Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.73 (urokinase-type plasminogen activator)
 10,685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among 366 unstable angina pectoris patients at our hospital, myocardial infarction was common (15.7%) in those with attacks of chest pain lasting for at least 20 min. There was also a high incidence (30.3%) when chest pain continued after the start of inpatient treatment. To investigate the etiology of unstable angina, coronary arteriography was performed in both the unstable and stable stages in these patients and the results were compared. The role of coronary spasm and coronary thrombosis in unstable angina was investigated, and the efficacy of continuous infusion of either diltiazem or isosorbide dinitrate as treatment for these patients was compared. Coronary arteriography in the unstable stage showed, no clear differences in the morphology of the stenotic site and the degree of stenosis between the patients with and without infarcts when urokinase or isosorbide dinitrate were injected into the coronary arteries. When drug treatment was effective, the angina was stabilized without any improvement in the degree of stenosis or the morphology of the involved coronary vessel. Thus, it was difficult to predict the response to treatment from coronary arteriography performed in the unstable stage. Diltiazem was more effective than isosorbide dinitrate, and it appears that some action other than coronary dilatation was involved in achieving the remission of unstable angina.
 ...
PMID:The response to drug therapy in unstable angina on the basis of coronary angiography findings. 145 41

Since Ca++-overloading is a major problem after myocardial reperfusion we studied the effects of Diltiazem on the left ventricular diastolic function in the early days following coronary thrombolysis. Twelve patients who had myocardial reperfusion by intracoronary urokinase in acute myocardial infarction were admitted to the study. Previous infarct, cardiogenic shock or late thrombolysis (greater than 4 h from symptoms onset) were exclusion criteria. All subjects were evaluated at control cardiac catheterization 5-8 days after the acute ischemia. Simultaneous left ventricular angiography and high-fidelity pressure recordings by means of a tip-micromanometer and angiographic catheter were performed at rest and after intravenous Diltiazem administration (16 mg over 2' + 0.008 mg/Kg/min). Indexes of myocardial relaxation and early ventricular filling were impaired at rest but improved significantly after Diltiazem (Tab. II). Isovolumic relaxation period fell from 92 +/- 8 msec to 77 +/- 12 msec (p less than .01), T constant of isovolumic pressure decay decreased from 61 +/- 7 msec to 55 +/- 7 msec (p = ns), first-third of filling rate increased from 64 +/- 7% to 79 +/- 6% (p less than .01). On the other hand, indexes of left ventricular compliance were altered after coronary reperfusion (left ventricular end-diastolic compliance 17 +/- 13 mmHg-1. 10(-3), modulus of chamber stiffness .045 +/- .008) but but did not change after calcium-blocker therapy. In conclusion, post-thrombolysis diastolic function is severely impaired at rest, probably because of raised intracellular Ca++ and delayed asynchronous relaxation. Diltiazem improves energy-dependent early diastole, but does not affect ventricular compliance.
 ...
PMID:[Hemodynamic effects of diltiazem in the subacute stage of myocardial infarct treated by thrombolysis]. 365 3