Coexistence of bicuspid aortic valve, aberrant right subclavian artery and common origin of carotid arteries

Background: Prevalence of bicuspid aortic valve (BAV) and right aberrant sub-clavian artery (ASA) separately is relatively common in general population, and much higher in some disorders. Surprisingly, coexistence of both valve and vessel anomalies has only been reported in single cases. Materials and methods: From 2008 to 2016, in a single, high-volume tertiary cardiac centre, patients who underwent chest computed tomography (CT) for various reasons, were retrospectively screened for the presence of right ASA. Results: Seventy-two patients with either right or left ASA were identified by CT. Among them 7 cases of BAV and right ASA coexistence were identified. Additionally, 1 case with coexisting common origin of carotid arteries (COCA) was visualised in this subgroup. Conclusions: Although coexistence of ASA and BAV has not been reported in paediatric population, it has been diagnosed in very few adults as well as in our series. Additional presence of COCA in this group seems to be very rare. From practical point of view, heart cannulation via the radial artery and subsequent ASA may be challenging. Similarly, COCA presence may have surgical implications during corrective procedures

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)