Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 48-year-old woman with Wolff-Parkinson-White syndrome underwent surgical division of the accessory pathway in the left lateral wall. At 6 months after the procedure, she developed dyspnea and chest oppression. Coronary angiography revealed total occlusion in the left circumflex coronary artery (segment 13) at the exact site where cryoablation had been performed. The coronary occlusion was treated with an intracoronary bolus injection of urokinase (960,000 U) and subsequent percutaneous transluminal balloon angioplasty. No significant residual stenosis remained after the balloon angioplasty, and no further evidence of myocardial ischemia was noted for 13 years to date after the procedure.
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PMID:Myocardial infarction after cryoablation surgery for Wolff-Parkinson-White syndrome. 1204 14

Various studies demonstrated an interdependence between rheological parameters and advanced stages not only of ischaemic heart disease and peripheral arterial occlusive disease, but also of chronic obstructive lung disease. In ischaemic heart disease, rheological alterations in the poststenotic circulation can result in impairment of the oxygen supply of the myocardium. Rheological therapies aim for a reduction in plasma viscosity and improved microcirculatory flow by means of a reduction of the elevated levels of fibrinogen. As an example, intermittent therapy with urokinase has been established as a treatment of refractory angina pectoris. Treatment with fibrates also can result in an improvement of microcirculation due to reduced hepatic fibrinogen synthesis. Treatment with statins leads to an improvement of microcirculation due to effects on serum lipids. In patients with chronic obstructive lung disease and cor pulmonale who, secondary to chronic hypoxia, develop polycythaemia and disturbances in pulmonary microcirculation, isovolumic haemodilution may result in a reduction of pulmonary arterial pressure with consecutively increased cardiac output and improved exercise capacity.
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PMID:[Rheological determinants of end-organ damage]. 1463 81

It has been reported that pulmonary thromboembolism (PTE) is a major complication in the post-operative period. However, there have been few reports on PTE after cardiopulmonary bypass (CPB). We report a case of PTE that occurred after cardiac surgery using CPB. A 76-year-old female patient underwent aorto-coronary graft bypass and mitral valve plasty because of ischemic heart disease and mitral valve regurgitation, respectively. The results of blood gas analysis after cardiopulmonary bypass showed no abnormalities. Immediately after ICU admission, the oxygenation index (PaO2/FIO2) of the patient was below 100, and the low level persisted despite decrease in interstitial fluid volume of the lung. Evaluations of hemodynamics using ultrasound echography and a Swan-Ganz catheter showed no findings associated with right heart failure. The results of lung perfusion scintigraphy performed on the 6th postoperative day (POD), revealed the decline in radioactivities in the upper and middle lobe areas of the right lung. Urokinase was therefore administered intravenously from the 6th to 9th POD. The oxygenation index increased dramatically after urokinase administration. Although the use of thrombolytic therapy in an early postoperative period is controversial, our patient was successfully treated with urokinase without a life-threatening bleeding tendency.
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PMID:[A case of pulmonary thromboembolism after cardiac surgery]. 1519 41

Cardiac plasmin activity is increased following myocardial ischemia. To test the hypothesis that macrophage-derived uPA is a key mediator of repair following myocardial infarction, we performed myocardial infarction on mice with macrophage-specific over-expression of uPA (SR-uPA mice). SR-uPA(+/0) mice and wild-type littermates were sacrificed at 5 days or 4 weeks after infarction and cardiac content of macrophages, collagen, and myofibroblasts was quantified. Cardiac function and dimensions were assessed by echocardiography at baseline and at 4 weeks post-infarction. At 4 weeks after myocardial infarction, macrophage counts were increased in SR-uPA(+/0) mice in the infarct (13.1 vs. 4.9%, P<0.001) and distant uninfarcted regions (5.9 vs. 2.4%, P<0.001). Infarct scar was thicker in SR-uPA(+/0) mice (0.54+/-0.03 mm vs. 0.45+/-0.03 mm, P<0.05) and infarct cardiac collagen content was increased (72.4+/-3.3% vs. 63.0+/-3.6%, P<0.06). Functionally, these changes resulted in mildly improved fractional shortening in SR-uPA(+/0) mice compared to controls (24.6+/-1.68 vs. 19.8+/-1.3%, P=0.03). At 5 days after infarction there was increased collagen content in the scar without increases in macrophages or myofibroblasts. To understand the mechanisms by which macrophage-derived uPA increases collagen, cardiac fibroblasts were treated with macrophage-conditioned medium or plasmin and expression of ColIalpha1 measured by qPCR. Conditioned media from SR-uPA(+/0) or plasmin-treated non-transgenic macrophages but not plasmin alone increased collagen expression in isolated cardiac fibroblasts. We hypothesize that plasmin generation in the heart in response to injury may induce activation of macrophages to a profibrotic phenotype to allow rapid formation of collagenous scar.
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PMID:The role of macrophage-derived urokinase plasminogen activator in myocardial infarct repair: urokinase attenuates ventricular remodeling. 2038 Aug 35


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