Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The finding of cardiac failure in a neonate led to the diagnosis of congenital mitral regurgitation complicating dystrophic valves. After failed surgical valvuloplasty, the child underwent mitral valve replacement with a Saint-Jude medical prosthesis at the age of 4 months. The child developed four episodes of prosthetic valve thrombosis in the two years that followed. The first was treated surgically but the three others were treated by thrombolysis associating plasminogen tissue activator and urokinase. All but one of the thromboses occurred in a context of recent destabilisation of oral anticoagulant therapy despite the initiation of heparin. Repeat thrombolysis was successfully undertaken, thereby widening the indications of this type of treatment in the infant. This case also underlines the difficulties of oral anticoagulants in infants.
 ...
PMID:[Repeated thrombolysis and difficulties in treatment with antivitamin K in an infant with mitral valve prosthesis]. 764 92

To determine whether pharmacologic reperfusion to Thrombolysis in Myocardial Infarction (TIMI) grade 2 flow during acute myocardial infarction confers the same clinical benefit as restoration of TIMI 3 flow, in-hospital clinical and angiographic outcomes in 1,229 patients prospectively enrolled in the Thrombolysis and Angioplasty in Myocardial Infarction trials were analyzed. Patients were treated with intravenous tissue plasminogen activator or urokinase, or both. Angiography of the infarct-related artery 90 minutes after initiation of thrombolytic therapy demonstrated TIMI grades 0, 1, 2, or 3 flow in 20%, 7%, 17%, and 55% of vessels, respectively. Rescue or adjunctive coronary angioplasty was performed in 80%, 27%, and 16% of patients with TIMI 0/1, 2, or 3 flow, respectively. Predischarge angiography was performed in 963 patients. A significant gradient of increasing mortality was seen in patients with lower TIMI flow (4.3%, 6.1%, and 10.1% with TIMI 3, 2, and 0/1 flow, respectively, p = 0.002). The incidence of congestive heart failure and recurrent ischemia was significantly higher in patients with TIMI 2 than with TIMI 3 perfusion (26% vs 19% for heart failure, p = 0.03; 23% vs 17% for recurrent ischemia, p = 0.05). Acute left ventricular ejection fraction and infarct zone regional wall motion were also significantly improved in patients with TIMI 3 than with TIMI 2 flow, with trends toward better improvement in global and regional function in the TIMI 3 group. These findings were not affected by the use of acute coronary angioplasty.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Significance of a coronary artery with thrombolysis in myocardial infarction grade 2 flow "patency" (outcome in the thrombolysis and angioplasty in myocardial infarction trials). Thrombolysis and Angioplasty in Myocardial Infarction Study Group. 773 92

In a 43-year-old patient with Ebstein's anomaly and a history of acute myocardial infarction by means of duplex ultrasonography and aortography the diagnosis of thrombotic occlusion of the a aorta was established, starting above the insertion of the renal arteries and reaching as far as the bifurcation of the aorta and the common iliac arteries. In the clinical picture dominated complete anuria with uraemia and marked hyperkaliaemia as a result of ischaemic affection of the extremities due to thrombosis of the aorta; at the onset of hospitalization also left ventricular failure with hyperhydration and later also signs of the hyperviscous syndrome. The latter developed after repeated haemofiltrations which led to a rise of the originally high haemoglobin and haemotocrit values a result of a righ-left shunt in Ebstein's anomaly. After improvement of the clinical condition local fibrinolytic treatment of the aortal thrombosis with urokinase (total dose 2,160,000 u. administered within 24 hours) was provided. The thrombus with a total length of 13.5 cm was dissolved except for a residual portion of 10 mm located in the area of insertion of the right renal artery. After dissolution of the thrombus it proved possible to restore the blood flow into the left kidney a and lower extremities, but not into the right kidney because of the residual thrombus. Seventy-two hours after terminated fibrinolysis - and after 31 days of anuria - the diuresis was restored and after a polyuric stage normalization of mineral, urea levels was restored and the creatinine value was slightly above the upper normal range. Concurrently with fibrinolytic therapy angioplasty of the aorta was carried out and a stent was placed on the left iliac artery. The clinical condition of the patient was improving, the patient started to mount stairs. Death occurred suddenly and the cause was cardiac failure due to very serious congenital heart disease.
 ...
PMID:[Subacute thrombosis of the abdominal aorta with suprarenal involvement and successful treatment with pharmacomechanical fibrinolysis]. 855 98

