Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrocardiograms of 90 patients with arteriographically documented acute submassive or massive pulmonary embolism and no associated cardiac or pulmonary disease were studied. Patients were derived from the Urokinase-Pulmonary Embolism Trial National Cooperative Study. In massive embolism, the electrocardiogram was normal in 6 per cent (3 of 50) of patients. With submassive embolism, 23 per cent of patients (9 of 40) had a normal electrocardiogram. Since one or more of the traditional manifestations of acute cor pulmonale (S1Q3T3, right bundle branch block, P pulmonale, or right axis deviation) occurred in only 26 per cent of patients, one could not rely exclusively upon these electrocardiographic abnormalities for the diagnosis of pulmonary embolism. The most common electrocardiographic abnormalities were nonspecific T wave changes which occurred in 42 per cent of patients and nonspecific abnormalities (elevation or depression) of the RST segment which occurred in 41 per cent of patients. Left axis deviation occurring in 7 per cent of the patients was as frequent as right axis deviation. Low voltage QRS complexes, previously undescribed in pulmonary embolism, occurred in 6 per cent of patients. None of the patients had atrial flutter or atrial fibrillation, which appears to occur more typically in patients with pulmonary embolism who have preexistent cardiac disease. All of the varieties of electrocardiographic abnormalities disappeared in some of the patients by 2 wk. Inversion of the T wave was the most persistent abnormality. Larger defects on the lung scan or pulmonary arteriogram occurred in patients with various abnormalities on the electrocardiogram than in patients with normal electrocardiograms. The pulmonary arterial mean pressure and/or right ventricular end-diastolic pressure was significantly higher in patients with several varieties of abnormal electrocardiograms, although the partial pressure of oxygen in arterial blood, in general, did not differ from that in patients with normal electrocardiograms. These hemodynamic correlations, made for the first time in patients, suggest that acute ventricular dilatation, possibly in combination with hypoxemia, is a causative factor of the electrocardiographic changes in acute massive or submassive pulmonary embolism.
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PMID:The electrocardiogram in acute pulmonary embolism. 12 74

Intraventricular extension of hemorrhage after intraparenchymal hemorrhage is associated with significant morbidity and mortality. Clinical improvement is reported in a patient with thalamic hemorrhage with intraventricular extension after third and fourth ventricular blood clot resolution with instillation of urokinase intraventricularly. A 49-year-old man with hypertension collapsed while at work. A computed tomography (CT) scan of the head revealed a left thalamic hemorrhage with extension into the lateral, third, and fourth ventricles and associated hydrocephalus. A left frontal intraventricular catheter (IVC) was placed and intraventricular urokinase was administered at a dose of 25,000 U every 12 hours. The CT scan revealed resolution of the lateral ventricular dilatation and blood clot but no decrease in third or fourth ventricular hemorrhage. No clinical improvement was noted. The IVC was reinserted on the right side with the catheter tip placed through the foramen of Monroe into the third ventricle. Twelve hours after receiving the first dose of urokinase through the new catheter, the patient's condition improved. The CT scan showed a reduction in the volume of blood of the third and fourth ventricles. This case report shows that treatment of hydrocephalus with an IVC was not sufficient to provide a therapeutic effect. Substantial clinical improvement occurred only after the blood clot was cleared from the third and fourth ventricles.
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PMID:Clinical improvement related to thrombolysis of third ventricular blood clot in a patient with thalamic hemorrhage. 1790 95

Enteroviruses, especially Coxsackie B3 virus (CVB-3), cause acute viral myocarditis, but the detailed mechanisms leading to chronic left ventricular dysfunction and dilatation remain elusive. Myocardial tissues of CVB-3 infected and sham infected male swr/J mice were analyzed after hemodynamic evaluation on days 4, 7, and 28 p.i. by RT-PCR, gelatin zymography, ELISA, immunohistochemistry, sirius red staining, and luxol fast blue staining. In the early phase after infection an abnormal diastolic function was the main hemodynamic finding. CVB-3 infection caused impairment of left ventricular function combined with ventricular dilatation 7 and 28days post-infection. These hemodynamic findings were associated with relevant upregulation of different cytokines (IL-1beta, IL-6, IL-10, INF-gamma, and TNF-alpha) in the acute phase with persistent over-expression of IL-6, IL-10, and INF-gamma in the chronic phase. This virus induced myocardial inflammation was linked to a significant induced MMP/TIMP system (MMP-2,-3,-8, TIMP-1, uPA, tPA-mRNA expression, and MMP-2-activity) in the acute and chronic phase leading to imbalance in the MMP/TIMP-ratio at day 28. This imbalance in the MMP/TIMP system was significantly correlated to the development of ventricular dilatation. Viral persistence induces chronic myocardial inflammation and an imbalance of the matrix degrading system, associated with the development of left ventricular dysfunction and dilatation in chronic murine myocarditis.
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PMID:Left ventricular enlargement in coxsackievirus-B3 induced chronic myocarditis--ongoing inflammation and an imbalance of the matrix degrading system. 2003 43

Fibrosis of the subarachnoid space (SAS) after infection, inflammation, or hemorrhage can impair cerebrospinal fluid absorption and circulation, causing diffuse ventricular dilatation. In the present study, we tested the hypothesis that urokinase (also known as urokinase-type plasminogen activator [uPA]), a fibrinolytic agent, attenuates fibrosis and ventriculomegaly in a rat model of kaolin-induced communicating hydrocephalus and thus may have potential as a therapy for these conditions. Thirty microliters of sterile 25% kaolin suspension was injected into the basal cisterns of adult Sprague-Dawley rats to induce hydrocephalus, and 2 intraventricular injections of either uPA or vehicle (saline) were administered immediately and 3 days thereafter. Ventricular volumes were measured by magnetic resonance imaging (MRI) on days 3, 14, and 28 after kaolin injection. Fibrosis and reactive astrogliosis were evaluated on day 28 by immunofluorescence and Western blotting. Neurocognitive features were tested using the Morris water maze from days 23 to 28. MRI analysis demonstrated that kaolin administration successfully induced hydrocephalus in rats and that uPA treatment significantly attenuated ventricular enlargement. In addition, uPA inhibited the deposition of laminin and fibronectin, extracellular matrix molecules, in the SAS, attenuated gliosis, and improved learning and memory in kaolin-treated rats. Therefore, we concluded that uPA prevents the development of kaolin-induced communicating hydrocephalus by preventing the development of subarachnoid fibrosis and by eliciting improvements in neurocognition. The results of this study indicate that uPA may be a novel clinical therapy for communicating hydrocephalus.
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PMID:Intraventricular administration of urokinase as a novel therapeutic approach for communicating hydrocephalus. 2761 13