Effects of Extended-Release Niacin on Quartile Lp-PLA2 Levels and Clinical Outcomes in Statin-treated Patients with Established Cardiovascular Disease and Low Baseline Levels of HDL-Cholesterol: Post Hoc Analysis of the AIM HIGH Trial.

BACKGROUND: Lipoprotein-associated phospholipase A2 (LpPLA2) is an inflammatory marker that has been associated with the presence of vulnerable plaque and increased risk of cardiovascular (CV) events. OBJECTIVE: To assess the effect of extended-release niacin (ERN) on Lp-PLA2 activity and clinical outcomes. METHODS: We performed a post hoc analysis in 3196 AIM-HIGH patients with established CV disease and low baseline levels of high-density lipoprotein cholesterol (HDL-C) who were randomized to ERN versus placebo on a background of simvastatin therapy (with or without ezetimibe) to assess the association between baseline Lp-PLA2 activity and the rate of the composite primary end point (CV death, myocardial infarction, stroke, hospitalization for unstable angina, and symptom-driven revascularization). RESULTS: Participants randomized to ERN, but not those randomized to placebo, experienced a significant 8.9% decrease in LpPLA2. In univariate analysis, the highest quartile of LpPLA2 activity (>208 nmol/min/mL, Q4) was associated with higher event rates compared to the lower quartiles in the placebo group (log rank P = .032), but not in the ERN treated participants (log rank P = .718). However, in multivariate analysis, adjusting for sex, diabetes, baseline LDL-C, HDL-C, and triglycerides, there was no significant difference in outcomes between the highest Lp-PLA2 activity quartile versus the lower quartiles in both the placebo and the ERN groups. CONCLUSION: Among participants with stable CV disease on optimal medical therapy, elevated Lp-PLA2 was associated with higher CV events; however, addition of ERN mitigates this effect. This association in the placebo group was attenuated after multivariable adjustment, which suggests that Lp-PLA2 does not improve risk assessment beyond traditional risk factors.

Bivalirudin fails to prevent atrial thrombus development in heparin-induced thrombocytopaenia and thrombosis syndrome.

An 81-year-old woman presented with acute decompensated heart failure due to new-onset atrial fibrillation and a flail myxomatous mitral valve which necessitated surgical mitral valve repair. No atrial thrombi were noted on transoesophageal echocardiograms performed prior to surgery and intraoperatively. Immediately postoperatively, while treated with unfractionated heparin, the patient developed thrombocytopaenia with positive platelet factor 4 antibodies and an abnormal serotonin functional platelet assay, consistent with heparin-induced thrombocytopaenia. The anticoagulation therapy was changed to the direct thrombin inhibitor bivalirudin with an improvement in the platelet count. Despite bivalirudin therapy, a left atrial layering thrombus was revealed on transoesophageal echocardiogram performed in preparation for cardioversion of the symptomatic atrial fibrillation. Anticoagulation was changed to warfarin, and the patient was discharged without thromboembolic complications neither during her hospital stay nor the 3-year outpatient follow-up.