Besides the thrombolytic therapy several adjuvant therapeutic measures were identified which significantly improve the prognosis of patients with acute myocardial infarction (AMI). These measures include the treatment by means of acetylsalicylic acid (ASA), beta-blockers and ACE inhibitors. Early administration of ASA and beta-blockers are indicated in all patients with AMI who have no contraindications for this therapy. They are especially the patients with manifest heart failure or asymptomatic left ventricular dysfunction who benefit from ACE inhibitors. The effectivity of routine administration of other medicaments such as anticoagulants, nitrates, calcium channel blockers and magnesium, have not been convincingly proved. However, some selected patients with AMI can benefit from these medicaments. Intravenous administration of heparin is unambiguously justified only in thrombolysis with t-PA. Thrombolyses with streptokinase, urokinase, and anistreplase are justified only at high risk of thromboembolic complications. Their prevention and therapy include also the necessity to restrict the administration of pelentan. The use of nitrates is indicated in patients with AMI in case of sustaining stenocardia, arterial hypertension and manifest heart left ventricular failure. Until the definitive standpoint is gained regarding the effect of magnesium in patients with AIM, its administration remains especially indicated in cases of arterial hypertension, tachycardiac disturbances of the heart rhythm and states of assumed or proved hypomagnesiemia. In AMI cases when magnesium is used in order to protect the patient from reperfusion lesion, it must be administered prior to the reperfusion therapy. An intensive research in the field of therapeutical measures in patients with AMI still continues. It is certain that it will soon bring further knowledge which will in turn improve the prognosis and quality of life of patients with AMI. (Tab. 4, Ref. 133.)
 ...
PMID:[Adjuvant therapy in patients with acute myocardial infarct]. 892 11

Long-term intermittent urokinase therapy has been developed for patients with severe coronary artery disease and refractory angina pectoris. This therapeutic approach is predominantly effective at the microcirculatory level based on a combination of rheologic and fibrinolytic effects; furthermore, plaque regression seems to be a possible mechanism. Patients with refractory angina pectoris are characterized by severe coronary artery disease without a therapeutic option for conventional revascularization procedures, only slight impairment of left ventricular systolic function and hyperfibrinogenemia, which results in further enhancement of myocardial ischemia due to microcirculatory impairment of blood flow. In this article data on the anti-ischemic effectiveness as well as first results on the impact of this therapeutic approach on hemodynamics are described. A dose-response study, which compared 3 x 50,000 IU with 3 x 500,000 IU urokinase three times a week over a treatment period of 12 weeks demonstrated subjective as well as objective antiischemic effectiveness. Only patients who were treated with 500,000 IU per injection achieved marked increases in exercise capacity, while some patients in the low-dose group presented even with a deterioration of exercise performance. First hemodynamic studies could not show marked changes of systolic parameters, either at rest or during exercise. But a decrease of pulmonary capillary wedge pressure at rest after treatment with 500,000 IU per injection indicates an improvement of diastolic function as a result of enhanced myocardial perfusion. Echocardiographic measurements of transmitral Doppler flow in 21 patients with end-stage coronary artery disease demonstrated normalization of early and late diastolic filling rates in most cases. These changes were accompanied by a reduction of clinical signs of heart failure. Long-term intermittent urokinase therapy is a valuable approach as it not only improves quality of life during the actual treatment period but by the persistence of therapeutic effects following the cessation of therapy.
 ...
PMID:[Chronic intermittent urokinase therapy: anti-ischemic and hemodynamic effects]. 917 24

