atorvastatin Lipitor
A pharmacoeconomic evaluation of the myocardial ischemia reduction with aggressive cholesterol lowering (MIRACL) study in Canada.

Casciano R, Tarride JE, Breton MC, Stern L, Langer A.

The Analytica Group, New York, New York, USA. rcasciano theanalyticagroup.com

OBJECTIVE: To determine a 16-week total healthcare cost and the cost-effectiveness of short-term, lipid-lowering therapy with atorvastatin 80 mg following acute coronary syndrome (ACS) in Canada. METHODS: The expected costs per patient on atorvastatin 80 mg per day and placebo were compared using clinical outcome data from the MIRACL study and cost data from the Ontario Case Costing Project and the Ontario Schedule of Benefits. The cost per event avoided was also assessed. The clinical outcomes measured included: death, cardiac arrest, non-fatal myocardial infarction (MI), fatal MI, angina pectoris, stroke, congestive heart failure, and surgical or percutaneous coronary revascularizations. All direct medical costs from the perspective of the Canadian health care system were taken into account. RESULTS: The total expected cost per patient was 2,590 dollars in the placebo group and 2,639 dollars in the atorvastatin group. The incremental cost of atorvastatin treatment (49.26 dollars per patient) corresponded to a cost of 1,285 dollars per event avoided. The cost savings obtained through the reduction in events offset 86% of the cost of atorvastatin treatment. Budget impact analysis revealed that increased rates of atorvastatin usage following ACS were associated with large numbers of events avoided at a small additional cost when projected to the Canadian population. CONCLUSIONS: In Canada, the clinical benefits of intensive short-term atorvastatin treatment administered within 96 hours after ACS were associated with a favorable cost-effectiveness ratio. The incremental cost of atorvastatin is mostly offset by savings due to the reduction in events in patients treated with atorvastatin.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15300960&dopt=Abstract atorvastatin Lipitor



atorvastatin Lipitor
[Effects of atorvastatin on the function of dendritic cells in patients with unstable angina pectoris]

[Article in Chinese]

Li DZ, Ranjit S, Zeng QT, Tian Y, Feng YB, Wang X, Cao LS.

Department of Cardiology, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, China. lidazhuhp sohu.com

OBJECTIVE: To investigate the function of dendritic cells (DC) in patients with unstable angina pectoris (UAP) and the effects of atorvastatin on it. METHODS: 27 patients with UAP were divided into two groups treated respectively with regular pharmacotherapy and regular pharmacotherapy plus atorvastatin. PBMC from the UAP patients (before and 2 weeks after the treatment) and 11 healthy subjects were incubated and induced to mature DC in a completed medium containing GM-CSF and IL-4. Flow cytometric analysis was used to detect the expression of co-stimulating factor CD86 (B7-2) on DC. The stimulating capacity of DC was determined in allogenic mixed lymphocyte reaction (MLR). ELISA was used to analyze the level of cytokines (IL-1beta, IL-6, IL-10 and TNF-alpha) in the medium of MLR. Relationship of expression of CD86 to risk factors and blood CRP level was also analyzed. RESULTS: When compared with normal group, CD86 on DC was much more expressed in UAP patients; the stimulating capacity of DC in MLR was higher; T lymphocytes in MLR secreted higher levels of pro-inflammation cytokines (IL-1beta, IL-6 and TNF-alpha) and lower level of anti-inflammation cytokine (IL-10). Blood LDL-C before treatment was positively related to the expression of CD86. Atorvastatin inhibited the function of DC and lowered blood level of CRP and CD86, the levels of which were significantly positively correlated. CONCLUSIONS: DC in UAP are activated, which may play an important role in initiating immune reaction in the plaque. LDL-C may be one of the activators of DC; inhibitory effect of atorvastatin on inflammation in UAP may be due to its inhibition on DC.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15312437&dopt=Abstract atorvastatin Lipitor



atorvastatin Lipitor
Atorvastatin induces tissue transglutaminase in human endothelial cells.

Soehnlein O, Eskafi S, Schmeisser A, Kloos H, Daniel WG, Garlichs CD.

Medical Clinic II, Friedrich-Alexander-University of Erlangen-Nuremberg, Ulmenweg 18, 91054 Erlangen, Germany.

