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These results support the need for a prospective, randomized, controlled study of BP changes during exenatide treatment in patients with hypertension and type 2 diabetes.

BackgroundPreceding release of the 2013 American College of Cardiology (ACC)/American Heart Association (AHA) cholesterol guidelines, prescribers aimed for specific low‐density lipoprotein cholesterol (LDL‐C) goals in patients with atherosclerotic cardiovascular disease (ASCVD). The 2013 guidelines changed this focus to treating patients with appropriate statin intensity given their ASCVD risk. We examined statin use and LDL‐C levels before and after the 2013 ACC/AHA guidelines in patients with clinical ASCVD as defined in the guidelines.Methods and ResultsWe conducted a retrospective cohort study of adult commercial and Medicare Advantage health plan enrollees in the Optum Research Database. Patients had ≥1 claim with a diagnosis of clinical ASCVD between November 1, 2012 and December 31, 2014 and were continuously enrolled 6 months before (baseline) and 7 months after (follow‐up) the first ASCVD visit. Patients were assigned to monthly cohorts based on ASCVD event month. Statin use and intensity were measured at baseline and first month of follow‐up. LDL‐C changes were assessed using ordinary least squares regression. For 90 287 patients, mean (SD) age was 68 (12) years; 50% were female; and 30% had commercial insurance. Statin use remained consistent before and after guidelines (32% and 31%, respectively). Of patients receiving statins, high‐intensity use increased by 4 percentage points 1 year after guidelines (P<0.001). Mean LDL‐C levels were 2.4 mmol/L (94 mg/dL) both pre‐ and postguidelines.ConclusionsStatin use and mean monthly LDL‐C before and after the guidelines remained largely unchanged; statin intensity increased modestly. More effort may be needed to increase guideline understanding and adherence to improve treatment of high‐risk patients.

Type 2 diabetes is a chronic disease characterized by impaired insulin action, progressive beta cell dysfunction as well as abnormalities in pancreatic alpha cell function and postprandial substrate delivery. These pathophysiologic defects result in both persistent and progressive hyperglycemia, resulting in increased risk of both microvascular and cardiovascular complications. Traditional treatments for type 2 diabetes have focused on impaired insulin secretion and insulin resistance. These strategies are typically used in a stepwise manner: employing oral glucose lowering agents, followed by insulin therapy. This traditional approach fails to address the progressive decline in beta cell function. Moreover, these therapies are often associated with weight gain in overweight or obese patients with type 2 diabetes. Both exogenous insulin and insulin secretagogues are associated with an increased risk of hypoglycemia. Recently, new treatments that leverage the glucoregulatory effects of incretin hormones, such as glucagon like peptide 1 have been introduced. Both incretin mimetics and DPP-4 inhibitors address both the underlying pathophysiology and overcome several of the limitations of established therapies by providing improvements in glycemia, and control of body weight with minimal risk of hypoglycemia.