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Gut Microbiota–Dependent Trimethylamine N-Oxide Predicts Risk of Cardiovascular Events in Patients With Stroke and Is Related to Proinflammatory Monocytes

Arteriosclerosis, thrombosis, and vascular biology, 2018-09, Vol.38 (9), p.2225-2235 [Peer Reviewed Journal]

2018 American Heart Association, Inc. ;ISSN: 1079-5642 ;EISSN: 1524-4636 ;DOI: 10.1161/ATVBAHA.118.311023 ;PMID: 29976769

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Title:
Gut Microbiota–Dependent Trimethylamine N-Oxide Predicts Risk of Cardiovascular Events in Patients With Stroke and Is Related to Proinflammatory Monocytes
Author: Haghikia, Arash ; Li, Xinmin S ; Liman, Thomas G ; Bledau, Nils ; Schmidt, David ; Zimmermann, Friederike ; Kränkel, Nicolle ; Widera, Christian ; Sonnenschein, Kristina ; Haghikia, Aiden ; Weissenborn, Karin ; Fraccarollo, Daniela ; Heimesaat, Markus M ; Bauersachs, Johann ; Wang, Zeneng ; Zhu, Weifei ; Bavendiek, Udo ; Hazen, Stanley L ; Endres, Matthias ; Landmesser, Ulf
Subjects: Animals ; Antigens, CD ; Antigens, Differentiation, T-Lymphocyte ; Brain Ischemia - complications ; Brain Ischemia - metabolism ; Cardiovascular Diseases - etiology ; CD4 Antigens ; Death, Sudden, Cardiac - etiology ; Female ; Gastrointestinal Microbiome - physiology ; Humans ; Inflammation ; Male ; Methylamines - blood ; Mice, Inbred C57BL ; Monocytes - immunology ; Monocytes - metabolism ; Prospective Studies ; Recurrence ; Risk Factors ; Stroke - complications ; Stroke - metabolism
Is Part Of: Arteriosclerosis, thrombosis, and vascular biology, 2018-09, Vol.38 (9), p.2225-2235
Description: OBJECTIVE—Gut microbiota–dependent metabolites, in particular trimethylamine N-oxide (TMAO), have recently been reported to promote atherosclerosis and thrombosis. Here, we examined for the first time the relation of TMAO and the risk of incident cardiovascular events in patients with recent first-ever ischemic stroke in 2 independent prospective cohorts. Moreover, the link between TMAO and proinflammatory monocytes as a potential contributing factor for cardiovascular risk in stroke patients was studied. APPROACH AND RESULTS—In a first study (n=78), higher TMAO plasma levels were linked with an increased risk of incident cardiovascular events including myocardial infarction, recurrent stroke, and cardiovascular death (fourth quartile versus first quartile; hazard ratio, 2.31; 95% CI, 1.25–4.23; P<0.01). In the second independent validation cohort (n=593), high TMAO levels again heralded marked increased risk of adverse cardiovascular events (fourth quartile versus first quartile; hazard ratio, 5.0; 95% CI, 1.7–14.8; P<0.01), and also after adjustments for cardiovascular risk factors including hypertension, diabetes mellitus, LDL (low-density lipoprotein) cholesterol, and estimated glomerular filtration rate (hazard ratio, 3.3; 95% CI, 1.2–10.9; P=0.04). A significant correlation was also found between TMAO levels and percentage of proinflammatory intermediate CD14CD16 monocytes (r=0.70; P<0.01). Moreover, in mice fed a diet enriched with choline to increase TMAO synthesis, levels of proinflammatory murine Ly6C monocytes were higher than in the chow-fed control group (choline9.2±0.5×10 per mL versus control6.5±0.5×10 per mL; P<0.01). This increase was abolished in mice with depleted gut microbiota (choline+antibiotics5.4±0.7×10 per mL; P<0.001 versus choline). CONCLUSIONS—The present study demonstrates for the first time a graded relation between TMAO levels and the risk of subsequent cardiovascular events in patients with recent prior ischemic stroke. Our data support the notion that TMAO-related increase of proinflammatory monocytes may add to elevated cardiovascular risk of patients with increased TMAO levels.
Publisher: United States: American Heart Association, Inc
Language: English
Identifier: ISSN: 1079-5642
EISSN: 1524-4636
DOI: 10.1161/ATVBAHA.118.311023
PMID: 29976769
Source: GFMER Free Medical Journals
MEDLINE
Alma/SFX Local Collection

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Gut Microbiota–Dependent Trimethylamine N-Oxide Predicts Risk of Cardiovascular Events in Patients With Stroke and Is Related to Proinflammatory Monocytes

2018 American Heart Association, Inc. ;ISSN: 1079-5642 ;EISSN: 1524-4636 ;DOI: 10.1161/ATVBAHA.118.311023 ;PMID: 29976769

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