IBD and ASCVD have been linked in several meta-analyses. In a 2017 meta-analysis of eleven cohort studies, researchers discovered a multivariate-adjusted independent link between IBD and coronary heart disease (pooled relative risk (RR) 1.24; 95 percent confidence interval (CI) 1.14-1.36). This link was also found in CD and UC subgroup analysis.
Similar relationships were seen in another meta-analysis between IBD and coronary heart disease (RR 1.17, CI 1.07-1.27), myocardial infarction (MI) (RR 1.12, CI 1.05-1.21), and acute cerebrovascular disease (RR 1.25, CI 1.08-1.44); these associations were more pronounced in women. 5 These findings were similar to those of a countrywide Danish retrospective cohort research of IBD patients followed for up to 13 years, as well as a 2019 US study based on cross-sectional data from 26 nationwide health care systems. 6,7 Younger patients were shown to have a stronger link in the study conducted in the United States.
Periods of active disease in IBD have also been linked to an increased risk of cardiovascular events. During IBD flares and periods of chronic IBD activity, the risks of MI, cerebrovascular illness, and cardiovascular death were significantly greater, according to a prospective Danish study, especially in the first year after IBD diagnosis. During remission, the hazards were the same as they were in the control group. 8 Despite the fact that there is a link between IBD and ASCVD, there hasn’t always been a link between IBD and ASCVD-related mortality. 5,9,10 The younger age of the IBD population and the low case-fatality rates of ASCVD events in this age group are possible factors.
Potential Mechanisms between IBD and ASCVD
Local and systemic inflammation, gut microbiota abnormalities, endothelial dysfunction, thrombosis, lipid dysfunction, and corticosteroids, which are utilised in IBD treatment and are known to raise ASCVD risk, are all possible contributors to elevated ASCVD risk in IBD. 3 Inflammatory indicators such as C-reactive protein, IL-6, and TNF-a are high in IBD patients, which can lead to endothelial dysfunction. 3,11
IBD also promotes hypercoagulability, especially during intense flares, and patients are at a higher risk of venous and arterial thromboembolic events. 3,12 Furthermore, lipid changes can be caused by changes in nutrition and absorption, as well as inflammation. 3,13 However, more research into the exact mechanisms of these connections is needed.
Proposed Strategies
1) Initiation of a Multi-disciplinary, Team-Based Approach
Because there is an elevated risk of ASCVD when IBD is first diagnosed, it is critical to begin preventative therapy as soon as possible. Gastroenterologists and preventive cardiologists should collaborate to establish patient-centered, shared-decision-making approaches.
2) Remission of Disease
ASCVD is exacerbated by increased disease activity. As a result, IBD management must be optimised, particularly during acute flares. 10 Steroids, 5-aminosalicylates, immunosuppressives, and biologics are used to treat IBD in a stepwise manner; 5-aminosalicylates and anti-TNF medications may help to reduce the risk of ASCVD. 6,15
3) Aggressive Reduction in Cardiovascular Risk Factors
At the time of diagnosis, all IBD patients should be evaluated for known risk factors and treated aggressively. Blood pressure, glucose, a lipid panel, and lifestyle behaviours are all included in the screening process. Given the proclivity for volume depletion due to gastrointestinal losses during flares, careful attention of blood pressure management is necessary. It’s also critical to quit smoking completely.
4) Implementation of ACC/AHA Guidelines
The current ACC/AHA guideline recommendations for risk assessment and management in patients with chronic inflammatory diseases should be followed in a systematic manner.
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