Pericoronary Adipose Tissue: A Novel Therapeutic Target in Obesity-Related Coronary Atherosclerosis

Abstract

Inflammation plays a crucial role in the development and destabilization of atherosclerotic plaques in coronary vessels. Adipose tissue is considered to act in paracrine manner, which modulates a number of physiological and pathophysiological processes. Perivascular adipose tissue has developed specific properties that distinguish it from the fat in other locations. Interestingly, its activity depends on several metabolic conditions associated with insulin resistance and weight gain. Particularly in obesity perivascular fat seems to change its character from a protective to a detrimental one. The present review analyzes literature in terms of the pathophysiology of atherosclerosis, with particular emphasis on inflammatory processes. Additionally, the authors summarize data about confirmed paracrine activity of visceral adipose tissue and especially about pericoronary fat influence on the vascular wall. The contribution of adiponectin, leptin and resistin is addressed. Experimental and clinical data supporting the thesis of outside-to-inside signaling in the pericoronary milieu are further outlined. Clinical implications of epicardial and pericoronary adipose tissue activity are also evaluated.

The role of pericoronary adipose tissue in obesity-related atherosclerosis is highlighted. In conclusion, the authors discuss potential therapeutical implications of these novel phenomena, including adipokine imbalance in pericoronary adipose tissue in the setting of obesity, the influence of lifestyle and diet modification, pharmaceutical interventions and the growing role of microRNAs in adipogenesis, insulin resistance and obesity.

Key teaching points:

• adipose tissue as a source of inflammatory mediators

• changes in the vascular wall as a result of outside-to-inside signaling

• anatomy, physiology, and clinical implications of epicardial and pericoronary adipose tissue activity

• adipokines and their role in obesity-related atherosclerosis

• therapeutic perspectives and future directions

Key words:

• insulin resistance, metabolism, obesity, type 2 diabetes, body composition

ACKNOWLEDGMENT

The authors thank Alan Lockwood for his contribution in the preparation of the article.

FUNDING

This work was supported by a grant from the Polish Ministry of Science and Higher Education (No. N402 383538).