Key result
Adipose-derived cytokines impair coronary microvascular function, driving coronary microvascular disease in obesity.
This review highlights the mechanistic link between obesity-induced adipose tissue inflammation and the development of coronary microvascular dysfunction.
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Should not change CMD management in obesity; extends mechanistic insights and warrants targeted clinical trials.
It is believed that obesity has detrimental effects on the coronary circulation. These include immediate changes in coronary arterial vasomotor responsiveness and the development of occlusive large coronary artery disease. Despite its critical role in regulating myocardial perfusion, the altered behavior of coronary resistance arteries, which gives rise to coronary microvascular disease (CMD) is poorly understood in obesity. A chronic, low-grade vascular inflammation has been long considered as one of the main underlying pathology behind CMD. The expanded adipose tissue and the infiltrating macrophages are the major sources of pro-inflammatory mediators that have been implicated in causing inadequate myocardial perfusion and, in a long term, development of heart failure in obese patients. Much less is known the mechanisms regulating the release of these cytokines into the circulation that enable them to exert their remote effects in the coronary microcirculation. This mini review aims to examine recent studies describing alterations in the vasomotor function of coronary resistance arteries and the role of adipose tissue-derived pro-inflammatory cytokines and adipokines in contributing to CMD in obesity. We provide examples of regulatory mechanisms by which adipokines are released from adipose tissue to exert their remote inflammatory effects on coronary microvessels. We identify some of the important challenges and opportunities going forward.
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Bagi et al. (2014) conducted a review in Obesity-associated coronary microvascular disease. Adipose tissue-derived pro-inflammatory cytokines and adipokines was evaluated. Adipose tissue-derived pro-inflammatory cytokines and adipokines impair coronary resistance artery vasomotor function, contributing to coronary microvascular disease in obesity.
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