthy young adults.

Department of Cardiology, Cardiovascular Research Centre, Royal Adelaide Hospital, and Disciplines of Physiology and Medicine, University of Adelaide, Adelaide, Australia

Corresponding Author InformationRequests for reprints should be addressed to Scott Willoughby, PhD, Department of Cardiology, Cardiovascular Research Centre, Level 5 McEwin Building, Royal Adelaide Hospital, Adelaide SA 5000, Australia

 Funding: Dr. Sanders is supported by the National Heart Foundation of Australia.

 Conflict of Interest: No author has a conflict of interest with this work.

 Authorship: All authors have had access to the data and a role in the manuscript.

PII: S0002-9343(09)00874-2

doi:10.1016/j.amjmed.2009.09.013


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