Arnold, Suzanne V., Bhatt, Deepak L., Barsness, Gregory W., Beatty, Alexis L., Deedwania, Prakash C., Inzucchi, Silvio E., Kosiborod, Mikhail, Leiter, Lawrence A., Lipska, Kasia J., Newman, Jonathan D., Welty, Francine K., and American Heart Association Council on Lifestyle and Cardiometabolic Health and Council on Clinical Cardiology
TYPE 2 diabetes, CORONARY disease, and GLYCEMIC control
Although cardiologists have long treated patients with coronary artery disease (CAD) and concomitant type 2 diabetes mellitus (T2DM), T2DM has traditionally been considered just a comorbidity that affected the development and progression of the disease. Over the past decade, a number of factors have shifted that have forced the cardiology community to reconsider the role of T2DM in CAD. First, in addition to being associated with increased cardiovascular risk, T2DM has the potential to affect a number of treatment choices for CAD. In this document, we discuss the role that T2DM has in the selection of testing for CAD, in medical management (both secondary prevention strategies and treatment of stable angina), and in the selection of revascularization strategy. Second, although glycemic control has been recommended as a part of comprehensive risk factor management in patients with CAD, there is mounting evidence that the mechanism by which glucose is managed can have a substantial impact on cardiovascular outcomes. In this document, we discuss the role of glycemic management (both in intensity of control and choice of medications) in cardiovascular outcomes. It is becoming clear that the cardiologist needs both to consider T2DM in cardiovascular treatment decisions and potentially to help guide the selection of glucose-lowering medications. Our statement provides a comprehensive summary of effective, patient-centered management of CAD in patients with T2DM, with emphasis on the emerging evidence. Given the increasing prevalence of T2DM and the accumulating evidence of the need to consider T2DM in treatment decisions, this knowledge will become ever more important to optimize our patients' cardiovascular outcomes. [ABSTRACT FROM AUTHOR]
Skulas-Ray, Ann C., Wilson, Peter W.F., Harris, William S., Brinton, Eliot A., Kris-Etherton, Penny M., Richter, Chesney K., Jacobson, Terry A., Engler, Mary B., Miller, Michael, Robinson, Jennifer G., Blum, Conrad B., Rodriguez-Leyva, Delfin, de Ferranti, Sarah D., and Welty, Francine K.
Hypertriglyceridemia (triglycerides 200–499 mg/dL) is relatively common in the United States, whereas more severe triglyceride elevations (very high triglycerides, ≥500 mg/dL) are far less frequently observed. Both are becoming increasingly prevalent in the United States and elsewhere, likely driven in large part by growing rates of obesity and diabetes mellitus. In a 2002 American Heart Association scientific statement, the omega-3 fatty acids (n-3 FAs) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were recommended (at a dose of 2–4 g/d) for reducing triglycerides in patients with elevated triglycerides. Since 2002, prescription agents containing EPA+DHA or EPA alone have been approved by the US Food and Drug Administration for treating very high triglycerides; these agents are also widely used for hypertriglyceridemia. The purpose of this advisory is to summarize the lipid and lipoprotein effects resulting from pharmacological doses of n-3 FAs (>3 g/d total EPA+DHA) on the basis of new scientific data and availability of n-3 FA agents. In treatment of very high triglycerides with 4 g/d, EPA+DHA agents reduce triglycerides by ≥30% with concurrent increases in low-density lipoprotein cholesterol, whereas EPA-only did not raise low-density lipoprotein cholesterol in very high triglycerides. When used to treat hypertriglyceridemia, n-3 FAs with EPA+DHA or with EPA-only appear roughly comparable for triglyceride lowering and do not increase low-density lipoprotein cholesterol when used as monotherapy or in combination with a statin. In the largest trials of 4 g/d prescription n-3 FA, non–high-density lipoprotein cholesterol and apolipoprotein B were modestly decreased, indicating reductions in total atherogenic lipoproteins. The use of n-3 FA (4 g/d) for improving atherosclerotic cardiovascular disease risk in patients with hypertriglyceridemia is supported by a 25% reduction in major adverse cardiovascular events in REDUCE-IT (Reduction of Cardiovascular Events With EPA Intervention Trial), a randomized placebo-controlled trial of EPA-only in high-risk patients treated with a statin. The results of a trial of 4 g/d prescription EPA+DHA in hypertriglyceridemia are anticipated in 2020. We conclude that prescription n-3 FAs (EPA+DHA or EPA-only) at a dose of 4 g/d (>3 g/d total EPA+DHA) are an effective and safe option for reducing triglycerides as monotherapy or as an adjunct to other lipid-lowering agents. [ABSTRACT FROM AUTHOR]
Welty, Francine K., Lewis, Sandra J., Friday, Karen E., Cain, Valerie A., and Anzalone, Deborah A.
Journal of Women's Health (15409996). Jan2016, Vol. 25 Issue 1, p50-56. 7p. 1 Diagram, 5 Charts, 1 Graph.
STATINS (Cardiovascular agents), CLINICAL trials, CONFIDENCE intervals, HYPERCHOLESTEREMIA, LOW density lipoproteins, MEDICAL cooperation, MEDICAL protocols, PATIENT safety, RESEARCH, RESEARCH funding, WOMEN'S health, TREATMENT effectiveness, ATORVASTATIN, DESCRIPTIVE statistics, SIMVASTATIN, ROSUVASTATIN, and ODDS ratio
Objective: Cardiovascular disease is the leading cause of mortality in women in the United States. Aggressive treatment of modifiable risk factors (e.g., hypercholesterolemia) is essential in reducing disease burden. Despite guidelines recommending the use of statin treatment in hypercholesterolemic women, this patient group is often undertreated. This subgroup analysis of the Statin Therapies for Elevated Lipid Levels compared Across doses to Rosuvastatin (STELLAR) trial examines the effects of statin therapy in hypercholesterolemic women. Methods: As part of the STELLAR trial, 1,146 women with elevated low-density lipoprotein cholesterol (LDL-C ≥160 and <250 mg/dL) and triglycerides <400 mg/dL were randomized to rosuvastatin 10-40 mg, atorvastatin 10-80 mg, simvastatin 10-80 mg, or pravastatin 10-40 mg for 6 weeks. Results: LDL-C reduction with rosuvastatin 10 mg, atorvastatin 10 mg, simvastatin 20 mg, and pravastatin 40 mg was 49%, 39%, 37%, and 30%, respectively, after 6 weeks. High-intensity statins (rosuvastatin 20-40 mg and atorvastatin 40-80 mg) reduced LDL-C to the greatest extent: 53% with rosuvastatin 20 mg, 57% with rosuvastatin 40 mg, 47% with atorvastatin 40 mg, and 51% with atorvastatin 80 mg. Similar results were observed for non-high-density lipoprotein cholesterol (non-HDL-C). Increases in HDL-C were greater with rosuvastatin across doses than with other statins. All treatments were well tolerated, with similar safety profiles across dose ranges. Conclusions: Statin therapies in the STELLAR trial led to reductions in LDL-C, non-HDL-C, and triglycerides and increases in HDL-C among hypercholesterolemic women, with rosuvastatin providing the greatest reductions in LDL-C and non-HDL-C. [ABSTRACT FROM AUTHOR]