Abstract

Objective: The AHA scientific statement on obesity identifies obesity as an important independent metabolic/genetic risk factor for ASCVD. For patients at high risk of ASCVD and with less-than-anticipated therapeutic response to statin therapy, the 2013 ACC/AHA cholesterol guideline recommends increasing statin intensity, or if on maximally tolerated statin intensity, considering non-statin therapy. The 2013 ACC/AHA cholesterol guideline evidence statements also describe the JELIS trial, in which 1.8 g/day of EPA added to statin therapy led to a 19% relative risk reduction in major coronary events in Japanese patients with hypercholesterolemia. Additionally, in the CHERRY trial of high-risk cardiac patients treated with moderate- to high-intensity statin therapy, the addition of 1.8 g/day of EPA resulted in significantly greater prevalence of coronary plaque regression compared to statin therapy alone (50% vs 24%; p<0.001). Further, in patients with DM, ASCVD is the primary cause of death. Methods: We reviewed the impact of initiating a prescription high-purity EPA drug, icosapent ethyl (2 g/day), in a morbidly obese (485 lb) 51-year-old African-American male patient with hypertension, DM, and ASCVD (evidenced by high CIMT) while on maximally tolerated statin therapy. Diet, exercise, and medications were stable for the duration of this report. Lipids, A1C, HOMA-IR, and CIMT were evaluated before and 4 months after initiating icosapent ethyl. Results: See table. Conclusions: Adding high-purity prescription EPA treatment (icosapent ethyl) to a maximally tolerated statin dose in a morbidly obese African-American patient with DM led to substantial regression of carotid intima-media thickness and to improvements in measured lipid parameters and two laboratory measures of DM. The clinical implications of adding icosapent ethyl to statin therapy is being evaluated in the ongoing cardiovascular outcomes trial, REDUCE-IT.

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