Gut microbiota and cardiovascular disease: implications for public health

Gut Microbiota-Dependent Trimethylamine N-Oxide in Acute Coronary Syndromes

Prospective study in 530 patients with acute chest pain (≤24h). Serial TMAO and cTnT (cardiac troponin T) measurements (baseline, 4, 8, 16h). MACE (major adverse cardiovascular events) follow-up at 1/6 months and annually.

Plasma TMAO levels demonstrated predictive utility for short- and long-term MACE in both cTnT-positive and cTnT-negative patients. These results support TMAO's clinical potential as a risk stratification biomarker in acute coronary syndrome.

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The gut microbiome across the cardiovascular risk spectrum

Metagenomic analysis of 411 fecal samples from individuals stratified by cardiovascular risk (low [n=130], intermediate [n=130], high [n=125] per Framingham scale) and STEMI patients (n=26).

Gradual increase in Collinsella stercoris, Flavonifractor plautii, and Ruthenibacterium lactatiformans abundance from low-risk to STEMI patients, while Streptococcus thermophilus showed inverse risk association. STEMI patients exhibited alterations in 8 bacterial species and 49 metabolic pathways, including reduced vitamin, lipid, and amino acid biosynthesis, suggesting direct microbiome impact on CVD progression.

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Gut microbiota-derived secondary bile acids, bile acids receptor polymorphisms, and risk of cardiovascular disease in individuals with newly diagnosed type 2 diabetes: a cohort study

5–7 year prospective cohort of type 2 diabetes patients assessing unconjugated secondary bile acids (SBAs: DCA, LCA, UDCA) and incident CVD risk (n=259 cases), adjusted for confounders.

Linear dose-response relationship between elevated unconjugated SBAs (particularly DCA) and increased CVD risk in type 2 diabetes. Findings suggest gut microbiota-derived SBAs may play a key role in cardiovascular pathogenesis in diabetic patients.

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The gut microbiome in atherosclerotic cardiovascular disease

Metagenomic comparison of gut microbiome through fecal sample analysis in 218 atherosclerotic cardiovascular disease (ASCVD) patients versus 187 healthy controls.

ASCVD patients exhibited an altered gut microbiome characterized by: (1) increased abundance of Enterobacteriaceae and Streptococcus spp.; (2) functional alterations in cardiovascular molecule metabolism pathways.

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Dietary Fiber Metabolism

Production of short-chain fatty acids (SCFAs: butyrate, propionate, acetate) reducing inflammation, improving blood pressure and insulin sensitivity.

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Choline/Carnitine/Lecithin Metabolism

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TMAO production promoting atherosclerosis, endothelial dysfunction, and thrombosis

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Gut Barrier Integrity

Prevents endotoxin translocation and reduces systemic inflammation

Dysbiosis increases intestinal permeability, allowing LPS entry and promoting chronic inflammation

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Immunomodulation

Induction of T-regulatory cells and IL-10 production; reduced vascular inflammation

Activation of proinflammatory cells (Th17, M1 macrophages) and elevation of proatherogenic cytokines

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Lipid metabolism

Reduced serum cholesterol and bile acid modulation

Alterations promoting atherogenic dyslipidemias

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Blood Pressure Regulation

SCFAs activate vascular tone-regulating receptors (GPR41/GPR43)

Dysbiosis associated with hypertension in animal models and humans

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Obesity/Metabolic Syndrome Impact

Specific bacteria (Akkermansia muciniphila) improve metabolism and reduce adiposity

Microbial imbalance linked to obesity, insulin resistance, and increased cardiovascular risk

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