The effect of inhomogeneities on the distance to the last scattering surface and the accuracy of the CMB analysis

The standard analysis of the CMB data assumes that the distance to the last scattering surface can be calculated using the distance-redshift relation as in the Friedmann model. However, in the inhomogeneous universe, even if =0, the distance relation is not the same as in the unperturbed universe. This can be of serious consequences as a change of distance affects the mapping of CMB temperature fluctuations into the angular power spectrum. In addition, if the change of distance is relatively uniform no new temperature fluctuations are generated. It is therefore a different effect than the lensing or ISW effects which introduce additional CMB anisotropies. This paper shows that the accuracy of the CMB analysis can be impaired by the accuracy of calculation of the distance within the cosmological models. Since this effect has not been fully explored before, to test how the inhomogeneities affect the distance-redshift relation, several methods are examined: the Dyer-Roeder relation, lensing approximation, and non-linear Swiss-Cheese model. In all cases, the distance to the last scattering surface is different than when homogeneity is assumed. The difference can be as low as 1% and as high as 80%. Excluding extreme cases, the distance changes by about 20-30%. Since the distance to the last scattering surface is set by the position of the CMB peaks, in order to have a good fit, the distance needs to be adjusted. After correcting the distance, the cosmological parameters change. Therefore, a not properly estimated distance to the last scattering surface can be a major source of systematics. This paper shows that if inhomogeneities are taken into account when calculating the distance then models with positive spatial curvature and with \Omega_\Lambda ~ 0.8-0.9 are preferred. The \Lambda CDM model in most cases, is at odds with the current data.Comment: 18 pages, 6 figure

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.)