Key result
An EPA-enriched diet reduced interstitial cardiac fibrosis and ameliorated LV diastolic dysfunction in spontaneously hypertensive rats despite continuous increases in blood pressure.
Why the study?
The treatment of cardiac fibrosis remains challenging and empiric, and whether EPA mitigates the exacerbation of cardiac remodeling and fibrosis induced by established hypertension was unknown.
Does an eicosapentaenoic acid (EPA)-enriched diet reduce cardiac fibrosis and LV diastolic dysfunction in spontaneously hypertensive rats?
RCT
randomized
Does an eicosapentaenoic acid (EPA)-enriched diet reduce cardiac fibrosis and LV diastolic dysfunction in spontaneously hypertensive rats?
In a rat model of established hypertension, an EPA-enriched diet ameliorated cardiac fibrosis and LV diastolic dysfunction, suggesting a potential novel treatment strategy for hypertensive cardiomyopathy.
Hypothesis-generating in hypertensive rat models; leaves open translation to human diastolic dysfunction.
Hypertension affects 1 in 3 adults in the United States and leads to left ventricular (LV) concentric hypertrophy, interstitial fibrosis, and increased stiffness. The treatment of cardiac fibrosis remains challenging and empiric. Eicosapentaenoic acid (EPA) is an omega-3 polyunsaturated fatty acid that is highly effective in reducing cardiovascular events in patients and cardiac fibrosis and hypertrophy in animals when administered before pressure overload by promoting the increase of anti-inflammatory M1 macrophages. In this study, we investigated whether EPA mitigates the exacerbation of cardiac remodeling and fibrosis induced by established hypertension, a situation that closely recapitulates a clinical scenario. Twelve-week-old spontaneously hypertensive rats were randomized to eat an EPA-enriched or control diet for 20 weeks. We report that rats eating the EPA-enriched diet exhibited a reduction of interstitial cardiac fibrosis and ameliorated LV diastolic dysfunction despite the continuous increase in blood pressure. However, we found that EPA did not have an impact on cardiac hypertrophy. Interestingly, the EPA diet increased mRNA expression of M2 macrophage marker Mrc1 and interleukin-10 in cardiac tissue. These findings indicated that the antifibrotic effects of EPA are mediated in part by phenotypic polarization of macrophages toward anti-inflammatory M2 macrophages and increases of the anti-inflammatory cytokine, interleukin-10. In summary, EPA prevents the exacerbation of cardiac fibrosis and LV diastolic dysfunction during sustained pressure overload. EPA could represent a novel treatment strategy for hypertensive cardiomyopathy.
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Gharraee et al. (2022) conducted an RCT in Hypertension. Eicosapentaenoic acid (EPA) vs. Control diet was evaluated on Interstitial cardiac fibrosis and LV diastolic dysfunction. An EPA-enriched diet reduced interstitial cardiac fibrosis and ameliorated LV diastolic dysfunction in spontaneously hypertensive rats despite continuous increases in blood pressure.
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