Effect of Intensive Atorvastatin Therapy on Periprocedural Phosphatase and Tension Homolog Deleted on Chromosome Ten (PTEN) Expression in CD4+T Lymphocytes of Patients with Unstable Angina Undergoing Percutaneous Coronary Intervention

Objectives: To investigate the effects of intensive atorvastatin therapy on Phosphatase and tension homolog deleted on chromosome ten (PTEN) expression by CD4+ T lymphocytes in patients with unstable angina (UA) who received percutaneous coronary intervention (PCI). Methods: All patients with UA wer...

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Bibliographic Details
Main Authors: Jiang-you Wang, Han Chen, Dan Song, Jian Peng, Xi Su
Format: Article
Language:English
Published: Barcaray International 2016-01-01
Series:International Cardiovascular Forum Journal
Subjects:
Online Access:http://icfjournal.org/index.php/icfj/article/view/246/Wang%20246%20pp85-90
Description
Summary:Objectives: To investigate the effects of intensive atorvastatin therapy on Phosphatase and tension homolog deleted on chromosome ten (PTEN) expression by CD4+ T lymphocytes in patients with unstable angina (UA) who received percutaneous coronary intervention (PCI). Methods: All patients with UA were randomly allocated to pretreatment with intensive atorvastatin (ATV, 80mg 12h before PCI, with a further 20mg every day after PCI, n = 56) or conventional dose (control group, only 20 mg/day, n = 56). Circulating CD4+ T cells were subsequently obtained prior to PCI and 18–24 h after successful PCI, using a magnetic cell sorting system. Plasma cardiac troponin I (cTnI), creatine kinase-MB (CK-MB), high sensitivity C reactive protein (hsCRP), interleukin-10 (IL-10) and tumor necrosis factor a(TNF-a) levels were measured just prior to the PCI and 18–24 h after PCI. PTEN mRNA and protein were determined by Real-time PCR and western blots, respectively. Results: PTEN mRNA and protein were dramatically decreased in ATV group (p < 0.05). In contrast, TNF-and hsCRP significantly increased following PCI in both groups, with the ATV group being higher than control group (p < 0.05). IL-10 also markedly increased following PCI for the two groups. However, higher values were associated with the ATV group (p < 0.05). Compared to the control group, the incidence of elevated cTnI levels post-PCI was lower in the ATV group (p < 0.05); however, no difference could be found between the two groups regarding the incidence of elevated CK-MB post-PCI (p >0.05). Conclusions: Intensive atorvastatin treatment reduced the post-PCI myocardial inflammatory response in patients with UA, possibly by enhancing PTEN expression in CD4+ T lymphocytes.
ISSN:2410-2636
2409-3424