Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intravenous thrombolytic therapy with streptokinase in the setting of acute MI has been shown to be effective in improving left ventricular function, limiting infarct size, and improving early mortality. The benefit of this therapy is greatest when administered within 3 hours and is of minimal benefit when given more than 6 hours from symptom onset. Newer second generation thrombolytic agents such as intravenous r-TPA have been shown to be more effective at establishing patency of acutely thrombosed coronary arteries. TPA treatment produces patency rates similar to those observed with intracoronary administration of streptokinase (65 to 75 per cent). This agent will probably become standard therapy for patients with acute MI. Unfortunately, there are significant problems with systemic thrombolytic therapy. The potential for bleeding complications contraindicates the use of this therapy in patients with recent cerebrovascular events, recent surgery, or other possible bleeding problems. Acute angioplasty of the infarct-related artery has been shown to be effective in restoring blood flow in 85 per cent of patients with acute MI. Preliminary studies have suggested that this therapy, when administered within 4 hours from symptom onset, improves global and regional left ventricular function to a greater degree than intracoronary streptokinase. Patients receiving acute PTCA as a primary reperfusion modality have a lower incidence of post-infarction angina and provokable ischemia by exercise testing. If facilities and skilled personnel are available to perform PTCA within 4 hours from symptom onset, this therapy remains an alternative revascularization modality in patients with acute infarction and contraindications to systemic thrombolytic therapy. However, the benefit of PTCA with regard to reduction in mortality when used in this manner is unproven. PTCA can also be used as an adjunctive therapy administered at some time following systemic thrombolytic therapy. Performing PTCA acutely offers the potential to restore blood flow in 90 per cent of the patients that initially fail thrombolytic therapy. However, despite the use of PTCA in this subgroup, benefits with regard to improved ventricular function and decreased mortality have yet to be conclusively demonstrated. Performing acute PTCA following systemic thrombolytic therapy also incurs a high incidence of bleeding complications. If initial thrombolytic therapy reestablishes vessel patency, similar improvements in ventricular function can be expected even if PTCA is deferred until clinically indicated by evidence of recurrent ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Percutaneous transluminal coronary angioplasty during acute myocardial infarction. 297 41

30 patients suffering from stable angina pectoris were studied by triaxicardiometric (polarcardiographic) method. Triaxicardiometry including the X, Y, Z Frank leads, azimuth (H degrees), elevation (V degrees) angle derivations and spatial magnitude (M) tracings were taken at rest and after submaximal bicycle ergometer exercise. After receiving 30 mg/day isosorbide dinitrate for a minimum of 5 days the whole procedure was repeated, stored by an analogue tape recorder and evaluated by a TPA/i computer. It has been stated that the method of triaxicardiometry has an excess sensitivity on the demonstration of ischemic alteration of anterior and posterobasal left ventricular wall compared to the traditional X, Y, Z leads. According to the pre- and post-exercise bicycle ergometer testing estimated by triaxicardiometry, isosorbide dinitrate caused a significant reduction of subendocardial myocardial ischemia.
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PMID:Polarcardiographic (triaxicardiometric) study on the effect of isosorbide dinitrate on exercise-induced myocardial ischemia. 731 94

We measured various coagulable factors and molecular markers in plasma and serum in the disease group including DIC, DIC suspect, thrombosis, acute myocardial infarction, angina pectoris, sepsis, malignant tumor and type II diabetes and the healthy subject group, and surmised the intravascular coagulative-fibrinolytic activity in each disease group compared with the healthy group. Additionally we selected parameters useful for early detection of the pre-thrombotic state and hypercoagulable state. As a result, of the parameters for the coagulative system, those considered useful were the assay of soluble fibrin monomer complexes using the synthetic substrate (FM.Oita), assay of soluble fibrin monomer complexes using HPLC(SFMC.Oita) and thrombin-anti-thrombin III complex (TAT) in this order. Of the parameters for the fibrinolytic system, those considered useful were FDP assay using ELISA (FDP.Oita) and plasmin-alpha 2 plasmin inhibitor complex (PIC). This FDP.Oita had a considerably high detection sensitivity compared with the FDP assay (Diayatron Co.) using the latex photometric immunoassay which has been commercially available. When measurement was made with plasma and serum in the subject disease group as the sample by the high sensitivity assays mentioned above, it was made clear that both the coagulative activity and fibrinolytic activity are increased, albeit with some differences in intensity, in all the disease groups compared with the healthy group. In order for the hypercoagulable state and pre-thrombotic state to be detected, it is important to know the balance between the coagulative activity and fibrinolytic activity. According to the results of the present experiment, a significant directly proportional correlation was recognized between FM.Oita and FDP.Oita and between TAT and FDP.Oita. Therefore, examination of these ratios will be a more detailed indicator of coagulative-fibrinolytic activity than the TAT/PIC ratio, PAI-1/TPA ratio and ATIII/alpha 2 PI ratio hitherto in use. If useful molecular markers such as FM.Oita are measured over time in various cases and these data are compiled and analyzed statistically, it will not be long before the criteria for the hypercoagulable state and pre-thrombotic state are established.
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PMID:[Molecular marker for detecting hypercoagulable state]. 810 79