Matthew J Pommerening1, Jessica C Cardenas1, Zayde A Radwan1, Charles E Wade1, John B Holcomb1, Bryan A Cotton2. 1. Department of Surgery and the Center for Translational Injury Research, The University of Texas Health Science Center, Houston, Texas. 2. Department of Surgery and the Center for Translational Injury Research, The University of Texas Health Science Center, Houston, Texas. Electronic address: bryan.a.cotton@uth.tmc.edu.
Abstract
BACKGROUND: Energy drink consumption in the United States has more than doubled over the last decade and has been implicated in cardiac arrhythmias, myocardial infarction, and even sudden cardiac death. We hypothesized that energy drink consumption may increase the risk of adverse cardiovascular events by increasing platelet aggregation, thereby resulting in a relatively hypercoagulable state and increased risk of thrombosis. METHODS: Thirty-two healthy volunteers aged 18-40 y were given 16 oz of bottled water or a standardized, sugar-free energy drink on two separate occasions, 1-wk apart. Beverages were consumed after an overnight fast over a 30-min period. Coagulation parameters and platelet function were measured before and 60 min after consumption using thrombelastography and impedance aggregometry. RESULTS: No statistically significant differences in coagulation were detected using kaolin or rapid thrombelastography. In addition, no differences in platelet aggregation were detected using ristocetin, collagen, thrombin receptor-activating peptide, or adenosine diphosphate-induced multiple impedance aggregometry. However, compared to water controls, energy drink consumption resulted in a significant increase in platelet aggregation via arachidonic acid-induced activation (area under the aggregation curve, 72.4 U versus 66.3 U; P = 0.018). CONCLUSIONS: Energy drinks are associated with increased platelet activity via arachidonic acid-induced platelet aggregation within 1 h of consumption. Although larger clinical studies are needed to further address the safety and health concerns of these drinks, the increased platelet response may provide a mechanism by which energy drinks increase the risk of adverse cardiovascular events.
BACKGROUND: Energy drink consumption in the United States has more than doubled over the last decade and has been implicated in cardiac arrhythmias, myocardial infarction, and even sudden cardiac death. We hypothesized that energy drink consumption may increase the risk of adverse cardiovascular events by increasing platelet aggregation, thereby resulting in a relatively hypercoagulable state and increased risk of thrombosis. METHODS: Thirty-two healthy volunteers aged 18-40 y were given 16 oz of bottled water or a standardized, sugar-free energy drink on two separate occasions, 1-wk apart. Beverages were consumed after an overnight fast over a 30-min period. Coagulation parameters and platelet function were measured before and 60 min after consumption using thrombelastography and impedance aggregometry. RESULTS: No statistically significant differences in coagulation were detected using kaolin or rapid thrombelastography. In addition, no differences in platelet aggregation were detected using ristocetin, collagen, thrombin receptor-activating peptide, or adenosine diphosphate-induced multiple impedance aggregometry. However, compared to water controls, energy drink consumption resulted in a significant increase in platelet aggregation via arachidonic acid-induced activation (area under the aggregation curve, 72.4 U versus 66.3 U; P = 0.018). CONCLUSIONS: Energy drinks are associated with increased platelet activity via arachidonic acid-induced platelet aggregation within 1 h of consumption. Although larger clinical studies are needed to further address the safety and health concerns of these drinks, the increased platelet response may provide a mechanism by which energy drinks increase the risk of adverse cardiovascular events.
Authors: Ryan A Grant; Branden J Cord; Lovemore Kuzomunhu; Kevin Sheth; Emily Gilmore; Charles C Matouk Journal: Interv Neuroradiol Date: 2016-08-01 Impact factor: 1.610
Authors: Dimitra Rafailia Bakaloudi; Kleo Evripidou; Ranil Jayawardena; João Breda; Theodoros Dardavessis; Kalliopi-Anna Poulia; Michail Chourdakis Journal: Int J Environ Res Public Health Date: 2022-04-26 Impact factor: 4.614