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Vascular Disease and SPMs

Coronary artery disease (CAD) is the most common form of heart disease and is a leading cause of death in the US among both men and women. CAD develops when plaque forms in the coronary arteries, limiting and blocking blood flow. Another cause of CAD, in addition to arterial plaques, is arterial inflammation.  A study by Tarec K. Elajami and colleagues found resolution of inflammation in the body may also lead to clot remodeling and reduce the incidence of CAD and coronary events in at risk patients.

The resolution phase of inflammation is facilitated in the body by specialized pro-resolving mediators (SPMs) which include lipoxins, resolvins, protectins, and maresins—which enhance microbial clearance as well as a variety of other functions including tissue remodeling, host defense, and others. Studies with patients with chronic inflammatory diseases such as cystic fibrosismetabolic syndromeasthma, and periodontal disease have lower levels of SPMs than do control participants. With regards to vascular disease,  it has also been found that patients with peripheral arterial disease have significantly lower levels of 17-HDHA than healthy subjects. These examples show that levels of SPMs may be lower in patients with chronic inflammatory diseases. Accordingly, Elajami et al. hypothesized patients with CAD having lower levels of SPMs, subsequently prevent them from resolving arterial inflammation and ultimately lead to the progression of CAD.

In the study conducted by Elajami et al., six men with stable CAD and lower than normal SPM levels were randomly assigned to take 3.36 g of an FDA-approved pharmacological therapy designed to increase circulating availability of SPMs, (precursors of SPMs), daily for one year.  EPA and DHA have been shown to reduce the risk of cardiovascular events. After one year of this treatment, patients who took the treatment, had twice the levels of proresolving and anti-inflammatory mediators as did those who did not take the nutritional treatment, and lower levels of prostaglandins compared to those who did not take use the treatment.

After one year of supplementation, CAD patients had more favorable SPM profiles, including improvements in lipid mediation and specific SPM biosynthesis. While the resolution properties of SPMs are known. This study indicates that a year of high-dose supplementation that increases availability of SPMs is highly effective. The results of this study indicate that supplementing the diet to increase SPMs may reduce the progression of atherosclerosis and CAD.

SPMs have a strong potential as a novel therapeutic strategy for inflammatory diseases, including CAD.

References

Elajami TK et al. Specialized proresolving lipid mediators in patients with coronary artery disease and their potential for clot remodeling. FASEB J. 2016;30(8):2792-2801.

Fredman G et al. Impaired phagocytosis in localized aggressive periodontitis: rescue by Resolvin E1. PLoS One. 2011;6(9).

Ho KJ et al. Aspirin-triggered lipoxin and resolving E1 modulate vascular smooth muscle phenotype and correlate with peripheral atherosclerosis. Am J Pathol. 2010; 177(4):2116-2123.

Karp CL et al. Defective lipoxin-mediated anti-inflammatory activity in the cystic fibrosis airway. Nat Immunol. 2004;5(4):388-392.

Levy BD et al. Diminished lipoxin biosynthesis in severe asthma. Am J Respir Crit Care Med. 2005;172(7):824-830.

Libby P et al. Inflammation and its resolution as determinants of acute coronary syndromes. Circ Res. 2014;114(12):1867-1879.

Serhan CN. Pro-resolving lipid mediators are leads for resolution physiology. Nature. 2014; 510(7503):92-101.

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