In the early stages of left ventricular hypertrophy (LVH) acute adaptive changes occur in the coronary vasculature as it remodels. Plasminogen activators (PAs) and inhibitors (PAIs) have the potential effects of proteolytic degradation that is relevant to tissue remodeling and angiogenesis. Our study focused on the possible roles of PAI-1, PAI-2, and uPA in tPA in myocyte hypertrophy and angiogenesis in the early and late stages of pressure overload induced left ventricular hypertrophy (LVH). We divided seventeen adult swine, weighing 24.2 +/- 6.5 kg, into four groups: control, sham-operated, early LVH and late heart failure LVH group. At surgery we placed a fixed constrictor on the ascending aorta immediately above the aortic valve. This increased LV systolic pressure from 133 +/- 15 to 193 +/- 24 mm Hg after the surgery. We subdivided the early group into groups of 3 animals each that we euthanized at 8, 24 and 72 h after operation and obtained heart samples for analysis. In the late heart failure group individual animals were euthanized at 55, 59, 62 and 72 days after the detection of congestive heart failure. We also obtained tissue samples from the control and sham-operated swine. Sections for histologic analysis were fixed in 10% buffered formalin. We isolated RNA, size fractionated it using 1% formaldehyde-agarose gel electrophoresis and then did Northern blots. The mRNAs from both PAI-1 and PAI-2 showed a remarkable increase at 8 and 24 h after acute aortic constriction and returned to control by 72 h. Regional differences showed that most of the increases were in the endocardium. Three animals in the late heart failure LVH group were determined to be in congestive heart failure at about 2 months after the onset of aortic constriction. In these animals PAI-1 and PAI-2 were increased in both the left and right ventricles but remained low in an animal of the same elevation in aortic pressure seen by the LV who did not have congestive failure. These data suggest that PA and PAI gene expressions change before morphologic changes occur in the early stages of developing LVH. Also at the time of onset of congestive heart failure this increased expression reappears. PAs and PA inhibitors mRNA levels vary in the different regions of the heart reflecting changing wall stresses. Thus, the PAs and PA inhibitors may play an important role in angiogenesis that occurs during the early stages of LVH. The increased expression in the late stage of LVH may reflect further changes in wall stresses since these animals also showed overt clinical signs of heart failure.
 ...
PMID:Increased gene expression of plasminogen activators and inhibitors in left ventricular hypertrophy. 940 71

Despite progress in the invasive revascularization procedures and even though conventional antianginal treatment has improved the quality of life in patients with symptomatic coronary artery disease considerably, an increasing number of patients suffers from end-stage coronary artery disease and refractory angina pectoris. For these refractory patients long-term intermittent urokinase therapy was developed as an antithrombotic intervention, which is based on its capacity to enhance thrombolysis and blood rheology, and may possibly lead to plaque regression. The coronary syndrome of refractory angina pectoris is characterized by a mismatch of severe coronary insufficiency and a relatively large amount of viable myocardium as indicated by an only moderately impaired left ventricular function. Prior to initiation of long-term intermittent urokinase therapy all potential measures to improve myocardial perfusion have to be considered in each patient. These supportive measures include rigorous reduction of LDL-cholesterol, which has proven antiischemic properties due to an improved endothelial function of epicardial conductance vessels possibly resulting in an antianginal effect. Apart from the proven antiischemic properties of long-term intermittent urokinase therapy in patients with refractory angina pectoris, objective signs of ischemic myocardial heart failure improve. Follow-up studies demonstrated a significant increase of left ventricular ejection fraction as evaluated with multi-gated blood pool analysis. Furthermore, left ventricular diastolic function normalized after a treatment period of 12 weeks. As the clinical effects last well beyond the actual treatment period and as they are accompanied by a remarkable increase in the quality of life, a complex approach as this one is justified in this highly symptomatic patient group.
 ...
PMID:[Conservative therapeutic approaches in terminal coronary heart disease. Chronic intermittent urokinase therapy]. 944 Nov 57

