5 research outputs found
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Eicosapentaenoic and Docosahexaenoic Acids Attenuate Progression of Albuminuria in Patients With Type 2 Diabetes Mellitus and Coronary Artery Disease
Background: Albuminuria is a marker of inflammation and an independent predictor of cardiovascular morbidity and mortality. The current study evaluated whether eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) supplementation attenuates progression of albuminuria in subjects with coronary artery disease. Methods and Results: Twoâhundred sixtyâtwo subjects with stable coronary artery disease were randomized to either Lovaza (1.86 g of EPA and 1.5 g of DHA daily) or no Lovaza (control) for 1 year. Percent change in urine albuminâtoâcreatinine ratio (ACR) was compared. Mean (SD) age was 63.3 (7.6) years; 17% were women and 30% had type 2 diabetes mellitus. In nondiabetic subjects, no change in urine ACR occurred in either the Lovaza or control groups. In contrast, ACR increased 72.3% (P<0.001) in diabetic subjects not receiving Lovaza, whereas those receiving Lovaza had no change. In diabetic subjects on an angiotensinâconverting enzymeâinhibitor or angiotensinâreceptor blocker, those receiving Lovaza had no change in urine ACR, whereas those not receiving Lovaza had a 64.2% increase (P<0.001). Change in ACR was directly correlated with change in systolic blood pressure (r=0.394, P=0.01). Conclusions: EPA and DHA supplementation attenuated progression of albuminuria in subjects with type 2 diabetes mellitus and coronary artery disease, most of whom were on an angiotensinâconverting enzymeâinhibitor or angiotensinâreceptor blocker. Thus, EPA and DHA supplementation should be considered as additional therapy to an angiotensinâconverting enzymeâinhibitor or angiotensinâreceptor blocker in subjects with type 2 diabetes mellitus and coronary artery disease. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT01624727
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Effect of Eicosapentaenoic and Docosahexaenoic Acids Added to Statin Therapy on Coronary Artery Plaque in Patients With Coronary Artery Disease: A Randomized Clinical Trial
Background: Although statins reduce cardiovascular events, residual risk remains. Therefore, additional modalities are needed to reduce risk. We evaluated the effect of eicosapentaenoic acid and docosahexaenoic acid in pharmacologic doses added to statin treatment on coronary artery plaque volume. Methods and Results: A total of 285 subjects with stable coronary artery disease on statins were randomized to omegaâ3 ethylâester (1.86 g of eicosapentaenoic acid and 1.5 g of docosahexaenoic acid daily) or no omegaâ3 (control) for 30 months. Coronary plaque volume was assessed by coronary computed tomographic angiography. Mean (SD) age was 63.0 (7.7) years; mean lowâdensity lipoprotein cholesterol â€80 mg/dL. In the intentionâtoâtreat analysis, our primary endpoint, noncalcified plaque volume, was not different between groups (P=0.14) but approached significance in the per protocol analysis (P=0.07). When stratified by age in the intentionâtoâtreat analysis, younger omegaâ3 subjects had significantly less progression of the primary endpoint, noncalcified plaque (P=0.013), and fibrous, calcified and total plaque. In plaque subtype analysis, controls had significant progression of fibrous plaque compared to no change in the omegaâ3 ethylâester group (median % change [interquartile range], 5.0% [â5.7, 20.0] versus â0.1% [â12.3, 14.5], respectively; P=0.018). Among those on lowâintensity statins, omegaâ3 ethylâester subjects had attenuation of fibrous plaque progression compared to controls (median % change [interquartile range], 0.3% [â12.8, 9.0] versus 4.8% [â5.1, 19.0], respectively; P=0.032). In contrast, those on highâintensity statins had no difference in plaque change in either treatment arm. Conclusions: Highâdose eicosapentaenoic acid and docosahexaenoic acid provided additional benefit to statins in preventing progression of fibrous coronary plaque in subjects adherent to therapy with wellâcontrolled lowâdensity lipoprotein cholesterol levels. The benefit on lowâintensity statin, but not highâintensity statin, suggests that statin intensity affects plaque volume. Clinical Trial Registration URL: http://www.ClinicalTrials.gov. Unique identifier: NCT01624727
Regression of Coronary Fatty Plaque and Risk of Cardiac Events According to Blood Pressure Status: Data From a Randomized Trial of Eicosapentaenoic Acid and Docosahexaenoic Acid in Patients With Coronary Artery Disease
Background Residual risk of cardiovascular events and plaque progression remains despite reduction in lowâdensity lipoprotein cholesterol. Factors contributing to residual risk remain unclear. The authors examined the role of eicosapentaenoic acid and docosahexaenoic acid in coronary plaque regression and its predictors. Methods and Results A total of 240 patients with stable coronary artery disease were randomized to eicosapentaenoic acid plus docosahexaenoic acid (3.36âg/d) or none for 30âmonths. Patients were stratified by regression or progression of coronary fatty plaque measured by coronary computed tomographic angiography. Cardiac events were ascertained. The mean±SD age was 63.0±7.7âyears, mean lowâdensity lipoprotein cholesterol level was <2.07âmmol/L, and median triglyceride level was <1.38âmmol/L. Regressors had a 14.9% reduction in triglycerides that correlated with fatty plaque regression (r=0.135; P=0.036). Compared with regressors, progressors had higher cardiac events (5% vs 22.3%, respectively; P<0.001) and a 2.89âfold increased risk of cardiac events (95% CI, 1.1â8.0; P=0.034). Baseline nonâhighâdensity lipoprotein cholesterol level <2.59âmmol/L (100âmg/dL) and systolic blood pressure <125âmmâHg were significant independent predictors of fatty plaque regression. Normotensive patients taking eicosapentaenoic acid plus docosahexaenoic acid had regression of noncalcified coronary plaque that correlated with triglyceride reduction (r=0.35; P=0.034) and a significant decrease in neutrophil/lymphocyte ratio. In contrast, hypertensive patients had no change in noncalcified coronary plaque or neutrophil/lymphocyte ratio. Conclusions Triglyceride reduction, systolic blood pressure <125âmmâHg, and nonâhighâdensity lipoprotein cholesterol <2.59âmmol/L were associated with coronary plaque regression and reduced cardiac events. Normotensive patients had greater benefit than hypertensive patients potentially due to lower levels of inflammation. Future studies should examine the role of inflammation in plaque regression. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT01624727