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Heart disease risk in IBD tied to chronic inflammation
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Patients with inflammatory bowel disease show a higher risk for acute myocardial infarction and heart failure, although they do not show an increased prevalence of traditional cardiovascular risk factors, according to new research.
“These findings support the role of chronic inflammation in IBD-associated [cardiovascular disease, and] should prompt physicians to be vigilant for the development of these disorders,” according to the study authors, including Healio Gastroenterology and Liver Disease Chief Medical Editor Edward V. Loftus, Jr., MD, of the division of gastroenterology and hepatology at the Mayo Clinic in Rochester, Minn.
Loftus and colleagues undertook this population-based cohort study because the data on whether IBD increases the risk for acute myocardial infarction (AMI) and heart failure (HF) are unclear. They estimated the risks for these cardiovascular conditions by reviewing data on 736 patients diagnosed with IBD in Olmstead County, Minn., between 1980 and 2010, and matching them to 1,472 controls without IBD.
Loftus said his team designed the study to overcome some of the limitations of previous research.
“I think it’s unique because it’s not only population-based, but the cases and controls were confirmed by direct medical record review and the endpoints of MI and HF were also confirmed by direct medical record review,” Loftus told us. “In other words, unlike a claims database, we didn’t use billing codes to identify the study population or the endpoints.”
A first AMI event occurred in 75 IBD patients and 59 controls during the study period, resulting in a significantly greater cumulative incidence of AMI among IBD patients (P < .001). A first HF event occurred in 53 IBD patients and 52 controls, again resulting in a significantly higher cumulative incidence of HF among IBD patients (P = .02).
After adjusting for traditional cardiovascular disease risk factors, the researchers found that IBD patients were almost three times as likely to develop AMI (adjusted HR = 2.82; 95% CI, 1.98-4.04) and about twice as likely to develop HF than controls (aHR = 2.03; 95% CI, 1.36–3.03). Compared with controls, the relative risk for AMI was higher for both Crohn’s disease (aHR = 2.89; 95% CI, 1.65–5.13) and ulcerative colitis (aHR = 2.7; 1.69–4.35), while the relative risk for HF was only higher in patients with ulcerative colitis (aHR = 2.06; 95% CI, 1.18–3.65).
Patients who used systemic corticosteroids were five times as likely to develop AMI than controls (aHR = 5.08; 95% CI, 3–8.81), but 2.5 times as likely to develop HF (aHR = 2.51; 95% CI, 1.93–4.57), “suggesting an association between disease activity and the developing AMI/HF,” Loftus and colleagues wrote.
While it can be difficult to assess disease activity retrospectively, “we used use of corticosteroids as a proxy for activity, and the risk of events was higher among the steroid users,” Loftus noted.
Notably, the patients with IBD showed a lower prevalence of traditional cardiovascular disease risk factors, (ie, age, sex, hypertension, diabetes, hyperlipidemia, familial coronary disease, current smoking and BMI), leading Loftus and colleagues to conclude that “the increased risk of AMI/HF in IBD patients might be due to chronic systemic inflammation-related atherosclerosis.”
Further research is warranted to determine if controlling systemic inflammation may prevent these cardiovascular events in patients with IBD, they noted.
Loftus and colleagues recently argued the same point in a previously published review article on the subject.
“Particular attention should be given to the increased risk observed during periods of increased disease activity and potential modification of the risk by immunosuppressive and biologic therapies for IBD that can modify the disease activity,” they wrote. “In addition, preclinical studies suggest that cardiovascular medications such as statins and angiotensin-converting enzyme inhibitors might also favorably modify IBD disease activity, which warrants further evaluation.” – by Adam Leitenberger
Reference:
Singh S, et al. Nat Rev Gastroenterol Hepatol. 2015;doi:10.1038/nrgastro.2014.202.
Disclosures: The authors report no relevant financial disclosures.
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