Microbiota-Dependent Marker TMAO Is Elevated in Silent Ischemia but Is Not Associated With First-Time Myocardial Infarction in HIV Infection

Haissman, Judith M.; Knudsen, Andreas; Hoel, Hedda; Kjær, Andreas; Kristoffersen, Ulrik Sloth; Berge, Rolf K.; Katzenstein, Terese L.; Svardal, Asbjørn; Ueland, Thor; Aukrust, Pål; Lebech, Anne‐Mette; Nielsen, Susanne Dam; Trøseid, Marius

doi:10.1097/qai.0000000000000843

Cited by 42 publications

(34 citation statements)

References 36 publications

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“…21 Consistent with this, patients commenced on drugs known to modulate tubular function, such as anti-retroviral protease inhibitors 22 and calcineurin inhibitors 23 , may exhibit elevations in plasma TMAO or reduced urinary TMAO clearance. 22,23 Potential cell membrane transporters for TMAO uptake and efflux have been identified. Overexpression of organic cation transporter 2 (Oct2) in…”

Section: Tmao Metabolism In Mammalsmentioning

confidence: 81%

“…30 In another HIV cohort, higher plasma TMAO levels were associated with advanced age, reduced kidney function and use of protease inhibitors, but not with coronary artery calcium scores or myocardial infarction. 22 Study of humans with variants of the FMO3 gene could provide opportunities to assess the impact of reduced TMAO production on CV disease.…”

Section: Tmao As a Mediator Of CV Disease: Clinical Datamentioning

confidence: 99%

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The role of trimethylamine N-oxide as a mediator of cardiovascular complications in chronic kidney disease

Tomlinson

Wheeler

2017

Kidney International

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Patients with chronic kidney disease (CKD) have an enhanced risk of cardiovascular (CV) morbidity and mortality when compared to age and gender- Cardiovascular disease in CKD -Unexplained riskPatients with chronic kidney disease (CKD) have an enhanced risk of cardiovascular (CV) morbidity and mortality when compared to age and gendermatched individuals with normal kidney function. 1 Advanced kidney disease (stage G5A3; estimated glomerular filtration rate (eGFR) <15 mL/min/1.73m 2 , albumin:creatinine ratio >30 mg/mM) carries an 8-fold increased adjusted CV mortality risk when compared to subjects with no kidney disease. 2 Traditional CV risk factors such as hypertension and dyslipidaemia are frequently present in

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Section: Tmao Metabolism In Mammalsmentioning

confidence: 81%

Section: Tmao As a Mediator Of CV Disease: Clinical Datamentioning

confidence: 99%

The role of trimethylamine N-oxide as a mediator of cardiovascular complications in chronic kidney disease

Tomlinson

Wheeler

2017

Kidney International

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“…Srinivasa and colleagues found no association between TMAO levels and coronary plaque burden in a group of HIV-infected and uninfected participants, instead finding that levels of its biologic precursor, trimethylamine (TMA), were significantly associated with calcified plaque burden independent of cardiovascular risk factors [18]. Haissman et al similarly did not find differences in TMAO levels between those with and without HIV [19]. However, they did find elevated levels of TMAO in HIV-infected individuals with myocardial perfusion defects on stress testing, which may be consistent with our results as perfusion defects typically occur with coronary stenosis.…”

Section: Discussionmentioning

confidence: 99%

“…These findings prompted an investigation into the association of HIV infection and TMAO levels, which found no association [18]. More recently, Haissman et al similarly found to difference in TMAO levels between HIV-infected and uninfected individuals [19]. We therefore designed a case-control study to further explore the association between coronary atherosclerosis and TMAO levels among participants in the Multicenter AIDS Cohort Study (MACS).…”

Section: Introductionmentioning

confidence: 99%

Brief Report

Miller

Haberlen

Brown

et al. 2016

JAIDS Journal of Acquired Immune Deficiency Syndromes

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Recent evidence has shown a complex relationship between the gut microbiota, dietary nutrients, and cardiovascular disease (CVD). Trimethylamine-N-oxide (TMAO) production, initiated by the microbiota, has been associated with CVD events. We sought to test if this association exists in HIV-infected persons. After adjusting for aspirin use and CVD risk factors, HIV-infected men were more likely to have coronary stenosis in the second and third TMAO quartiles compared to the first quartile, but did not differ significantly in the fourth quartile. We found an inverted U-shaped association between TMAO levels and the presence of coronary artery stenosis among HIV-infected men.

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“…The metabolite Trimethylamine-N-oxide (TMAO), a derivative of Trimethylamine (TMA) that is produced as a waste product of carnitine and choline metabolism by intestinal bacteria, is strongly linked to increased risk for CVD[76-78]. Given that HIV-1 infection is associated with both microbiome changes and with increased CVD risk, a number of recent studies have investigated potential links between TMAO and various aspects of CVD in HIV-1 infected individuals[79-82]. In these pilot studies with relatively small sample sizes, serum and plasma levels of TMAO were not higher in HIV-1 infected study participants compared to uninfected controls and limited evidence for an important role of TMAO in the pathogenesis of coronary heart disease in HIV-1 infected individuals was observed.…”

Section: Linking Alterations In Microbe-associated Metabolites To Hivmentioning

confidence: 99%

The gut microbiome and HIV-1 pathogenesis

Dillon

Frank²,

Wilson³

2016

Aids

143

127

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HIV-1 infection is associated with substantial damage to the gastrointestinal (GI) tract resulting in structural impairment of the epithelial barrier and a disruption of intestinal homeostasis. The accompanying translocation of microbial products and potentially microbes themselves from the lumen into systemic circulation has been linked to immune activation, inflammation, and HIV-1 disease progression. The importance of microbial translocation in the setting of HIV-1 infection has led to a recent focus on understanding how the communities of microbes that make up the intestinal microbiome are altered during HIV-1 infection and how they interact with mucosal immune cells to contribute to inflammation. This review details the dysbiotic intestinal communities associated with HIV-1 infection and their potential link to HIV-1 pathogenesis. We detail studies that begin to address the mechanisms driving microbiota-associated immune activation and inflammation and the various treatment strategies aimed at correcting dysbiosis and improving the overall health of HIV-1 infected individuals. Finally, we discuss how this relatively new field of research can advance to provide a more comprehensive understanding of the contribution of the gut microbiome to HIV-1 pathogenesis.

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Microbiota-Dependent Marker TMAO Is Elevated in Silent Ischemia but Is Not Associated With First-Time Myocardial Infarction in HIV Infection

Abstract: TMAO was elevated in HIV-infected persons with myocardial perfusion defects, but was not associated with first-time MI. Our data question TMAO as a useful biomarker of cardiovascular risk in HIV infection, at least in ART-treated individuals.

Cited by 42 publications

References 36 publications

The role of trimethylamine N-oxide as a mediator of cardiovascular complications in chronic kidney disease

The role of trimethylamine N-oxide as a mediator of cardiovascular complications in chronic kidney disease

Brief Report

The gut microbiome and HIV-1 pathogenesis

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