Renal disease in patients with nonalcoholic fatty liver disease and chronic heart failure

Summary: in the present-day routine clinical practice, measurement of GFR in the absence of risk factors for the development of CKD is not common. However, recent research shows that evaluation of GFR in patients with NAFLD is imperative even in the absence of classical risk factors for CKD. Early detection of kidney damage in patients with CHF and NAFLD will enable to define the right dose of pharmacotherapy and avoid overdose

Rosuvastatin in patients with arterial hypertension and dyslipidemia: effects on microcirculation and pulse wave parameters

Aim. To investigate the parameters of pulse wave contour analysis (PWCA) and microcirculation (MC) in patients with arterial hypertension (AH), dyslipidemia (DLP), and high cardiovascular risk levels (SCORE >5%); to compare the dynamics of these parameters during the treatment with rosuvastatin or atorvastatin. Material and methods. The study included 82 patients (mean age 53±10 years) with the high-risk AH (SCORE levels >5%), DLP, and no strict contraindications to statins. All patients were randomised into two comparable groups: Group I (n=40; mean age 51±10 years), receiving atorvastatin and standard AH treatment; and Group II (n=42; mean age 52±10 years), receiving rosuvastatin and standard AH treatment. At baseline and after 5 weeks, all patients underwent the MC assessment (conjunctival biomicroscopy) and PWCA (AngioScan-01). The following parameters were assessed: stiffness index (SI), reflection index (RI), augmentation index (AIx), and increased pulse wave amplitude (PWA). Results. In the atorvastatin group, mean SI values were 5,87±2,05 m/s, RI values 35,64±19,98%, mean AIx values for heart rate of 75 beats per minute (AIx75) 41,21±14,56%, and mean central blood pressure (BP, Spa) levels 144,35±22,31 mm Hg. In the rosuvastatin group, the respective values were 5,01±2,56 m/s (SI), 37,01±14,56% (RI), 41,23±14,35% (AIx75), and 148,98±7,89 mm Hg (BP, Spa). All participants demonstrated PW Types A and B, as a marker of increased arterial stiffness, and positive AIx and AIx75 values. The treatment with atorvastatin and rosuvastatin was associated with a significant reduction in ∆SI (-0,87 and -0,89 m/s, respectively). Both groups demonstrated a non-significant reduction in ∆RI (-7,89 and -7,21%, respectively) and ∆AIx (-1,88 and -1,92%, respectively). PWA increased by 1,82±0,62 times in the atorvastatin group and by 1,95±0,81 times in the rosuvastatin group. At baseline, both groups demonstrated disturbed conjunctival MC (arterio-venular coefficient 1:3, stasis, and Stage III erythrocyte aggregation). Atorvastatin and rosuvastatin treatment was linked to a regression in the last two parameters, which could be explained by the improved vascular wall elasticity. Conclusion. In high-risk patients with AH, the PWCA data suggested an increase in arterial stiffness, which was combined with conjunctival MC disturbances. Statin therapy improved not only blood lipid levels, but also MC, vascular stiffness, and endothelial function parameters, which was more pronounced in the rosuvastatin group

Edoxaban versus warfarin in patients with atrial fibrillation

Contains fulltext : 125374.pdf (publisher's version ) (Open Access)BACKGROUND: Edoxaban is a direct oral factor Xa inhibitor with proven antithrombotic effects. The long-term efficacy and safety of edoxaban as compared with warfarin in patients with atrial fibrillation is not known. METHODS: We conducted a randomized, double-blind, double-dummy trial comparing two once-daily regimens of edoxaban with warfarin in 21,105 patients with moderate-to-high-risk atrial fibrillation (median follow-up, 2.8 years). The primary efficacy end point was stroke or systemic embolism. Each edoxaban regimen was tested for noninferiority to warfarin during the treatment period. The principal safety end point was major bleeding. RESULTS: The annualized rate of the primary end point during treatment was 1.50% with warfarin (median time in the therapeutic range, 68.4%), as compared with 1.18% with high-dose edoxaban (hazard ratio, 0.79; 97.5% confidence interval [CI], 0.63 to 0.99; P<0.001 for noninferiority) and 1.61% with low-dose edoxaban (hazard ratio, 1.07; 97.5% CI, 0.87 to 1.31; P=0.005 for noninferiority). In the intention-to-treat analysis, there was a trend favoring high-dose edoxaban versus warfarin (hazard ratio, 0.87; 97.5% CI, 0.73 to 1.04; P=0.08) and an unfavorable trend with low-dose edoxaban versus warfarin (hazard ratio, 1.13; 97.5% CI, 0.96 to 1.34; P=0.10). The annualized rate of major bleeding was 3.43% with warfarin versus 2.75% with high-dose edoxaban (hazard ratio, 0.80; 95% CI, 0.71 to 0.91; P<0.001) and 1.61% with low-dose edoxaban (hazard ratio, 0.47; 95% CI, 0.41 to 0.55; P<0.001). The corresponding annualized rates of death from cardiovascular causes were 3.17% versus 2.74% (hazard ratio, 0.86; 95% CI, 0.77 to 0.97; P=0.01), and 2.71% (hazard ratio, 0.85; 95% CI, 0.76 to 0.96; P=0.008), and the corresponding rates of the key secondary end point (a composite of stroke, systemic embolism, or death from cardiovascular causes) were 4.43% versus 3.85% (hazard ratio, 0.87; 95% CI, 0.78 to 0.96; P=0.005), and 4.23% (hazard ratio, 0.95; 95% CI, 0.86 to 1.05; P=0.32). CONCLUSIONS: Both once-daily regimens of edoxaban were noninferior to warfarin with respect to the prevention of stroke or systemic embolism and were associated with significantly lower rates of bleeding and death from cardiovascular causes. (Funded by Daiichi Sankyo Pharma Development; ENGAGE AF-TIMI 48 ClinicalTrials.gov number, NCT00781391.)