Why the study?
Pathogenetic cellular and biochemical mechanisms underlying increased cardiovascular risk in chronic inflammatory diseases remain elusive, animal models are limited, and treatments have varying effects on cardiac function.
This review highlights the complex interplay between chronic inflammatory diseases, their treatments, and cardiovascular risk, emphasizing the need for therapies that alleviate CID-related cardiovascular disease.
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Calls for integrated CV risk management in chronic inflammatory diseases; extends mechanistic insights but leaves optimal cardioprotection strategies open.
The association between chronic inflammatory diseases (CIDs) and increased cardiovascular (CV) risk is well documented and can be a most threatening complication in these patients. However, the pathogenetic mechanisms underlying increased CV risk remain elusive, especially in their cellular and biochemical pathways. Using animal models to understand mechanisms underlying cardiac involvement are limited. Additionally, treatments may influence cardiovascular events through different outcomes. Some drugs used to treat CIDs can negatively affect cardiac function by a direct toxicity, whereas others may protect the myocardium. In the present article, we focus on the cardiac manifestations and risk factors, the pathogenetic mechanisms, and the effect of treatments on myocardial function and cardioprotection for five common worldwide CIDs (rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, psoriasis and inflammatory bowel disease). We also give recommendations in order to evaluate common targets between CID and CV disease (CVD) and to design therapies to alleviate CID-related CVD. LINKED ARTICLES: This article is part of a themed issue on Risk factors, comorbidities, and comedications in cardioprotection. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.23/issuetoc.
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Lazou et al. (2020) studied this question.
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