Zawartość metalicznych i niemetalicznych pierwiastków w homogenatach próbek tkankowych pobranych z amputowanych na poziomie uda z powodu miażdżycy kończyn dolnych. Doniesienie wstępne

Background: Metallic and non-metallic elements have influence on the development the changes within structure and function of arteries in different regions of vascular tree. The content of elements into arterial walls varies according to geographical origin of people. Material and methods: Tissue specimens were taken from the six lower limbs amputated on the level of thigh due to atherosclerosis. The mean age was 69 (57 to 84). Tissue specimens were collected from the limbs from the level of amputation, the popliteal fossa and the dorsal artery of foot. After chemical processing of the tissues homogenates determination of the content of elements using atomic emission spectrometry method with inductively coupled plasma (inductively coupled plasma optical emission spectroscopy) was performed. The content of Al, Ba, Ca, Cu, Fe, K, Mg, Mn, P, S, Sr and Zn was determined. Results: As a point of reference mean absolute value occurred from six specimens on the level of thigh was assumed as 100%. Content of non-metallic elements such as Ca, P and S rise towards to periphery of amputated limb reaching few times higher values on the level of dorsal artery of foot. Content of some metallic elements such as: Fe, Zn, K and Sr also rise towards to periphery of extremity. The Cu accumulation was the highest on the level of popliteal fossa, while Mn, Al and Mg concentration was the lowest on this same level and the highest in dorsal artery of foot. Conclusions: The influence of individual elements on development the atherosclerosis especially on necrotic changes requires further investigations. Described problem pose a preliminary report only in order to indicate the issue and to check the method of analysis

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.)