| Background:Acute coronary syndrome (ACS) is one kind of acute syndromes, ranging from unstable angina pectoris to acute myocardial infarction. Its pathological process is characterized by rupture of a stable or unstable atherosclerotic plaque, base collagen fibers exposure, thrombus due to assemblage of plates and several kinds of inflammatory cytokines such as C-reactive proteins (CRP), interleukin-6 (IL-6) or tumour necrosis factor (TNF). As the acute and sub-acute thrombus is the most serious complication in the early stage of percutaneous transluminal coronary angioplasty and stenting, the therapy of anti-plate and anti-thrombus is very important role in the pre-operation of interventional therapy of acute coronary syndrome.The main effects of Prostaglandin El are 1. Effect on the vascular smooth muscle directly, to expand the artery and vein, to lower the peripheral vascular resistance, to lessen the preload and after loading of heart, 2. To inhibit the adhesion and aggregation of platelets, so as to improve the hemodynamics, 3. to protective effect in reperfusion injury,4. To increase the myocardial contractile force as well as improvecoronary artery circulation and protect myocardium, it also increase the blood and oxygen supply, 5. To inhibit the release of catecholamine, to protect myocardial cells' membrane, to stable liposomal membrane, 6. To clean up circulating immune complex, to decrease the injury of myocardium, 7. To inhibit the arteriosclerosis forming and so on. So it has pharmacological actions widely.This article is to aim directly on the effects of liposomal prostaglandin E, in the peri-percutaneous coronary interventional (PCI) of ACS, and observe the effects on the patients' plasma coagulation system and inflammatory cytokines.Method:2. 1 Eligible criteria as following:(1) Age 18 years old, but 80 years old,(2) Working diagnosis of acute coronary syndromes:1) Unstable angina episode within the preceding 24 hours,2) AMI with at least 2 of following criteria:a. Persistent chest pain >20 minutes,b. ST elevation in at least 2 corresponding leads ( 0. 05mV), or with new onset of complete left bundle block,c. Elevation of cardiac enzymes or markers,d. New regional wall motion abnormality on echocardiography. 2. 2 Thirty-seven consecutive patients who diagnosed as ACS (coronaryartery angiography showed one or more coronary artery stenosis 70%) underwent PCI were included. Lipo-PGEl was given at a dosage of 20Hg, two times a day by intravenously after PCI for three days. Aspirin, ticlid (or Plavix), heparin (or low molecular weight heparin) and statins, 6-blocker as well as ACEI were used at same time in usually dosage. PT, INR, KPTT, platelets and CRP, IL-6, TNF was monitored before PCI and onthe third day. PT, INR, KPTT, platelets was also retest when the patients were discharged. Another thirty-four ACS cases were as placebo group without any Lipo-PGEl using. PT, INR, KPTT, platelets and CRP, IL-6, TNF was tested on the same time.2. 3 Rate nephelometry with Beckman systems was used to measure the plasma levels of CRP of two groups. And Elisa (Enzyme-linked immunoadsordent assay) method was used to test the levels of IL-6 and TNF. PT, INR, KPTT and platelets were measured by routine method.2.4 The results of two groups were compared by t test.Result:3. 1 PT and KPTT on the third day were prolonged in both groups. But it' s much more longer in Lipo-PGE, group, and it' s also prolonged significantly than control group (Lipo-PGEi group/control group: PT 23. 2 1.5/13. 1 1.2s; KPTT 38. 4 3. 6/30. 8 4. 0s, P<0. 05), and platelet count did not change any more in two groups of all times.3.2 CRP, TNF were elevated in both two group in early stage of ACS. But IL-6 did not change obviously. On the third day, CRP, TNF decreased significantly in Lipo-PGEl group (from 22.32 17.15 mg-L'Vl69.33 32. 74 pg-ml'1 to 10.87 7. 54 mg-L'V76.58å¤22.51 pg-ml-1, P<0. 05), and it did not decrease any more in control group.3. 3 Subgroup analys...
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