Gut microbiota and coronary microvascular dysfunction in obesity: narrative review of mechanisms
This narrative review proposes that gut dysbiosis mediates obesity-induced coronary microvascular dysfunction via metabolites such as TMAO and SCFAs, but provides no original primary data to establish causality.
| Outcome | Grade | Direction | Effect | Studies |
|---|---|---|---|---|
| Coronary flow reserve (CFR) in obese individuals | B | ▼ Unfavorable | reducao 47.7% IC -80.2/-15.2 (meta-analise citada, n=422) | 1 |
| Stress myocardial blood flow (MBF) in obese individuals | B | ▼ Unfavorable | reducao 47.8% IC -73.7/-21.8 (meta-analise citada, n=409) | 1 |
| Cardiovascular event risk per CFR unit decrease | B | ▼ Unfavorable | HR 1.95 IC 1.41/2.69 (estudo longitudinal citado, n=827) | 1 |
| Resting myocardial blood flow (MBF) in obese individuals | B | — Neutral | diferenca 15% IC -24/+53 (nao significativo, meta-analise citada) | 1 |
| Role of TMAO in coronary endothelial dysfunction | D | — Insufficient | mecanistico; sem efeito quantificado em humanos nesta revisao | — |
| Role of SCFAs in inflammation and vascular function | D | — Insufficient | mecanistico; sem efeito quantificado em humanos nesta revisao | — |
| Gut microbiota diversity in obesity | C | ▼ Unfavorable | reducao de diversidade em obesos vs eutróficos; sem efeito quantificado agregado | — |
Context
Coronary microvascular dysfunction (CMD) occurs in obese patients even without large-vessel obstruction and predicts major cardiovascular events. The gut microbiota has emerged as a potential link between obesity and CMD, but mechanisms remain largely inferred from heterogeneous studies. Understanding this pathway is relevant as half of all adults globally may have obesity by 2050.
What the study showed
The review cites a meta-analysis (n=1,399; 456 obese) showing a 47.7% reduction in CFR in obese individuals (n=422; 95% CI −80.2% to −15.2%) and a 47.8% reduction in stress MBF (n=409; 95% CI −73.7% to −21.8%), with no significant difference in resting MBF (15%; 95% CI −24% to +53%). A longitudinal study of 827 patients (median follow-up 5.6 years) reported a negative correlation between CFR and BMI (p<0.0001) and that each 1-unit decrease in CFR nearly doubled cardiovascular event risk (HR 1.95; 95% CI 1.41–2.69). Proposed mechanisms involve TMAO, SCFAs, LPS, and pro-inflammatory cytokines, but the review presents no primary data directly linking microbiota to CMD.
How it was done
Narrative review without a registered protocol, without a described systematic search, and without explicit inclusion/exclusion criteria. Integrates data from meta-analyses, longitudinal studies, experimental models, and in vitro studies non-systematically. No primary data collection.
Effect magnitude
Highest-magnitude data come from cited studies: ~48% reduction in CFR and stress MBF in obese individuals (wide CIs) and HR 1.95 (95% CI 1.41–2.69) for cardiovascular events per unit CFR decrease. These figures do not derive from the review's own methodology.
Limitations
Narrative review without systematic methodology (AMSTAR-2 not applicable), with high risk of selection and confirmation bias. Does not distinguish causality from association between microbiota and CMD. Most mechanistic evidence derives from animal or in vitro models with limited direct clinical translation.
In clinical practice
Clinicians should recognize CMD as a relevant entity in obese patients with normal angiography. No microbiota-targeted intervention has sufficient evidence for clinical recommendation based on this review alone. Monitoring CFR in obese patients with ischemic symptoms is supported by the cited studies, not by this article itself.
What is still missing
Randomized controlled trials testing microbiota modulation (probiotics, prebiotics, fecal transplant) on measurable CMD outcomes in obese populations. Mechanistic studies in humans establishing causality between specific microbial metabolites and CFR.