Abstract
BACKGROUND: Chronic inflammation is a focal process in the pathophysiology and pathogenesis of coronary heart disease (CHD). Dietary Inflammatory Index (DII) has been demonstrated as a potential useful marker to identify individuals at higher risk of adverse outcomes in CHD patients. AIM: This paper examined how dietary inflammatory potential is related to negative clinical outcomes in the population with angiographically confirmed CHD. METHODS: This is a retrospective cohort study that involved 500 adults with CHD, who were followed up a median of 38 months. The baseline dietary intake was measured, and the DII scores were computed and placed in quartiles. Major adverse cardiovascular events (MACE), death by any cause, and cardiovascular-related re-hospitalization were registered. The associations between DII and clinical outcomes were estimated with the help of cox proportional hazards and logistic regression models that took into consideration demographic, clinical, and lifestyle confounders. The correlation of DII and circulating inflammatory biomarkers were also studied. RESULTS: A positive association was found between higher DII scores and the negative cardio-metabolic phenotype and high systemic inflammation. The incidence of MACE over time was more and more increased with DII quartiles (11.2% in Q1 and 29.6% in Q4; p-trend <0.001). Once fully adjusted, the participants in the top quartile of DII had a much greater probability of MACE (HR 1.82, 95% CI 1.27-2.61) and of all-cause mortality (HR 1.68, 95% CI 1.05-2.69) than the participants in the lowest quartile. Every one unit rise in DII corresponded to a 21 percent increase in the risks of MACE. Greater DII scores were also associated with higher cardiac-related hospital readmission rates and high levels of inflammatory biomarkers, such as hs-CRP. CONCLUSION: Pro-inflammatory dietary pattern (high DII scores) are associated with adverse cardiovascular outcomes and mortality in this cohort. Such results indicate that dietary inflammation is an associated factor in CHD outcomes, and further research is warranted to examine whether modifying dietary inflammatory potential could influence clinical outcomes.