A recent study published in Arthritis Care & Research reveals that individuals with rheumatoid arthritis (RA) face a higher risk of developing certain types of heart failure, particularly heart failure with preserved ejection fraction (HFpEF), compared to those without RA.
The findings underscore the role of inflammation in heart health and point to potential strategies for reducing this risk.
The research, led by Dr. Yumeko Kawano from Brigham and Women’s Hospital in Boston, analyzed data from 1,445 patients with RA and 4,335 matched controls without the condition.
RA is an autoimmune disease characterized by chronic inflammation, which has been linked to an increased risk of various cardiovascular problems. This study aimed to better understand the connection between RA and heart failure subtypes.
Heart failure occurs when the heart is unable to pump blood efficiently, and it is categorized into two main subtypes: HFpEF, where the heart’s pumping strength is preserved but filling is impaired, and heart failure with reduced ejection fraction (HFrEF), where the heart’s ability to pump blood is significantly weakened.
The researchers found that HFpEF was the most common type of heart failure in both groups, affecting 65% of heart failure cases in RA patients compared to 59% in non-RA individuals.
After accounting for cardiovascular risk factors like high blood pressure and diabetes, RA patients were found to have a 79% higher overall risk of developing heart failure.
Specifically, their risk of HFpEF was nearly double (hazard ratio of 1.99) compared to those without RA. However, there was no significant difference in the rates of HFrEF between the two groups.
These findings suggest that the increased heart failure risk in RA patients is primarily driven by HFpEF. According to the authors, this highlights the potential role of chronic inflammation—a hallmark of RA—in contributing to HFpEF.
Unlike HFrEF, which is often linked to structural damage from conditions like heart attacks, HFpEF is more strongly associated with systemic inflammation.
The study’s authors emphasize the importance of exploring anti-inflammatory treatments to address this risk.
Since inflammation is modifiable with medications commonly used to treat RA, such as biologics or disease-modifying antirheumatic drugs (DMARDs), future research could investigate whether these therapies might also help prevent or reduce HFpEF in RA patients.
“This elevated risk was driven by HFpEF, supporting a role for inflammation in HFpEF and highlighting potential opportunities to address this excess risk in RA,” the authors noted.
While the study provides valuable insights, further research is needed to confirm whether controlling inflammation through specific treatments can effectively lower the risk of HFpEF in RA patients and others with chronic inflammatory conditions.
The study also disclosed that several authors have financial ties to industry, which is a standard practice in many large-scale research efforts.
Despite this, the findings contribute to a growing body of evidence linking inflammation to cardiovascular health and emphasize the need for tailored prevention strategies for individuals with RA.
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The research findings can be found in Arthritis Care & Research.
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