A complete heart with surface coronary vessels appears beside an artery cross-section with eccentric pale-gold wall material and an open lumen.
Cardiovascular pathology reconstruction Editorially reviewed

Coronary anatomy with one representative atherosclerotic arterial-wall process. Coronary artery disease also includes congenital and non-atherosclerotic processes; this reconstruction does not show occlusion, infarction, severity, or diagnosis.

WikiBiome / Microbiome MedicineNLM-MeSH-condition-, NHLBI-coronary-plaque-, open-lumen-, and literal-output-audit-informed reconstruction
Scientific media record1 verified identifier
Subject
Coronary Artery Diseasecondition
Identifiers
MeSH:D003324
Review
Editorial review completeIdentifiers authority-verified · Accessibility validated · · coronary-artery-disease|coronary-artery-disease-pathology-v1.webp
Digital source
Trained-algorithmic mediaCreated with a trained generative algorithm and reviewed by WikiBiome for subject identity, scientific framing, identifiers, provenance, and accessibility.
License
CC BY-SA 4.0Created

Coronary artery disease (CAD)—the progressive narrowing of coronary arteries by atherosclerotic plaque—is the single leading cause of death globally, responsible for approximately 9 million deaths annually. CAD encompasses stable angina, unstable angina, and myocardial infarction (heart attack).

While conventional risk factors (hypertension, dyslipidemia, smoking, diabetes) are well established, the Gut Microbiome adds an underappreciated dimension: microbial metabolites directly promote plaque formation, bacteria translocate into arterial plaques, and the metal environment modulates both microbial and vascular pathology.

CAD is closely related to the broader Cardiovascular Disease and Atherosclerosis pages in this wiki, but is distinguished by its focus on coronary-specific pathology and the increasingly detailed metabolomic-microbiome data linking gut bacteria to plaque severity.

Evidence map4 cited passagesInspect provenance +
01
Gut Microbiome in CAD

CAD patients have distinct gut microbial communities compared to healthy controls:

02
Metabolomic Correlation with Stenosis Severity

A critical observation: gut microbiome metabolic capacity correlates with CAD severity:

03
Key Studies

gut microbiome composition in CAD

04
Key Studies

metabolomic correlation with stenosis severity

Integrated microbiome signature

One disease. Five evidence layers.

A generated systems view of the metals, organisms, host sequestration signals, ecological conditions, and microbial functions indexed for Coronary Artery Disease.

01

Evidence layer

Metallomic signature

Elements and antioxidants reported as elevated, accumulated, depleted, or systemically altered.

Elevated or accumulated

0

No structured signals indexed yet.

Depleted or redistributed

0

No structured signals indexed yet.

02

Evidence layer

Taxonomic signature

Organisms reported as enriched or depleted, with their indexed functional context kept beside the name.
Enriched taxa0

No structured taxa indexed yet.

Depleted taxa0

No structured taxa indexed yet.

03

Evidence layer

Nutritional immunity

Host metal-withholding, inflammatory, antioxidant, and microbial-metabolite signals indexed in the signature.

Elevated host signals

0

No structured signals indexed yet.

Depleted protective signals

0

No structured signals indexed yet.

04

Evidence layer

Ecological state

The environmental conditions that connect the organism-level observations into a system.
WB.ECO / SYSTEM MODEL0 connected states

No structured ecological features indexed yet.

EnvironmentCommunity structureHost response
05

Evidence layer

Virulence functions

Microbial structures, enzymes, and acquisition systems implicated by the linked evidence.

No structured virulence functions indexed yet.

Encyclopedia article

The disease record, in full.

The original WikiBiome disease narrative remains intact beneath the generated signature atlas.

Metallomic Signature#

CAD shares the metallomic profile described for acute cardiovascular events (see Cardiovascular Disease):

MetalDirectionMechanism
CopperElevatedCeruloplasmin acute-phase response; oxidative damage to LDL
SeleniumDepletedImpaired selenoprotein antioxidant defense (GPX1, GPX4)
IronDysregulatedFree iron catalyzes LDL oxidation; heme iron from dietary red meat
LeadChronic elevationHypertension, endothelial dysfunction, accelerated atherosclerosis
CadmiumChronic elevationSmoking-associated; vascular endothelial toxicity

Cu/Se Ratio#

The copper (Cu)/selenium (Se) ratio is the most discriminating metallomic marker for acute coronary events, capturing both copper elevation and selenium depletion in a single metric. This ratio, combined with iron (Fe)/copper, achieves an AUC of 0.942 for AMI prediction in random forest modeling.

