The link between periodontal disease and heart failure (HF) was reinforced by long-term data from the Atherosclerosis Risk in Communities (ARIC) cohort.
Among study participants with full-mouth periodontal exams in 1996-1998, those with a finding of periodontal disease were significantly more likely to experience incident HF over approximately 13 years of follow-up — namely HF with reduced ejection fraction (HFrEF; adjusted HR 1.69, 95% CI 1.18-2.43), with a nonsignificant trend of excess HF with preserved ejection fraction (HFpEF; adjusted HR 1.35, 95% CI 0.98-1.86) as well.
People whose gum health deteriorated to a state of edentulism had roughly double the risk of HFrEF (adjusted HR 2.19, 95% CI 1.43-3.36) and HFpEF alike (adjusted HR 2.00, 95% CI 1.37-2.93), according to epidemiologist Ryan Demmer, MPH, PhD, of University of Minnesota in Minneapolis, and colleagues. Their manuscript was published online in JACC: Heart Failure.
“Results for overall HF and HFpEF/HFrEF specifically remained significant after extensive adjustment for sociodemographic, behavioral, and HF risk biomarkers along with other pre-existing health conditions and incident coronary heart disease,” the authors noted.
Periodontal disease results from a person’s inflammatory response to bacteria under the gums. “Although numerous studies have reported associations between periodontal status and coronary artery disease, stroke, or diabetes, few have examined HF,” Demmer’s group noted.
Incidentally, chronic systemic inflammation is commonly observed in HF and is believed to be directly related to disease pathogenesis. Recent research suggests potential benefit to intravenous corticosteroids in acute HF if patients have elevated levels of C-reactive protein (CRP), a biomarker of systemic inflammation.
Based on the ARIC data, Demmer and colleagues reported that periodontal disease tracked with unfavorable changes in CRP. Edentulism was associated with CRP and heart failure marker N-terminal pro-B-type natriuretic peptides (NT-proBNP).
“Our findings support nascent literature linking oral infection to HF risk and support the need for more research exploring the potential for anti-infective periodontal therapies as a preventative strategy for minimizing HF burden. If future studies provide evidence of causal association, the population-level implications could be notable given the high prevalence of treatable periodontal disease and the burden of HF on our aging society,” the investigators suggested.
Their ARIC analysis included 7,514 people (55% women, mean age 63 years) with full-mouth periodontal exams at visit four of the study (1996-1998). Results were healthy gums in 23%, periodontal disease in 59%, and edentulism in 18%.
For the analysis by HF subtype, the authors relied on a subset of 6,707 people who were living and free of HF in 2005 when ARIC first began adjudication by HFrEF versus HFpEF.
Cumulative incidence of HF from ARIC visit four to 2018 was 21%, or 112.3 cases per 10,000 person-years.
Demmer and colleagues cautioned that they could not account for changes in participants’ oral health as periodontal examinations were conducted just once in ARIC. The study design also left room for confounding and selection bias.
“Given the aforementioned knowledge linking inflammation to both periodontal disease and HF, coupled with the demonstrated ability to reduce inflammation by intervening on oral dysbiosis, the potential for anti-infective periodontal therapy for the reduction in risk for HF development merits further consideration,” they maintained.
ARIC has been supported by NIH grants.
Demmer had no disclosures.