No abstract

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.

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.

Background: We have investigated outcomes of contemporary management in patients undergoing stress echocardiography for evaluation of chest pain. Methods: Records of 294 consecutive patients who underwent a stress echocardiogram at a single tertiary care center were reviewed. Demographic, clinical data, and outcomes were collected. ANOVA, chi-square, and logistic regression analyses were used. Mean follow up length was 37 months. The study was approved by the IRB. Results: This study cohort included 46% women, with an average age of 61 +/- 10.6 years old; 20% were current smokers, with history of CAD in 26%, CHF in 4%, hypertension in 40%, diabetes in 14%, and peripheral vascular disease in 4%. Baseline medical treatment included beta blockers in 46% and ACE inhibitors in 24%. The majority (94%) of these patients underwent a dobutamine stress echocardiogram. Fifty five of the 294 patients had ischemia during the test. Males were twice as likely to have ischemia during the stress test compared to females (24% vs. 12% p=0.009). There was a trend towards increased prevalence of ischemia in diabetics (26% vs. 17% p=0.175) and in smokers (24% vs. 17% p=0.262). The presence of ischemia was associated with a 40% increase in mortality (14.5% vs. 10.5%) and an approximately 3-fold increase in MI (9.1% vs. 2.9% p=0.0679). Patients with ischemia during stress testing were ten times more likely to have invasive cardiac evaluation and changes in medications compared to patients without ischemia during stress testing (41.5% vs. 4.1% p<0.001) or undergo invasive evaluation without a change in medications (24.5% vs. 3.3% p<0.001). Invasive evaluation was not associated with a reduction in mortality (13.4% vs. 10.4% p=0.349). However, change in medications alone was associated with increased mortality (16.7% vs. 9.7% p=0.04). Conclusions: In the majority of contemporary managed patients with suspected coronary artery disease, stress testing is likely to have a normal result. When abnormal, it typically leads to invasive evaluation and/or medication changes. The small sample size of patients with ischemia in our study limits our ability to discern the effects of invasive evaluation and/or medicine changes on outcomes. Additional studies of this important subject are needed.