Optimal secondary prevention medication use in acute myocardial infarction patients with nonobstructive coronary artery disease is modified by management strategy: insights from the TRIUMPH Registry.

BACKGROUND: Patients with acute myocardial infarction (AMI) and nonobstructive coronary artery disease (nonobCAD) may be perceived to be at lower risk for cardiac events, relative to those with obstructive CAD (obCAD), and thus less likely to receive optimal preventive medications in the year following AMI. HYPOTHESIS: We aimed to determine if AMI patients with nonobCAD, compared to obCAD, received lower rates of prevention medications in the year following AMI. METHODS: We compared optimal prevention medication use at hospital discharge, 1, 6, and 12 months after hospitalization. Optimal medication use was defined as the receipt of all prevention medications for which that patient was eligible (eg, aspirin, clopidogrel, statins, ß-blockers, and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers). We used multivariable logistic regression analyses to determine the association between nonobCAD to medication use and adjusted for potential confounders. RESULTS: Three thousand six hundred thirty AMI patients were studied, of whom 200 (5.2%) had nonobCAD. Fewer nonobCAD patients received optimal medication use compared to obCAD patients at discharge (31% vs 65%, P < 0.001), driven primarily by lower rates of clopidogrel use (40.5% vs 83.3%, P < 0.001). After adjustment for percutaneous coronary intervention (PCI), differences in medication use were similar at discharge and 1 year after hospitalization. Stratified analyses by receipt of PCI suggested patients confined to medical management had less optimal medication use, regardless of their CAD burden. CONCLUSIONS: Lower rates of unadjusted optimal medication use were seen in nonobCAD patients, driven by low clopidogrel use among medically managed patients, suggesting improvement efforts should focus on these patients.

Aldosterone Does Not Predict Cardiovascular Events Following Acute Coronary Syndrome in Patients Initially Without Heart Failure.

BACKGROUND: Aldosterone may have adverse effects in the myocardium and vasculature. Treatment with an aldosterone antagonist reduces cardiovascular risk in patients with acute myocardial infarction complicated by heart failure (HF) and left ventricular systolic dysfunction. However, most patients with acute coronary syndrome do not have advanced HF. Among such patients, it is unknown whether aldosterone predicts cardiovascular risk. METHODS AND RESULTS: To address this question, we examined data from the dal-OUTCOMES trial that compared the cholesteryl ester transfer protein inhibitor dalcetrapib with placebo, beginning 4 to 12 weeks after an index acute coronary syndrome. Patients with New York Heart Association class II (with LVEF <40%), III, or IV HF were excluded. Aldosterone was measured at randomization in 4073 patients. The primary outcome was a composite of coronary heart disease death, nonfatal myocardial infarction, stroke, hospitalization for unstable angina, or resuscitated cardiac arrest. Hospitalization for HF was a secondary endpoint. Over a median follow-up of 37 months, the primary outcome occurred in 366 patients (9.0%), and hospitalization for HF occurred in 72 patients (1.8%). There was no association between aldosterone and either the time to first occurrence of a primary outcome (hazard ratio for doubling of aldosterone 0.92, 95% confidence interval 0.78-1.09, P=0.34) or hospitalization for HF (hazard ratio 1.38, 95% CI 0.96-1.99, P=0.08) in Cox regression models adjusted for covariates. CONCLUSIONS: In patients with recent acute coronary syndrome but without advanced HF, aldosterone does not predict major cardiovascular events. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00658515.

The Emerging Role of PCSK9 Inhibitors in Preventive Cardiology.

Low-density lipoprotein cholesterol (LDL-C) is a most important risk factor for developing coronary artery disease (CAD) and other forms of atherosclerotic cardiovascular disease (CVD) and a major focus of CVD risk reduction with lifestyle and statins. Unfortunately residual risk of CVD remains in patients with familial hypercholesterolaemia and/or statin intolerance in whom adequate LDL-C lowering is not accomplished with lifestyle and statins. PCSK9 is a serine protease that binds the LDL receptor (LDL-R) and acts as a chaparone for endocytosis and shuttling the PCSK9-LDLR complex to lysosomes for degradation. In the absence of PCSK9 the LDLR-LDL-C complex dissociates and LDL-R is recycled back to the cell surface. Humanised monoclonal antibodies (evolocumab, alirocumab, bocolicumab) have been developed that increase LDL-R by ~2-fold and lower LDL-C by up to 75 percent. This effect is synergistic to that of statins with the only common adverse effect is a local injection site reaction. At present, ongoing Phase III CVD outcome trials with PCSK9 inhibitors offer promise that patients with LDL-C levels that remain elevated can decrease CVD events and related mortality.