Background and Purpose: Often in clinical practice, stroke patients with elevated triglycerides more than 150 mg/dl are seen despite being treated with moderate to high-intensity statins and with even in settings of low-density lipoprotein (LDL) <70 mg per deciliter (mg/dl). This analysis aims to understand the role of icosapent ethyl (IPE) for controlling the elevated triglycerides in cardiovascular and cerebrovascular high-risk populations.
Methods: We performed the subgroup analysis of the REDUCE-IT double-blinded controlled study. The patient population included had either established cardiovascular disease or diabetes and other risk factors, who had been receiving statin therapy and who had a fasting triglyceride level of 135 to 499 mg/dl and a low-density lipoprotein cholesterol level of 41 to 100 mg/dl. The patients were randomly assigned to receive 2 g of IPE twice daily (total daily dose, 4 g) or placebo. The primary outcomes assessed as nonfatal myocardial infarction, nonfatal stroke, coronary revascularization, or unstable angina. The secondary outcomes were death from any cause, cardiovascular, or cerebrovascular related mortality.
Results: Almost 8179 patients were studied (70.7%) for secondary prevention of cardiovascular and cerebrovascular events and were followed for a median of 4.9 years. The rate of death from any cause was 6.7% in the IPE group and 7.6% in the placebo group (hazard ratio [HR], 0.87; 95% confidence interval [CI] 0.74 to 1.02). The time to event analysis over 4.5 years follow up showed better primary outcomes by 17.2% in the IPE group than 22% in placebo, HR 0.75; 95% CI, 0.68 to 0.83; p<0.001). The secondary outcomes in terms of overall mortality from cerebrovascular or cardiovascular accidents were reduced by 25% in IPE compared to placebo (HR: 0.74; 95% CI 0.65-0.83; p<0.001).
Conclusion: The combination therapy of IPE with moderate to high dose statins reduces the overall risk of cardiovascular and cerebrovascular accidents and mortality. The better primary and secondary outcomes were achieved irrespective of triglyceride levels at one year and it does explain the other metabolic effects of IPE.
Why does the top bullet point claim 36% RRR when according to whichever link you quoted the RRR is reported to be only 28%? That's what I seem to recall from the original R-IT papers.