Dysbiosis of gut bacteria is a factor in several diseases, possibly including heart failure.
An altered intestinal microbiome could be part of the pathogenesis and progression of heart failure, according the results of a recent study. Conducted by Dr. Mark Luedde (pictured) of the Department of Internal Medicine at the University Medical Center Schleswig-Holstein in Kiel, Germany and colleagues, the study examined the intestinal microbiomes of 20 patients with heart failure (HF).
Several studies have made connections between HF and gut microbiota. Due to the poor prognosis and high mortality associated with chronic HF, even with modern treatment options, viewing heart failure as a systemic multi-organ failure may lead to a better understanding of the pathophysiology of the disease.
Previous studies have shown dysbiosis of gut bacteria is a factor in several diseases, possibly including HF. Additionally, reduced intestinal perfusion and ischemia, bowel wall thickness, epithelial permeability, and absorptive function may all be associated with heart failure. In conducting the present study, researchers said they sought to provide a “comprehensive description of the intestinal bacterial profile in patients with acute decompensated or stable HF."
The study population included 20 patients with heart failure, all of whom had a left ventricular ejection fraction of 35% or less, making it highly reduced compared to healthy controls. Most of the HF patients had etiologies, such as ischemic cardiomyopathy and dilated cardiomyopathy. The researchers report that 70% of the HF participants were in an "acute state of cardiac decompensation” and 30% were stable.
Body height, weight, systolic and diastolic blood pressure, body temperature, blood samples, and fecal samples were taken from the HF patients. Blood pressure, height, and weight, and fecal samples were obtained from the controls.
The researchers assessed the composition and structure of the intestinal luminal microbiota through analysis of the fecal samples. The microbiomes of the HF patients were then compared to that of the healthy controls, which the researchers confirmed were consistent with the normal gut microbiome constellation, according to previously conducted research. The present study is the “first systematic analysis of the intestinal bacterial microbiota of HF patients using high-throughput sequencing of bacterial 16S rRNA gene sequences,” according to the study.
The analysis revealed distinct differences between the gut bacteria of the controls versus the HF patients, but the researchers did not find an enhanced abundance of any certain potentially pathogenic bacteria in the HF patients. Rather, they found differences that could indicate adaptations to altered environments. Instead of seeing more of any particular bacteria, the researchers found significant decreases in some bacterial families and genera.
The small sample size used in this study represents a clear limitation. The authors noted there are multiple possible external factors which may be confounders, such as food intake, drug usage, environment. Though the researchers attempted to minimize the effect of such confounders, they added that other factors such as the chronic inflammation and fluid imbalance associated with HF may also play a role in the bacterial profile in the gut of an HF patient.
The researchers concluded by suggesting that more, larger-scale studies are necessary, and those studies should focus on the pathomechanisms involved.
"It seems possible that altered bacterial gut colonization, most likely the depletion of distinct core intestinal microbiota, acts as a risk factor and disease marker for HF, enhancing disease progression in a vicious cycle," the study read.
The full study can be found in the journal ESC Heart Failure.