Abstract
Simple SummaryThere is a strong potential of n-3 polyunsaturated fatty acid (n-3 PUFA) consumption to reduce cardiovascular risk and prevent adverse outcomes in existing cardiovascular diseases. This study aimed to test the effect of n-3 PUFA supplementation in the form of enriched hen eggs on serum lipid and free fatty acid profiles, inflammatory and oxidative stress biomarkers, and microvascular reactivity in patients with acute and chronic coronary artery disease. Consumption of three n-3 PUFA-enriched hen eggs for three weeks had a favorable effect on serum free fatty acid profile (a lower n-6/n-3 PUFA ratio) and mild anti-inflammatory effects but did not significantly affect microvascular reactivity in patients with coronary artery disease. Because consumption of both regular and n-3 PUFA eggs had no negative effects on any of the measured biological and functional vascular parameters, the results of the present study indicate that eggs can be safely consumed in the daily diet of patients with coronary artery disease.This study aimed to test the effect of n-3 polyunsaturated fatty acid (PUFA)-enriched hen egg consumption on serum lipid and free fatty acid profiles, inflammatory and oxidative stress biomarkers, and microvascular reactivity in patients with coronary artery disease (CAD). Forty CAD patients participated in this study. Of those, 20 patients had acute CAD (Ac-CAD), and 20 patients had chronic CAD (Ch-CAD). The control group (N = 20) consumed three regular hen eggs/daily (249 mg n-3 PUFAs/day), and the n-3 PUFAs group (N = 20) consumed three n-3 PUFA-enriched hen eggs/daily (1053 g n-3 PUFAs/day) for 3 weeks. Serum n-3 PUFA concentration significantly increased (in all CAD patients), while LDL cholesterol and IL-6 (in Ac-CAD patients), and hsCRP and IL-1a (in all CAD patients) significantly decreased in the n-3 PUFAs group. Glutathione peroxidase (GPx) activity significantly decreased, and forearm skin microvascular reactivity in response to vascular occlusion (postocclusive reactive hyperemia (PORH)) remained unchanged in both the n-3 PUFAs and control groups in total CAD, Ac-CAD, and Ch-CAD patients. Potentially, n-3 PUFA-enriched hen eggs can change the free fatty acid profile to a more favorable lower n6/n3 ratio, and to exhibit mild anti-inflammatory effects but not to affect microvascular reactivity in CAD patients.
Highlights
Coronary artery disease (CAD), characterized by atherosclerotic plaque accumulation in the epicardial arteries, is the most common type of heart disease and the leading cause of death in developed countries in both men and women [1,2]
N-3 polyunsaturated fatty acid (PUFA) supplementation in the form of capsules (2g n-3 PUFAs per day/3 months) significantly decreased IL-6 and TNFα levels in patients with chronic heart failure [37], and CRP and IL-6 levels were significantly decreased in overweight women with an inflammatory phenotype [38]. Consistent with these results, the present study demonstrated that n-3 PUFA-enriched hen egg consumption significantly decreased IL-1 and IL-6 levels, while TNF-α, interleukin 10 (IL-10), and monocyte chemoattractant protein-1 (MCP-1) levels remained unchanged following the respective diet protocol
The present study showed the anti-inflammatory potential of n-3 PUFAs egg consumption in coronary artery disease (CAD) patients
Summary
Coronary artery disease (CAD), characterized by atherosclerotic plaque accumulation in the epicardial arteries, is the most common type of heart disease and the leading cause of death in developed countries in both men and women [1,2]. CAD is often accompanied by established metabolic syndrome with insulin-resistant hyperglycemia, dyslipidemia, abdominal obesity, and hypertension, all of which contribute to the etiopathogenesis of CAD and to its complications, worsening the outcome of the disease [3,4]. Both CAD and metabolic syndrome are clinically manifested with established endothelial dysfunction (ED), which presents one of the earliest symptoms underlying various cardiovascular diseases (CVDs) (e.g., hypertension, diabetes mellitus, obesity, hyperlipidemia, and atherosclerosis) [5,6]. Increased oxidative stress levels [8], as well as generation of high levels of proinflammatory cytokines (e.g., IL-1, IL-6, and TNFα), resulting in vascular or systemic inflammation [9], are key pathophysiological mechanisms mediating the development of ED [10]. Oxidative stress affects the production of vasoactive and proinflammatory prostaglandins, leading to impaired endothelium-dependent vasoreactivity [11]
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