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Association of weight gain with coronary artery disease, inflammation and thrombogenicity

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Abstract

Obese individuals, despite having increased cardiovascular (CV) risk factors experience adverse CV outcomes less frequently than non-obese. Little is known about association of long-term weight gain to development of coronary artery disease (CAD), inflammation and thrombogenicity. 418 consecutive patients with suspected CAD undergoing elective cardiac catheterization were included in a sub-analysis of the multi analyte, thrombogenic, and genetic markers of atherosclerosis study. Maximum weight gain (MWG) was defined as percentage increase in weight since age 17 years to year of heaviest weight and categorized as: minor (<30 %), moderate (30–47 %), severe (>47–69 %), and extreme (>69 %). Lipid profiling was determined by vertical density gradient ultracentrifugation, thrombin-induced platelet fibrin clot strength (TIP–FCS) by thrombelastography, and urinary 11-dehydrothromboxane B2 (11-dhTxB2) by ELISA. CAD severity was defined as minimal (<20 %), moderate (20–75 %), and severe (>75 %) luminal diameter obstruction of any major coronary vessel. The mean MWG was 53 ± 33 %. Extreme MWG group had a higher incidence of diabetes mellitus (48 %), hypertension (81 %), depression (25 %), and were most often female (60 %) (p < 0.05 for all). In women, CAD severity was inversely associated to MWG (p = 0.05), whereas in men no such association was observed (p = 0.18). TIP–FCS increased in a stepwise fashion with MWG (p = 0.001). 11-dTxB2 levels were higher in the extreme MWG group, regardless of lipid lowering therapy (p < 0.05). Our data suggest that maximal weight gain since age 17 years is associated with heightened thrombogenicity, inflammation and a poorer lipid profile but not an increased risk for severe CAD development.

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Acknowledgments

This study was supported by Platelet and Thrombosis Research, LLC and Haemonetics. VAP© testing was provided by Atherotech® Inc. Urinary 11-dehydrothromboxane B2 and AtherOx testing were provided by Corgenix Medical Corp. We wish to acknowledge Tania Gesheff, RN, MSN, Kiran Kalra, MBBS, and Cescelle Barbour RN, MSN for their contributions to this study.

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Authors and Affiliations

  1. Inova Center for Thrombosis Research and Drug Development, Inova Heart and Vascular Institute, 3300 Gallows Rd. Falls Church, Fairfax, VA, 22042, USA

    Rahul Chaudhary, Kevin P. Bliden, Udaya S. Tantry, Nafees Mohammed, Denny Mathew, Martin G. Gesheff, Christopher J. Franzese & Paul A. Gurbel

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  1. Rahul Chaudhary
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  2. Kevin P. Bliden
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Correspondence to Paul A. Gurbel.

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Conflicts of interest

Dr. Gurbel reports serving as a consultant for Daiichi Sankyo/Lilly, Bayer, AstraZeneca, Accumetrics, Merck, Medtronic, Janssen, CSL, and Haemonetics; receiving grants from the National Institutes of Health, Daiichi Sankyo, Lilly, CSL, AstraZeneca, Haemetics, Harvard Clinical Research Institute, and Duke Clinical Research Institute; receiving payment for lectures, including service on speakers’ bureaus, from Lilly, Daiichi Sankyo, and Merck; receiving payment for development of educational presentations from Merck, the Discovery Channel, and Pri-Med; Dr. Gurbel is holding stock or stock options in Merck, Medtronic, and Pfizer; and holding patents in the area of personalized antiplatelet therapy and interventional cardiology. Dr. Gurbel has received consulting fees from Corgenix Medical Corp. Dr. Toth reports either serving as a consultant and/or on speakers’ bureau for Amarin, GSK, Aegerion, Amgen, AstraZeneca, Kowa, Liposcience, and Merck. No other authors report any potential conflicts of interest.

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Chaudhary, R., Bliden, K.P., Tantry, U.S. et al. Association of weight gain with coronary artery disease, inflammation and thrombogenicity. J Thromb Thrombolysis 41, 394–403 (2016). https://doi.org/10.1007/s11239-015-1327-y

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  • DOI: https://doi.org/10.1007/s11239-015-1327-y

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