International geographic variation in event rates in trials of heart failure with preserved and reduced ejection fraction.
Total cholesterol, triglycerides and low-density lipoprotein decreased significantly (P = 0.000) and maintained at a low level. The carotid artery IMT decreased significantly (P = 0.022) at the end of this study, but the femoral and iliac artery IMT did not show any obvious change. There were no serious adverse events noticed, during the study period.
The results of our pilot study suggest possible gender-dependent effects of the rs4149056 variant within the SLCO1B1 gene on statin treatment efficacy.
Soluble TF (sTF) significantly correlated with thrombin generation as measured by prothrombin fragment F1.2 at baseline. This correlation was lost 6 weeks and 6 months after initiation of statin therapy. In vivo, F1.2 was significantly lowered after 6 months of statin therapy by both, low dose (0 vs. 10 mg: 1.3+/-0.3 vs. 0.7+/-0.2 ng/ml; P<0.05) and high dose (0 vs. 80 mg: 1.2+/-0.3 vs. 0.6+/-0.2 ng/ml; P=0.01) atorvastatin compared to control. However, sTF and free TFPI did not change significantly with atorvastatin therapy when compared to baseline or control.
A pooled, subgroup analysis of three randomized, controlled, double-blind, 12-week trials.
Atorvastatin (10 mg daily) was administrated orally during 5 months to 17 men with normal plasma lipid and standard semen parameters. Spermatozoa parameters, accessory gland markers, semen lipid levels and blood levels of gonadal hormones were assayed before statin intake, during the treatment, and 3 months after its withdrawal.
Of the 18,889 patients participating in the 2 trials, 199 had RA, 46 had AS, and 35 had PsA. Lipid-lowering therapy consisted of an intensive regimen of atorvastatin 80 mg or a conventional/low-dose regimen of atorvastatin 10 mg or simvastatin 20-40 mg. The median duration of followup was nearly 5 years. Changes in lipid levels were examined by analyses of covariance. The effect on CVD was examined by Cox regression analyses, and heterogeneity tests were performed.
The two cases reported here and the brief literature review emphasize the impact of genetic factors on the risk of myopathy with statins. Although genotyping all patients before initiating therapy is not recommended at present, pharmacogenetic testing may be useful for new patients who have a family history of statin-induced myopathy.
Six studies from 2006-2008 that have influenced clinical management of stroke and threatened stroke are presented. The ABCD2 score effectively stratifies the short-term risk of stroke following transient ischemic attack into those with a high (12%), moderate (6%), and low (1%) 7-day stroke risk. High-dose atorvastatin reduces recurrent stroke in patients with recent stroke, but probably slightly increases central nervous system hemorrhage (SPARCL). Intravenous tissue plasminogen activator is of overall benefit to selected patients when given 3 to 4.5 hours after ischemic stroke onset (ECASS III). Adjusted-dose warfarin is far superior to aspirin and is relatively safe for very old people with atrial fibrillation (BAFTA). Despite results from 3 recent randomized trials (SAPPHIRE, EVA-3S and SPACE) the optimal role of carotid angioplasty/stenting vs. endarterectomy remains unclear. Enoxaparin once daily is an efficacious alternative to unfractionated heparin twice daily for prevention of venous thromboembolism after acute ischemic stroke (PREVAIL). These recent studies add important pieces to the complex puzzle of optimal stroke prevention and treatment.
Adult male Wistar rats were subjected to SDH and successful establishment of SDH was confirmed by magnetic resonance imaging (MRI). The treatment was initiated 6 hours after SDH induction. For the treatment, rats suffering SDH were randomly divided into saline group (the control group, rats were treated by saline, n=29) and atorvastatin group (rats were treated by atorvastatin, 3mg/kg/day, n=30). The volume of lesion before treatment as well as on day 2 and day 7 after initial treatment was measured by MRI, respectively. The behaviors before SDH induction and on the days 1, 3, 5 and 7 after the initial treatment were dynamically evaluated. Gene expression, cytokine secretion and the number of neutrophilic granulocyte and vascular density were measured in both neomembrane and SDH lesion on the day 2 and day 7 after the initial treatment.
We studied the effect of atorvastatin on insulin sensitivity and the plasma adiponectin and leptin concentrations. Our randomized open labeled study had 29 hyperlipidemic Type 2 diabetic patients (14 females, 15 males, mean age 60.0+/-2.2 yr). They were randomized into three 12-week atorvastatin intervention types. Each day patients were given either 10 mg (no.=10), 20 mg (no.=10) or 40 mg (no.=9). Evaluations were performed before and after intervention.
Niemann-Pick C1-like 1 protein (NPC1L1) plays a key role in lipoprotein metabolism. We examined the association of common genetic polymorphisms in NPC1L1 on apolipoprotein (apo) B-100 metabolism and the response to statin treatment in 37 men with central obesity.