Clinical Study Of Small Does Thromblytic On Unstable Angina

Unstable angina is the second highest risk clinical syndrome afteracute myocardial infarction with high rate of hospitalization and acutecoronary artery events. The evidences of that unstable angina iscorrelated with thrombus includes ( 一 ) data from autopsy: ①Rupture or bleeding of an atherosclerotic plaque in the coronaryartery, both rupture and bleeding can induce the aggregation ofplatelet and dysfunction of coagulation to the local and cause thesevere stenosis of the coronary arterry cavity. It is estimated that about50~70% UA patients has thrombus formation. More than 70% of UApatients has the stenosis of convex and secund with irregular margin,while only less than 20% of this kind of stnosis in the patients ofstable angina. ② Damage of the endothelium, the roughening of theendothelium on the one hand disturbs the blood flow, and on the otherhand collide with the tangible particles like platelet, and further morerelease large quantity of vessel contractors like TXA2 that cause thespasm of the coronary artery. This spasm can exist alone and combinewith thrombus in the coronary artery and cause the 20% cardiacischemia in UA. ③Acute swelling of the atherosclerotic plaquecaused by the infiltrating of lipid, 10~20% UA patients are causedby this acute swelling of the atherosclerotic plaque which inducessevere stenosis of the coronary artery and significant reduce of bloodflow. (二) data from newly-developed coronary aretery endoscopicexamination: As presented in acute myocardial infarction patients,more than 90% of UA patients have thrombus within the first 8 hours(10% occlusive and 80% non-occlusive) or combine with bleeding ofthe atherosclerotic plaque. Most thrombus attaches to the wall of theartery with irregular margin and rough endothelium, consisting withplatelet white thrombus, minority has red thrombus with minordamage to the endothelium compared with acute myocardial infarction.The argument about whether adopting thrombolytic therapy or not toUA patients exist at all times. In the late 10 years, most small sampleresult of thrombolytic therapy to UA controlled by coronary arteryangiography shows significant effective outcome. In the study ofTIMI-IIIB, the rate of more than 10~20% reduction of the stenosis inthe group of thrombolytic is much higher than that of the controlgroup, although the enrollment criteria is not so strict. The thrombusof UA is mostly white thrombus (platelet and fibrin thrombus), whilethat of acute myocardial infarction is mostly red thrombus(red bloodcell fibrin thrombus). Thrombolytic therapy is effective to redthrombus and uneffective to white thrombus. However, from the newforeign data of coronary artery endoscopic examination, not only theangina after acute myocardial infarction, but also unstable angina andeven Prinzmetal's angina, there exist thrombus much or less at thefocal of ischemic correlated artery, including white thrombus, redthrombus and sometimes coexist with bleeding of the plaque. Thataffirms the critical clinical value that the thrombolytic therapy onunstable angina is unarguable. But much attention should be paied tochoose the right patients and select the right chance to take actionduring the clinical practice. Thrombolytic agents can resolve the redthrombus at the head and tail of the diseased plaque, while the whitethrombus can be resolved gradually by the combination of thethrombolytic agents, anti-platelet agents, systemic fibrinolytic activityand the force of blood flow. The prognosis of unstable patientsimproved greatly after the alleviation of the stenosis of coronary artery.Through long-term clinical observation, jointly use tpA and stronganti-platelet agents is significantly preceded to use only one drugseperately. That affirms that like treating acute myocardial infarctionby thrombolytic therapy, unstable angina should be treated by thecombination of thrombolytic, anti-platelet and anti-thrombin together,while the drug doses should be reduced greatly. In this study, 120 UApatients were assigned randomly into two groups, which were treatedwith whether heparin and urokinase or heparin alone. The resultshows that the former group can release the symptom of ischemicangina, reduce the frequence of attack, improve the outcome of ECGand function of endothelium. It has great effect on improving the long-term prognosis and life quality of the patients by reducing the rate ofacute myocardial infarction and cardiac sudden death.