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Gut microbiome and its role in cardiovascular diseases

Ahmadmehrabi, Shadia; Tang, W.H. Wilsonb,c

doi: 10.1097/HCO.0000000000000445
ISCHEMIC HEART DISEASE: Edited by Peter H. Stone

Purpose of review In recent years, an interest in intestinal microbiota–host interactions has increased due to many findings about the impact of gut bacteria on human health and disease. Dysbiosis, a change in the composition of the gut microbiota, has been associated with much pathology, including cardiovascular diseases (CVD). This article will review normal functions of the gut microbiome, its link to CVD, and potential therapeutic interventions.

Recent findings The recently discovered contribution of gut microbiota-derived molecules in the development of heart disease and its risk factors has significantly increased attention towards the connection between our gut and heart. The gut microbiome is virtually an endocrine organ, arguably the largest, capable of contributing to and reacting to circulating signaling molecules within the host. Gut microbiota–host interactions occur through many pathways, including trimethylamine-N-oxide and short-chain fatty acids. These molecules and others have been linked to much pathology including chronic kidney disease, atherosclerosis, and hypertension.

Summary Although our understanding of gut microbiota–host interactions has increased recently; many questions remain about the mechanistic links between the gut microbiome and CVD. With further research, we may one day be able to add gut microbiota profiles as an assessable risk factor for CVD and target therapies towards the gut microbiota.

aCleveland Clinic Lerner College of Medicine at Case Western Reserve University

bHeart and Vascular Institute

cCenter for Clinical Genomics, Cleveland Clinic, Cleveland, Ohio, USA

Correspondence to W.H. Wilson Tang, MD, 9500 Euclid Avenue, Desk J3–4, Cleveland, OH 44195, USA. Tel: +1 216 444 2121; fax: +1 216 445 6165; e-mail: tangw@ccf.org

Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved.