No abstract

Nonsteroidal antiinflammatory drugs (NSAIDs) are used in the management of a variety of conditions, but their prevalence is likely underreported as a result of widespread availability and the perception that nonprescription therapies are unnecessary to report during medication history taking. However, NSAIDs are associated with a number of adverse effects, especially in patients with cardiovascular disease (CVD). Patients with CVD and comorbidities for which NSAIDs may provide symptomatic relief (e.g., osteoarthritis, rheumatoid arthritis) tend to be older, which places them at greater risk of harm. For these reasons, the use of NSAIDs in patients with CVD is a significant public health concern. An understanding of the risks associated with NSAIDs is critical for clinicians across practice settings. In this review, we detail the safety of NSAIDs in patients with CVD, provide recommendations on their use in specific disease states, and discuss therapeutic alternatives.

Hospitals that used inpatient AQCV pharmacists performed better on process of care measures than hospitals that do not use inpatient AQCV pharmacists. However, improvements in process of care performance measures observed in AQCV hospitals did not translate into improved 30-day clinical outcomes.

Reduction in low-density lipoprotein cholesterol (LDL-C) is associated with a decrease in coronary heart disease (CHD). Statins are currently the most effective medications for LDL-C lowering; however, there continues to be a residual risk for cardiovascular events. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a protease that promotes LDL receptor degradation, leading to an increase in LDL-C blood levels. Patients with PCSK9 gain-of-function mutations can have up to a 20-fold increase in associated CHD compared with patients without these mutations. Conversely, patients with PCSK9 loss-of-function mutations can have up to an 88% reduction in CHD without any deficits in neurologic or physiologic functions. PCSK9 can be modulated by current antihyperlipidemic therapies. In particular, statins lead to an increase in PCSK9, which may attenuate their full lipid-lowering effects. These attributes have made PCSK9 inhibition a desirable target for future drug therapies. Current investigational modalities inhibiting PCSK9 will also be discussed.