Measurement of Thrombus Precursor Protein in the Diseases Associated with Thrombosis and Changes after Heparin Therapy.
- Author:
Nan Young LEE
1
;
Tae Yeob KIM
;
Dong Kil JUNG
;
Jang Soo SUH
Author Information
1. Department of Clinical Pathology, School of Medicine, Kyungpook National University, Daegu, Korea.
- Publication Type:Original Article
- Keywords:
Thrombus precursor protein;
Thrombosis;
Atherosclerosis;
Acute myocardial infarction;
Unstable angina;
Aortic dissection;
Cerebral infarction;
Heparin
- MeSH:
Angina, Unstable;
Atherosclerosis;
Cerebral Infarction;
Chest Pain;
Emergency Service, Hospital;
Enzyme-Linked Immunosorbent Assay;
Fibrinolytic Agents;
Heparin*;
Humans;
Myocardial Infarction;
Plasma;
Thrombosis*
- From:Korean Journal of Clinical Pathology
2001;21(6):431-436
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: The relationship between thrombosis and atherosclerosis has long been recognized. It is important to diagnose them earlier and utilize thrombolytic agents earlier in the clinical diseases associated with thrombosis and atherosclerosis. So we measured the thrombus precursor protein (TpP) in these diseases and intended to investigate the changes after heparin therapy. METHODS: TpP concentration was measured in 17 patients with acute myocardial infarction (AMI), 7 patients with unstable angina (UA), 2 patients with aortic dissection (AD), 10 patients with other chest pain, and 9 patients with cerebral infarction and 18 healthy controls. We divided AMI into two groups, early presenters (n=10) who presented to the emergency room (ER) within 6 hours and late presenters (n=7) who presented to the ER after 6 hours of the onset of chest pain. Among the patients, in 24 patients treated with unfractionated heparin, the level of TpP was measured from plasma at 8 hours after therapy. We used the microtiter plate ELISA procedure. RESULTS: TpP was significantly increased in AD (mean+/-SD; 51.21+/-8.08 microgram/mL), AMI (12.07+/-9.62 microgram/mL), early AMI (11.39+/-9.25 microgram/mL), late AMI (13.05+/-10.78 microgram/mL), cerebral infarction (7.34+/-4.67 microgram/mL), and UA (7.05+/-4.72 microgram/mL) compared with healthy controls (3.03+/-1.48 g/ mL). Abnormal concentrations of TpP were observed in 2 of 2 patients (100%) with AD, 12 of 17 patients (70.6%) with AMI, 8 of 10 patients (80.0%) with early AMI, 4 of 7 patients (57.1%) with late AMI, 5 of 9 patients (55.6%) with cerebral infarction, 3 of 7 patients (42.9%) with UA, and 2 of 10 patients (20.0%) with other chest pain. Among the 24 patients following heparin therapy, the level of TpP did not show significant decrease after heparin therapy in the group of UA and AMI with increased TpP above the upper limit of normal (n=14). CONCLUSTIONS: TpP appears to be a sensitive marker of the clinical diseases associated with thrombosis and atherosclerosis. But, TpP measurement does not allow for the accurate monitoring in the treatment with unfractionated heparin.