Tissue transglutaminase (tTgase) contributes to the organisation of the basement membrane and is therefore thought to be important for the integrity and stability of the vessel wall. In the present study, we hypothesised that the HMG-CoA reductase inhibitor atorvastatin may up-regulate the tTgase expression in endothelial cells and thereby exert beneficial effects on endothelial function. Treatment of human umbilical vein endothelial cells (HUVEC) with atorvastatin (1-10 microM) caused a clear increased expression of tTgase in both permeabilised and non-permeabilised HUVEC. In contrast, stimulation of HUVEC with TNFalpha had no substantial effect on tTgase expression or localisation but inhibited the atorvastatin-induced up-regulation and externalisation of tTgase. Propidium iodide staining revealed that statin-induced apoptosis is not responsible for the enhanced expression. By inducing the expression of tTgase, statins may promote tTgase-mediated stabilisation of the basement membrane. This effect of atorvastatin may contribute to the beneficial role of statins on endothelial function.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15313180&dopt=Abstract atorvastatin Lipitor



atorvastatin Lipitor
Histological and morphometrical examinations of suprarenal glands in rats after experimental administration of atorvastatin and ethanol.

Zarebska A, Izdebska M, Sekita-Krzak J, Matusiewicz J, Visconti J.

Department and Institute of Histology and Embryology with the Laboratory for Experimental Cytology, Medical University of Lublin, Lublin, Poland.

The experiment was carried out on Wistar rat males weighting about 250 g. Animals from control group I received water and standard granulated fodder ad libitum. Animals from control group II received 20% ethanol instead of water. Animals from experimental group I received Atorvastatin in the dose of 0.28 mg/24h, animals from experimental group II received Atorvastatin in the dose of 2.8 mg/24h, animals from experimental group III received 20% ethanol + Atorvastatin in the dose of 0.28 mg. After 6 weeks the animals were decapitated. H+E staining, PAS method for detection of neutral mucopolysaccharides and Thomas's reaction for detection of lipids were made on 6 micron thick sections. The surface areas of the nuclei sections were assessed in the zona fasciculata. It was stated that ethanol causes strong hyperemia of suprarenal cortex, the high dose of atorvastatin--2.8 mg/24h and small dose of atorvastatin--0.28 mg/24h administered with ethanol cause the decrease of lipid amount in the whole suprarenal cortex and degenerative changes in many cells of the zona fasciculata.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15314998&dopt=Abstract atorvastatin Lipitor



atorvastatin Lipitor
The lipid-regulating effects of atorvastatin on type 2 elder diabetes patients with hyperlipidemia.

Tu L, Liu X, Li R, Huang K, Yao H, Fan Q.

Department of Integration, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

To investigate the effect of atorvastatin on lipid metabolism in type 2 elder diabetes patients with hyperlipidemia, 26 patients with type 2 elder diabetes complicated with hyperlipidemia were treated with atorvastatin (10 mg/d) for 8 weeks. The serum triglyceride (TG), high density protein cholesterol (HDL-C) and low density protein cholesterol (LDL-C) were measured before and after the treatment. Meanwhile, the non-denaturing polyacrylamide gradient gel electrophoresis was used for detection of small-sized LDL(SLDL). Our results showed that TG dropped from 4.88 +/- 0.72 mmol/L to 2.65 +/- 0.32 mmol/L; HDL-C was increased from 0.85 +/- 0.31 mmol/L to 1.28 +/- 0.29 mmol/L; LDL-C was declined from 3.71 +/- 2.98 mmol/L to 2.10 +/- 1.22 mmol/L, sLDL-A was increased from (42.49 +/- 8.1)% to (53.27 +/- 7.5)%; LDL-B was decreased from (57.91 +/- 8.1)% to (46.73 +/- 7.5% ) (P<0.05). The level of blood glucose was not changed at the end of 8th week. It is concluded that atorvastatin has satisfactory lipid-regulating effects on type 2 elder diabetes patients with hyperlipidemia.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15315163&dopt=Abstract atorvastatin Lipitor



atorvastatin Lipitor
Lipid-altering changes and pleiotropic effects of atorvastatin in patients with hypercholesterolemia.

Sakabe K, Fukuda N, Wakayama K, Nada T, Shinohara H, Tamura Y.

Department of Cardiology and Clinical Research, National Zentsuji Hospital, 2-1-1 Senyu-cho, Zentsuji, Kagawa 765-8507, Japan. ksakabe jun.ncvc.go.jp

In this prospective study, we found beneficial short-term effects from atorvastatin therapy, including effects on low-density lipoprotein subfractions and remnant-like lipoprotein particle cholesterol, antioxidant effects, and alterations in endothelial function that may be important in early benefit from statin therapy; some effects would support much earlier benefit than previously reported. We also found long-term effects of atorvastatin, including decreased plasminogen activator inhibitor type-1 and additional significant alterations in low-density lipoprotein subfractions and endothelial function, supporting benefits from continuous long-term atorvastatin therapy beyond early reversal of hypercholesterolemia.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15325939&dopt=Abstract atorvastatin Lipitor