Microbiome Associations#

Gut Microbiome in CAD#

CAD patients have distinct gut microbial communities compared to healthy controls:[1]Coronary artery disease is associated with an altered gut microbiome compositionTakumi Toya, Michel T. Corban, Eric Marrietta et al. · 2020Open reference 1

Metabolomic Correlation with Stenosis Severity#

A critical observation: gut microbiome metabolic capacity correlates with CAD severity.[2]Alterations in the gut microbiome and metabolism with coronary artery disease severityHonghong Liu, Xi Chen, Xiaomin Hu et al. · 2019Open reference 2 Patients with more severe coronary stenosis (higher Gensini scores) show more pronounced Dysbiosis. TMAO-producing bacterial pathways are enriched in proportion to plaque burden.

SCFA-producing pathways are depleted in proportion to disease severity.

This suggests a dose-response relationship between microbial metabolic output and coronary pathology.

TMAO: The Microbial Metabolite Driving Plaque#

Trimethylamine N-oxide (TMAO) is the most direct metabolite link between gut bacteria and CAD:

1. Dietary choline, carnitine, and betaine (red meat, eggs, dairy) are metabolized by gut bacteria to trimethylamine (TMA) 2. TMA is absorbed and oxidized to TMAO by hepatic FMO3 3. TMAO promotes atherosclerosis through: - Enhanced macrophage foam cell formation (cholesterol uptake, impaired efflux) - Increased platelet hyperreactivity and thrombosis risk - Promotion of endothelial Metal-Driven Inflammation - Altered bile acid and cholesterol metabolism

TMAO levels predict cardiovascular events independent of traditional risk factors, and the TMAO-producing capacity of an individual's microbiome is a modifiable risk factor.

Oral-to-Coronary Bacterial Translocation#

Oral bacteria, particularly Porphyromonas gingivalis and other periodontal pathogens, have been detected within coronary atherosclerotic plaques.

Periodontal disease is an independent CAD risk factor. Oral bacteria reach coronary arteries via transient bacteremia during dental procedures, eating, and tooth brushing. Within plaques, bacteria sustain local inflammation and may contribute to plaque instability.

The oral microbiome is therefore a direct contributor to coronary pathology, not merely a systemic inflammation marker.

SCFA Protection#

Butyrate and propionate from gut commensals protect against CAD through:

  • Anti-inflammatory signaling: Butyrate suppresses NF-kB in vascular endothelial cells
  • Blood pressure regulation: Propionate activates Olfr78 and GPR41 receptors, modulating renin secretion
  • Barrier integrity: SCFAs maintain intestinal barrier, preventing LPS-driven endothelial activation
  • Cholesterol metabolism: SCFAs influence hepatic cholesterol synthesis

The depletion of SCFA-producing bacteria in CAD removes these protective effects.

Associated Conditions#

ConditionRelationshipShared Metallomic/Microbiome Features
AtherosclerosisCAD is atherosclerosis of the coronary arteriesSame process, same taxa, same metals
Type 2 DiabetesMajor risk factor; 2-4x CAD riskCadmium, Enterobacteriaceae enrichment, SCFA depletion
HypertensionMajor risk factorLead, cadmium vascular toxicity
Chronic Kidney DiseaseBidirectional riskLead/cadmium retention, uremic toxins, TMAO
Erectile DysfunctionSentinel marker (ED precedes CAD by 3-5 years)Shared endothelial dysfunction, same gut-vascular axis

Open Questions#

Unresolved questions identified by the current evidence record.

01Can TMAO-lowering interventions (dietary or microbial) reduce coronary events in clinical trials?

The current WikiBiome record identifies this as an unresolved evidence gap.

02Does the oral microbiome composition predict CAD independent of periodontal disease severity?

The current WikiBiome record identifies this as an unresolved evidence gap.

03Can the copper (Cu)/selenium (Se) ratio serve as a screening biomarker for subclinical CAD?

The current WikiBiome record identifies this as an unresolved evidence gap.

04Do statin-microbiome interactions (see Statins) contribute to cardiovascular protection beyond cholesterol lowering?

The current WikiBiome record identifies this as an unresolved evidence gap.

