Heart failure developed after myocardial infarction does not affect gut microbiota composition in the rat

Abstract

There is a body of evidence that supports the notion that gut dysbiosis plays a role in the pathogenesis of cardiovascular diseases. Decreased cardiac function can reduce intestinal perfusion, resulting in morphological alterations, which may contribute to changes in the gut microbiota composition in patients with heart failure (HF). In this regard, a germane question is whether changes in gut microbiota composition are a cause or consequence of the cardiovascular disturbance. We tested the hypothesis that the development of HF, after myocardial infarction, would cause gut dysbiosis. Fecal samples were collected before and 6 wk after myocardial infarction or sham surgery. Gut microbiota were characterized by sequencing the bacterial 16S ribosomal DNA. The composition of bacterial communities in the fecal samples was evaluated by calculating three major ecological parameters: 1) the Chao 1 richness, 2) the Pielou evenness, and 3) the Shannon index. None of these indices was changed in either sham or HF rats. The Firmicutes/Bacteroidetes ratio was not altered in HF rats. The number of species in each phylum was also not different between sham and HF rats. β-Diversity analysis showed that the composition of gut microbiota was not changed with the development of HF. Bacterial genera were grouped according to their major metabolic end-products (acetate, butyrate, and lactate), but no differences were observed in HF rats. Therefore, we conclude that HF induced by myocardial infarction does not affect gut microbiota composition, at least in rats, indicating that the dysbiosis observed in patients with HF may precede cardiovascular disturbance. NEW & NOTEWORTHY Our study demonstrated that, following myocardial infarction in rats, heart failure (HF) development did not affect the intestinal microbiota despite distinct differences reported in the gut microbiota of humans with HF. Our finding is consistent with the notion that dysbiosis observed in patients with HF may precede cardiovascular dysfunction and therefore offers potential for early diagnosis and treatment.

A Mouse Model Suggests That Heart Failure and Its Common Comorbidity Sleep Fragmentation Have No Synergistic Impacts on the Gut Microbiome

“…In previous studies, Ruminococcaceae_UCG.014 abundance was found as significantly positively associated with serum trimethylamine N-oxide (TMAO) levels, which were associated with coronary atherosclerotic plaque and increased cardiovascular disease risk [42]. The genus Ruminococcus was also found increased in HF models [43], and was related to the inflammation that is observed in HF patients by the disruption of the gut barrier through either the translocation of gut bacterial DNA, endotoxins, or both, into the bloodstream [44]. It is known that both a high-fat diet (calorie-dense obesogenic) and aging cause inflammation in HF through an alteration of the microbiome such as increasing the phylum Firmicutes, specifically the genus Allobaculum [45], which in our study was found as significantly more abundant in HF than in C. Both Alistipes and Oscillibacter were also reported in previous studies as decreased in chronic HF patients [43].…”

Impact of sleep fragmentation, heart failure, and their combination, on the gut microbiome

“…When we restrict our attention to the HF models, we observed an increase in the with serum trimethylamine N-oxide (TMAO) levels, which were associated with coronary atherosclerotic plaque and increased cardiovascular disease risk (Gao et al, 2020). The genus Ruminococcus was also found increased in HF models (Cui et al, 2018), and was related to the inflammation that is observed in HF patients by the disruption of the gut barrier through the translocation of gut bacterial DNA and/or endotoxins into the bloodstream (Lataro et al, 2019). It is known that both a high-fat diet (calorie-dense obesogenic) and aging cause inflammation in HF through an alteration of the microbiome such as increasing the phylum Firmicutes, specifically the genus Allobaculum (Kain et al, 2019), which in our study was found as significantly more abundant in HF than in C. Both…”

Spermidine Affects Cardiac Function in Heart Failure Mice by Influencing the Gut Microbiota and Cardiac Galectin-3

“…However, different results were also observed in other studies. Lataro et al thought that the Firmicutes / Bacteroidetes ratio was not altered in HF model rats subjected to myocardial infarction ( 42 ). However, Marques et al found that a high fiber diet led to a decrease in the Firmicutes / Bacteroidetes ratio and prevented the development of hypertension and heart failure in hypertensive mice ( 43 ).…”