Effect of platelet activation on pulmonary hypertension in chronic obstructive pulmonary diseases. |
Hyung Jung Kim1, Moon Suk Nam1, Hyuck Moon Kwon1, Chul Min Ahn1, Sung Kyu Kim1, Won Young Lee1, Kyung Soon Song2 |
1Department of Intemal Medicine, College of Medicine, Yonsei University, Seoul, Korea 2Department of Clinical Pathology, Yonsei University, Seoul, Korea |
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Abstract |
Background There is evidence that platelet is activated in chronic obstructive pulmonary disease and activated platelet with injured endothelium contribute to the pathogenesis of pulmonary hyper. tension, prognostic factor of chronic obstructive pulmonary disease. So, we have investigated platelet function further in chronic obstructive pulmonary disease and effect of platelet activation on pulmonary hypertension.
Methods We studied platelet aggregation ratio and alpha-granule products such as platelet factor 4 (PF4) and beta.thrombomodulin ( β -TG) in control subjects and COPD without and with pulmonary hypertension subjects.
Results 1) The platelet aggregation ratio (PAR) was 0.99 ± 0.04 in control subjects. 0.98 ± 0.05 in COPD without pulmonary hypertension subjects and 0.89 ± 0.08 in COPD with pulmonary hypertension subjects. The platelet aggregation ratio of COPD subjects was tend to decrease than that of control subjects and the ratio of COPD with pulmonary hypertension subjects was significantly lower than that of control subjects. 2) The platelet factor 4 (PF4 , IU/ ml) was 4. 7 ± 1. 2 in control subjects, 18.6 ± 4.9 in COPD without pulmonary hypertension subjects, and 57.2 ± 12.7 in COPD with pulmonary hypertension subjects. The level of COPD subjects was significantly higher than that of control subjects and the level of COPD with pulmonary hypertension subjects was significantly higher than that of COPD without pulmonary hypertension subjects. 3) The beta.thromboglobulin ( β -TG , IU/ ml) was 34. 4 ± 5 . 8 in control subjects. 80.4 ± 18.1 in COPD without pulmonary hypertension subjects and 93.0 ± 14.0 in COPD with pulmonary hypertension subjects. The level of COPD subjects was significantly higher than that of control subjects and the level of COPD with pulmonary hypertension subjects was tend to increase than that of COPD without pulmonary hypertension subjects. 4) There was no correlation between the clinical parameters and PAR, PF4 and β -TG but there was significant correlation among PAR, PF4 and β-TG.
Conclusion The platelet is activated in chronic obstructive pulmonary disease and the platelet of COPD with pulmonary hypertension is tend to be activated more than that of COPD without pulmonary hypertension. So, activated platelet may involve in the pathogenesis and maintenance of pulmonary hypertension in COPD subjects and modulation of platelet activity that might reduce pulmonary hypertension needs to be determined. |
Key Words:
Platelet activation, Pulmonary hypertension, Chronic obstructive pulmonary disease |
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