Short-term atorvastatin preload reduces levels of adhesion molecules in patients with acute coronary syndrome undergoing percutaneous coronary intervention. Results from the ARMYDA-ACS CAMs (Atorvastatin for Reduction of MYocardial Damage during Angioplasty-Cell Adhesion Molecules) substudy
ABSTRACT In patients with stable angina receiving percutaneous coronary intervention (PCI) prevention of periprocedural myocardial infarction by atorvastatin pretreatment was associated with reduction of endothelial activation. This mechanism was not evaluated in patients with acute coronary syndrome (ACS). The aim was to investigate effects of atorvastatin load on adhesion molecules in ACS patients undergoing PCI.
In a planned subanalysis of the ARMYDA-ACS trial, a subgroup of 44 patients were blind-tested for measurement of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin plasma levels; 21 patients belonged to the atorvastatin (80 mg 12 h before PCI, with a further 40 mg preprocedure dose) and 23 to the placebo arm. Adhesion molecules were evaluated at randomization (12 h before intervention), immediately before PCI and after 8 and 24 h.
Reduction of procedural myocardial injury after statin pretreatment was confirmed in this subgroup. ICAM-1, VCAM-1 and E-selectin levels were similar at randomization and before intervention in both arms. At 8 h, ICAM-1 increase was similar in the two arms, whereas 24-h levels were lower in the atorvastatin vs. placebo group (241 ± 25 vs. 261 ± 30 ng/ml; P = 0.019). Significant attenuation of VCAM-1 elevation occurred both at 8 and 24 h in the atorvastatin group (509 ± 56 vs. 545 ± 59 ng/ml; P = 0.044 and 561 ± 58 vs. 600 ± 53 ng/ml; P = 0.025). E-selectin levels were not different at any time-point in the two arms.
In ACS patients undergoing PCI, reduction of procedural myocardial injury after atorvastatin load is associated with attenuation of endothelial inflammatory response. This may contribute to mechanisms of statin cardioprotection in this setting.
- SourceAvailable from: Simona Pisanti
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- "Other adhesion molecules in monocytes and T cells have been shown to be inhibited by statins, ICAM-1, CD11b, CD18, and CD49 (Weitz-Schmidt, 2003). A recent study in patients with acute coronary syndrome confirmed the reduced levels of adhesion molecules ICAM-1 and vascular cell adhesion molecule-1 after short-term atorvastatin preload (Patti et al., 2010). These effects might result in reduced migration and infiltration of the leukocytes along with strongly reduced T-cell activation. "
ABSTRACT: Statins, among the most commonly prescribed drugs worldwide, are cholesterol-lowering agents used to manage and prevent cardiovascular and coronary heart diseases. Recently, a multifaceted action in different physiological and pathological conditions has been also proposed for statins, beyond anti-inflammation and neuroprotection. Statins have been shown to act through cholesterol-dependent and -independent mechanisms and are able to affect several tissue functions and modulate specific signal transduction pathways that could account for statin pleiotropic effects. Typically, statins are prescribed in middle-aged or elderly patients in a therapeutic regimen covering a long life span during which metabolic processes, aging, and concomitant novel diseases, including cancer, could occur. In this context, safety, toxicity, interaction with other drugs, and the state of health have to be taken into account in subjects treated with statins. Some evidence has shown a dichotomous effect of statins with either cancer-inhibiting or -promoting effects. To date, clinical trials failed to demonstrate a reduced cancer occurrence in statin users and no sufficient data are available to define the long-term effects of statin use over a period of 10 years. Moreover, results from clinical trials performed to evaluate the therapeutic efficacy of statins in cancer did not suggest statin use as chemotherapeutic or adjuvant agents. Here, we reviewed the pharmacology of the statins, providing a comprehensive update of the current knowledge of their effects on tissues, biological processes, and pathological conditions, and we dissected the disappointing evidence on the possible future use of statin-based drugs in cancer therapy.Pharmacological reviews 11/2011; 64(1):102-46. DOI:10.1124/pr.111.004994 · 18.55 Impact Factor
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ABSTRACT: The pupil is one objective marker of vision and autonomic pathways. A good understanding of its anatomy and careful examination techniques are the essential tools for proper clinical diagnosis of pupillary disorders.Ophthalmology Clinics of North America 04/2001; 14(1):149-68.
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ABSTRACT: Many previous studies have demonstrated that statins pre-treatment before percutaneous coronary intervention (PCI) reduced myocardial infarction (MI) in statin-naive patients with both stable angina and acute coronary syndrome. However, clinical benefit of statins is controversial as some studies have shown different results. A search of MEDLINE, EMBASE using the term statins AND PCI, statins AND percutaneous coronary intervention. The review was limited to articles published in English between January 1990 and July 2011. Most trials noted that statins pretreatment before PCI in patients are associated with risk reduction of periprocedural myocardial infarction (PMI) and major adverse cardiovascular events (MACE). The mechanisms underlying this protective action of statins possibly attribute to the pleiotropic effects. However, controversial results were also reported in some trials that early use of statins before PCI did not influence occurrence of PMI or long-term clinical outcomes. Statins therapy among PCI patients seems to be associated with a significant mortality advantage at early and long-term follow-up. However, currently early statins use before intervention still cannot serve as a routine strategy of treatment. Further large-scale randomized studies are critically required to demonstrate the importance of early treatment with statins in pre-PCI.Journal of Interventional Cardiology 01/2012; 25(2):156-62. DOI:10.1111/j.1540-8183.2011.00709.x · 1.32 Impact Factor