Although an increasing incidence of upper extremity venous thrombosis (U/E-DVT) has been reported, a relative paucity of information regarding the etiologic categories, precipitating causes, and proper management for this disorder is available. To settle on a strategy for the management of U/E-DVT, retrospective analyses were performed using records from the authors' hospital. In 12 patients (seven men, five women), 61 (mean) years of age, diagnosed as having symptomatic venography-proved U/E-DVT and followed up for 41 (mean) months, etiologic factors, precipitating causes, treatments, and outcomes were retrospectively analyzed. As etiologic factors, five of the patients had neoplastic disease, one had hemodialysis, and two had transvenous pacemaker implantations. Among various precipitating causes of U/E-DVT, hypoproteinemia was most frequently noted (67%). Various types of therapeutic management were selected: from thrombolysis with urokinase in six, balloon angioplasty in two, thrombectomy in two, and venous bypass surgery in one patient. Pulmonary embolism did not occur in any of the patients and only three of them complained of mild intermittent arm swelling during the follow-up period. Four patients died of neoplastic disease or heart failure (three within the first 6 months). This study, though limited, suggests that the rate of mortality depends on multiple underlying medical problems in U/E-DVT patients. Low incidences of late postthrombotic sequelae and pulmonary embolism were noted in this series. Symptomatic U/E-DVT patients could be managed conservatively with a revised supplementary therapy for their precipitating causes of U/E-DVT.
 ...
PMID:Upper extremity vein thrombosis: etiologic categories, precipitating causes, and management. 1043 94

Cardiac rupture is a fatal complication of acute myocardial infarction lacking treatment. Here, acute myocardial infarction resulted in rupture in wild-type mice and in mice lacking tissue-type plasminogen activator, urokinase receptor, matrix metalloproteinase stromelysin-1 or metalloelastase. Instead, deficiency of urokinase-type plasminogen activator (u-PA-/-) completely protected against rupture, whereas lack of gelatinase-B partially protected against rupture. However, u-PA-/- mice showed impaired scar formation and infarct revascularization, even after treatment with vascular endothelial growth factor, and died of cardiac failure due to depressed contractility, arrhythmias and ischemia. Temporary administration of PA inhibitor-1 or the matrix metalloproteinase-inhibitor TIMP-1 completely protected wild-type mice against rupture but did not abort infarct healing, thus constituting a new approach to prevent cardiac rupture after acute myocardial infarction.
 ...
PMID:Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure. 1050 7

Three patients presenting with massive venous pulmonary thrombo-embolism are described, who have been selected from a series of 22 patients treated with thrombolysis during a 6-year period. A 23-year-old female presented with tachycardia and dyspnoea. She had pulmonary angiography following scintigraphy with a perfusion deficit of more than 60%. Thrombolysis resulted in open blood vessels and a disappearance of the complaints. A 51-year-old woman presented with profound hypoxemia, probably due to a patent foramen ovale, with shunting and tachycardia. Perfusion defects on scintigraphy combined with a normal chest radiograph in the absence of pre-existent pulmonary disease established the diagnosis. She responded favourably to intravenous streptokinase. The third patient was an 80-year-old woman with hypertension. She developed dyspnoea, tachycardia and shock following immobilisation due to a fractured hip. Despite an initial improvement on streptokinase, she deteriorated and died from right-sided heart failure. The diagnostic tests should be limited and aimed at ruling out left-sided heart failure and pericardial tamponade. Echocardiography is often diagnostic in these patients. Thrombolysis may be life saving but there are no randomised trials to prove that survival rate is indeed better compared to heparin therapy. Streptokinase is less expensive than alteplase and there is no evidence from trials to suggest that it is inferior to more expensive thrombolytics such as alteplase or urokinase.
 ...
PMID:[Three patients with massive pulmonary embolism]. 1199 57


<< Previous 1 2 3 4 5 Next >>