Background
Patients with acute myocardial infarction (AMI) and non-obstructive 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. We aimed to determine if AMI patients with nonobCAD, compared to obCAD, received lower rates of prevention medications in the year following AMI.
Methods and Results
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 (e.g. aspirin, clopidogrel, statins, beta-blockers and ACEI/ARBs). We used multivariable logistic regression analyses to determine the association between nonobCAD to medication use and adjusted for potential confounders. 3630 AMI patients were studied, of which 200 (5.2%) had nonobCAD. Fewer nonobCAD patients received optimal medication use compared to obCAD patients at discharge (31% v. 65%, p<0.001), driven primarily by lower rates of clopidogrel use (40.5% v. 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.
Conclusion
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.
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.
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