The Role of Omega-3 Fatty Acids in the Setting of Coronary Artery Disease and COPD: A Review

Alex Pizzini, Lukas Lunger, Thomas Sonnweber, Guenter Weiss, Ivan Tancevski, Alex Pizzini, Lukas Lunger, Thomas Sonnweber, Guenter Weiss, Ivan Tancevski

Abstract

Chronic obstructive pulmonary disease (COPD) is a growing healthcare concern and will represent the third leading cause of death worldwide within the next decade. COPD is the result of a complex interaction between environmental factors, especially cigarette smoking, air pollution, and genetic preconditions, which result in persistent inflammation of the airways. There is growing evidence that the chronic inflammatory state, measurable by increased levels of circulating cytokines, chemokines, and acute phase proteins, may not be confined to the lungs. Cardiovascular disease (CVD) and especially coronary artery disease (CAD) are common comorbidities of COPD, and low-grade systemic inflammation plays a decisive role in its pathogenesis. Omega-3 polyunsaturated fatty acids (n-3 PUFAs) exert multiple functions in humans and are crucially involved in limiting and resolving inflammatory processes. n-3 PUFAs have been intensively studied for their ability to improve morbidity and mortality in patients with CVD and CAD. This review aims to summarize the current knowledge on the effects of n-3 PUFA on inflammation and its impact on CAD in COPD from a clinical perspective.

Keywords: CAD; CHD; COPD; PUFA; coronary artery disease; inflammation; ischemic heart disease; n-3 PUFA; omega 3.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Interplay between smoking, pulmonary and systemic inflammation, coronary artery disease and omega-3 polyunsaturated fatty acids (n-3 PUFAs). COPD = chronic obstructive pulmonary disease, CAD = coronary artery disease.
Figure 2
Figure 2
Inflammatory response and inflammatory resolution: the role of molecular mediators derived from n-3 PUFA and n-6 PUFA. EPA = eicosapentaenoic acid, DHA = docosahexaenoic acid, AA = arachidonic acid, PGI = prostaglandins, TNFα = tumor necrosis factor α.

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Source: PubMed

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