© 2005 European Society of Cardiology
Effects of Atorvastatin on Th polarization in patients with acute myocardial infarction*
a The Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology Wuhan 430022, China
b The Center for Experimental Therapeutics, University of Pennsylvania School of Medicine 816 BRB II/III, 421 Curie Boulevard, Philadelphia, PA 19104, USA
* Corresponding author. Tel.: +86 27 85726376; fax: +86 27 85727140. E-mail address: liaoyh27{at}hotmail.com
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Abstract |
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Background: The development of heart failure after acute myocardial infarction (AMI) has been shown to be associated with inflammation, which is positively and negatively regulated by T helper (Th) 1 and Th2 lymphocytes, respectively. Several studies have indicated that statins can improve heart function after AMI.
Aims: To study the effects of atorvastatin on Th polarization in patients with AMI.
Methods: Peripheral blood mononuclear cells were collected from 20 patients with AMI treated with oral atorvastatin (10 mg/d, group AMI-A) and 18 patients with AMI (group AMI-C) who did not receive treatment with statins. Cytokine-producing Th lymphocytes were quantified by 3-color flow cytometry. After in vitro culturing in the presence or absence of atorvastatin (0, 0.3, 1 and 3 µmol/L) for 6 days, cytokine-producing Th lymphocytes were quantified again in AMI-C group.
Results: The ratio of IFN-
-producing T cells was significantly higher in AMI-C group (17.8%±6.4%) than in the AMI patients treated with oral atorvastatin (AMI-A, 13.1%±4.6%). In vitro culturing with atorvastatin significantly reduced Th1 development in the AMI-C group. There was no significant difference on the frequencies of interleukin (IL)-4-producing T cells between each group.
Conclusions: Atorvastatin can reduce Th1 development but has no effect on Th2 cell-functions in AMI patients. Our findings suggest that atorvastatin can regulate the polarization of Th1/Th2, this may be one of the mechanisms through which atorvastatin improves heart function after AMI.
Key Words: HMG-CoA reductase inhibitor • Acute myocardial infarction • T lymphocyte • helper • Heart failure
Received August 28, 2004; Revised November 14, 2004; Accepted January 27, 2005
* This study was supported by grants from National Natural Science Foundation of China (No. 30370574).
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