05Can precision probiotics targeting butyrate production reduce CAD progression?

The current WikiBiome record identifies this as an unresolved evidence gap.

Key Studies#

  • [1]Coronary artery disease is associated with an altered gut microbiome compositionTakumi Toya, Michel T. Corban, Eric Marrietta et al. · 2020Open reference 1—gut microbiome composition in CAD
  • [2]Alterations in the gut microbiome and metabolism with coronary artery disease severityHonghong Liu, Xi Chen, Xiaomin Hu et al. · 2019Open reference 2—metabolomic correlation with stenosis severity

Cross-References#

Generated evidence record

References 8

Numbered by first appearance in the article, then reconciled with its declared source list.

  1. 1

    Takumi Toya, Michel T. Corban, Eric Marrietta et al. (2020). Coronary artery disease is associated with an altered gut microbiome composition. PLOS ONE.

  2. 2

    Honghong Liu, Xi Chen, Xiaomin Hu et al. (2019). Alterations in the gut microbiome and metabolism with coronary artery disease severity. Microbiome.

  3. 3

    Kevin T. McVary (2007). McVary 2007 — Erectile Dysfunction Clinical Practice Review. New England Journal of Medicine.

  4. 4

    Md. Mominur Rahman, Fahadul Islam, Md. Harun-Or-Rashid et al. (2022). The Gut Microbiota (Microbiome) in Cardiovascular Disease and Its Therapeutic Regulation. Frontiers in Cellular and Infection Microbiology.

  5. 5

    Andrea Tonelli, Evelyn N. Lumngwena, Ntobeko A. B. Ntusi (2023). The oral microbiome in the pathophysiology of cardiovascular disease. Nature Reviews Cardiology.

  6. 6

    Xiao-Ce Dai, Yi Yu, Si-Yu Zhou et al. (2024). Assessment of the causal relationship between gut microbiota and cardiovascular diseases: a bidirectional Mendelian randomization analysis. BioData Mining.

  7. 7

    Dan Wang, Xiaoyan Chen, Zhen Li et al. (2023). Association of the Gut Microbiota with Coronary Artery Disease and Myocardial Infarction: A Mendelian Randomization Study. Frontiers in Genetics.

  8. 8

    Jing Zhen, Zhou Zhou, Meng He et al. (2023). The gut microbial metabolite trimethylamine N-oxide and cardiovascular diseases. Frontiers in Endocrinology.

Knowledge graph

Article network

Researcher discussion

Connect the evidence

Publicly readable discussion by ORCID-authenticated researchers. Questions, interpretation, methods, corrections, and new evidence stay attached to this record.

0 posts

No discussion yet. Start with a precise question or a source-backed observation.

Transparent record

Activity and accepted changes

Accepted researcher context, editorial status, public discussion, and upstream Git revisions are shown together. Pending, declined, and withdrawn proposals remain private.

8 events
  1. published revision

    Consolidate microbial metabolite knowledge

    Karen Pendergrass · +1 −1

    Inspect exact Git diff ↗
  2. published revision

    Backfill butyrate concept links

    Karen Pendergrass · +2 −2

    Inspect exact Git diff ↗
  3. published revision

    Backfill gut microbiome concept links

    Karen Pendergrass · +1 −1

    Inspect exact Git diff ↗
  4. published revision

    Backfill inflammation concept links

    Karen Pendergrass · +1 −1

    Inspect exact Git diff ↗
  5. published revision

    Complete corpus-wide Dysbiosis linking

    Karen Pendergrass · +1 −1

    Inspect exact Git diff ↗
  6. published revision

    massive wiki expansion: 149 stubs fixed, 100+ new pages, Rule 15 scan, keystone papers

    WikiBiome Deploy Bot · +30 −24

    Inspect exact Git diff ↗
  7. published revision

    nightly maintenance: 94 stub demotions, 181 source_count fixes, 22 auto-discovered stubs, 5 adversarial audits, 3 boundary fixes, 3 evidence-level corrections

    WikiBiome Deploy Bot · +2 −0

    Inspect exact Git diff ↗
  8. published revision

    pre-overnight checkpoint 2026-04-18

    WikiBiome Deploy Bot · +130 −0

    Inspect exact Git diff ↗
Continue exploring

Follow the disease network.

Generated from the WikiBiome Markdown vault; disease and signature records are reconciled at build time.

8 references · 1 content records · 822 corpus pages