Less invasive fractional flow reserve measurement from 3-dimensional quantitative coronary angiography and classic fluid dynamic equations

AIMS: The aim of this study was to develop a simplified model of FFR calculation (FFRsim) derived from three-dimensional (3D) coronary angiographic data and classic fluid dynamic equations without using finite element analysis. METHODS AND RESULTS: Intracoronary pressure measurements were performed by pressure wire sensors. The lumens of the interrogated vessel segments were reconstructed in 3D. The coronary artery volumetric flow was calculated based on the velocity of the contrast material. Pressure gradients were computed by classic fluid dynamic equations. The diagnostic power of the simplified computation of the FFR (FFRsim) was assessed by comparing the results with standard invasive FFR measurements (FFRmeas) in 68 vessels with a single stenosis. We found a strong correlation between the FFRsim and the FFRmeas (r=0.86, p0.88 and the FFRsim ≤0.8 ranges. In our patient population, these ranges were found in 69% of the cases. CONCLUSIONS: According to our simplified model, the invasive FFR measurement can be omitted without misclassification in pre-specified ranges of the calculated FFRsim

Association between use of oral anti-diabetic drugs and the risk of sepsis: A nested case-control study

[[abstract]]Although oral antidiabetic drugs (OADs) have been associated with immunomodulation in preclinical studies, little is still known about the association between the use of OADs and the risk of sepsis. Using a cohort of patients, extracted from Taiwan's National Health Insurance Research Database, with type 2 diabetes who were newly diagnosed between 2010 and 2012 and treated with OADs, we conducted a nested case-control study involving 43,015 cases (patients who were first hospitalized for sepsis) and 43,015 matched controls. Compared with non-use, metformin use was associated with a decreased risk of developing sepsis (adjusted odds ratio [OR] 0.80, 95% confidence interval [CI] 0.77-0.83, P < 0.001), but meglitinide (adjusted OR 1.32, 95% CI 1.25-1.40, P < 0.001) use was associated with the increased risk of developing sepsis. The risk for development of sepsis was also lower among current (adjusted OR 0.87, 95% CI 0.78-0.96) and recent (adjusted OR 0.83, 95% CI 0.73-0.94) thiazolidinedione users. Current or recent sulfonylurea use and dipeptidyl peptidase-4 inhibitor use were not significantly associated with the development of sepsis. Our results highlight the need to consider the potential pleiotropic effect of OADs against sepsis in addition to the lowering of blood glucose

Thrombin-receptor antagonist vorapaxar in acute coronary syndromes

BACKGROUND Vorapaxar is a new oral protease-activated–receptor 1 (PAR-1) antagonist that inhibits thrombin-induced platelet activation. METHODS In this multinational, double-blind, randomized trial, we compared vorapaxar with placebo in 12,944 patients who had acute coronary syndromes without ST-segment elevation. The primary end point was a composite of death from cardiovascular causes, myocardial infarction, stroke, recurrent ischemia with rehospitalization, or urgent coronary revascularization. RESULTS Follow-up in the trial was terminated early after a safety review. After a median follow-up of 502 days (interquartile range, 349 to 667), the primary end point occurred in 1031 of 6473 patients receiving vorapaxar versus 1102 of 6471 patients receiving placebo (Kaplan–Meier 2-year rate, 18.5% vs. 19.9%; hazard ratio, 0.92; 95% confidence interval [CI], 0.85 to 1.01; P = 0.07). A composite of death from cardiovascular causes, myocardial infarction, or stroke occurred in 822 patients in the vorapaxar group versus 910 in the placebo group (14.7% and 16.4%, respectively; hazard ratio, 0.89; 95% CI, 0.81 to 0.98; P = 0.02). Rates of moderate and severe bleeding were 7.2% in the vorapaxar group and 5.2% in the placebo group (hazard ratio, 1.35; 95% CI, 1.16 to 1.58; P<0.001). Intracranial hemorrhage rates were 1.1% and 0.2%, respectively (hazard ratio, 3.39; 95% CI, 1.78 to 6.45; P<0.001). Rates of nonhemorrhagic adverse events were similar in the two groups. CONCLUSIONS In patients with acute coronary syndromes, the addition of vorapaxar to standard therapy did not significantly reduce the primary composite end point but significantly increased the risk of major bleeding, including intracranial hemorrhage