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Relationship between Two Blood Stasis Syndromes and Inflammatory Factors in Patients with Acute Coronary Syndrome
Authors:MA Cai-yun  LIU Jian-xun  SHI Da-zhuo and LIU Jing-hua
Institution:1.Department of Cardiology, Beijing Anzhen Hospital,Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Diseases,Beijing,China;2.Institute of Basic Medical Sciences, Xiyuan Hospital,China Academy of Chinese Medical Sciences,Beijing,China;3.Cardiovascular Diseases Center, Xiyuan Hospital,China Academy of Chinese Medical Sciences,Beijing,China;4.Department of Cardiology,Aviation General Hospital,Beijing,China
Abstract:

Objective

To investigate the relationship between inflammatory factors and two Chinese medicine (CM) syndrome types of qi stagnation and blood stasis (QSBS) and qi deficiency and blood stasis (QDBS) in patients with acute coronary syndrome (ACS).

Methods

Sixty subjects with ACS, whose pathogenesis changes belongs to qi disturbance blood stasis syndrome, were divided into 2 groups: 30 in the QSBS group and 30 in the QDBS group. The comparative analysis on them was carried out through comparing general information, coronary angiography and inflammatory factors including intracellular adhesion molecule-1 (ICAM-1), chitinase-3-like protein 1 (YKL-40) and lipoprotein-associated phospholipase A2 (Lp-PLA2).

Results

Compared with the QSBS group, Lp-PLA2 and YKL-40 levels in the QDBS group showed no-significant difference (P>0.05); ICAM-1 was significantly higher in the QDBS group than in the QSBS group in the pathological processes of qi disturbance and blood stasis syndrome of ACS (P<0.05).

Conclusions

Inflammatory factor ICAM-1 may be an objective basis for syndrome typing of QSBS and QDBS, which provides a research direction for standardization research of CM syndrome types.
Keywords:coronary heart disease  Chinese medicine  qi deficiency and blood stasis syndrome  qi stagnation and blood stasis syndrome  inflammation  intracellular adhesion molecule-1  chitinase-3-like protein 1  lipoprotein-associated phospholipase A2
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