Patients with chronic heart failure (CHF) are likely to have "intestinal overgrowth" of pathogenic gut flora and permeability that is associated with disease severity, new research suggests.
A study of 80 total participants showed that the CHF patients had "massive quantities" of pathogenic bacteria and candida vs a group of healthy controls. Specific types of the increased pathogens found in stool samples included Campylobacter, Shigella, Salmonella, Yersinia enterocolitica, and Candida species. Those with CHF also had significantly increased inflammation, intestinal permeability, and right atrial pressure (RAP), which is a signal of venous blood congestion.
In addition, most associations were stronger in those with moderate-severe HF (NYHA 3-4) vs those with mild HF (NYHA 1-2).
Interestingly, 100% of the CHF group had increased permeability and 78.3% of them had altered gut flora.
The full CHF group had substantially greater amounts of campylobacter vs the healthy controls group (85.3 vs 1.0 colony-forming units/mL, respectively; P<0.001). They also had larger quantities of shigella (38.9 vs 1.6) and candida (21.3 vs 0.8; both comparisons, P<0.001), as well as of salmonella (31.3 vs 0) and Yersinia E (22.9 vs 0; both comparisons, P<0.0001).
In addition, the CHF group had increased RAP (12.6 mm Hg) and systemic inflammation, as measured with C-reactive protein (12.5 mg/dL), and greater intestinal permeability vs the healthy controls (10.2 vs 1.5 mg, P<0.001).
The subgroup of moderate-severe CHF patients had significantly greater development rates of candida, campylobacter, and shigella compared with the subgroup with mild CHF. They also had greater intestinal permeability.
"Further studies are needed to confirm the link between gut pathogenic bacteria and CHF severity," write the investigators, "If confirmed, this link could suggest additional personalized therapeutic strategies . . . in support of traditional drugs," they write.
However, they note that there are currently "no clinical gut-flora modifiers available," and using probiotics could be potentially dangerous. "At present, reestablishing the gut microbiota may be the only option for patients to reverse intestinal dysbiosis," they write.
Consequence, Not Cause of HF?
The study's main take-home message, according to Hazen, is a reemphasis of the connection between cardiac function and bowel-wall edema, "and the breakdown of the barrier function of the intestines" in HF. In addition, "I think a lot of what was shown in the paper was a consequence of the heart failure and not a cause of the heart failure."
Hazen and other colleagues from Cleveland Clinic have written before about these issues and continue to study the associations. A new preclinical study published in Cell earlier today, for which Hazen was the principal investigator, showed that targeting and inhibiting gut microbes may prevent the development of atherosclerosis.