Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 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

During the acute phase of myocardial infarction, the generation of thrombin is reflected in the sudden rise of fibrinopeptide A (FPA) and the thrombin-antithrombin III (TAT) complex in blood. We have systematically determined the FPA and TAT plasma concentrations over a period of 14 days after acute myocardial infarction in 100 patients. Mean levels of both thrombin markers were the highest on admission, remained elevated over the following few days, and then gradually declined after day 5. Still, by the end of the first week two thirds of the patients had distinctly elevated TAT and FPA levels, and by the end of the second week such an abnormality was present in half of them. Continuous intravenous heparin infusion at a dose of 20,000 units/day, administered for 1 week to patients who had either received (n = 21) or not received (n = 17) streptokinase, led to a significant depression (p less than 0.05) of thrombin markers over the first 48 hours, an effect that did not persist over the subsequent days of treatment. In patients not assigned to heparin treatment, those in heart failure had significantly (p less than 0.05) higher mean TAT and FPA values on days 3, 5, and 7 compared with patients in whom heart failure was absent. Infarct extension, pulmonary embolism, and death were also associated with a rise in one or both thrombin markers, often preceding the onset of clinical symptoms. Thrombinogenesis was not accompanied by changes in mean plasma concentrations of prothrombin, antithrombin III, or alpha 2-macroglobulin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Persistent generation of thrombin after acute myocardial infarction. 157 16

A 18-year-old boy was admitted to hospital in an unconsciousness state as a result of taking a large dose of several psychotropic drugs simultaneously in an attempt to commit suicide. Blood studies revealed hypoxia (55.7 mmHg) and hypercapnia (59.7 mmHg). Hypoxia (74.3 mmHg) and hypercapnia (46.7 mmHg) were still present on the fourth day after admission, and the patient was becoming lethargic. Reduced vascular markings in the right upper lung field on chest roentgenogram in spite of hypercapnia suggested that the persistent hypoxia was the result of a pulmonary embolism. This diagnosis was supported by a perfusion defect on 99mTc-MAA scintigram and arterial obstruction in right pulmonary angiogram. Hypercapnia is an unusual finding in pulmonary embolism, and in this case was considered due to depression of respiration by psychotropic drugs.
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PMID:[A case of pulmonary embolism following acute respiratory failure with hypercapnia]. 180 86

The presence of depression in consecutive admissions with life-threatening illness was assessed using the Montgomery-Asberg Depression Rating Scale (MADRS). The 211 patients had one of four conditions, myocardial infarction (N = 100), subarachnoid haemorrhage (N = 41), pulmonary embolism (N = 40), and acute upper gastrointestinal haemorrhage (N = 30). Depression was measured using both the standard MADRS, and a modified version excluding somatic items which might be influenced by the underlying illness. The patients were also assessed for severity of illness and cognitive dysfunction. The results showed that immediately following a life-threatening illness approximately 34% of the patients were depressed, using the modified scale, but that the depressed group did not have a more severe physical illness. However, the depressed patients had a significantly poorer outcome over the 28 days following admission, with 47% of the depressed patients dying or having life-threatening complications, as opposed to 10% of the non-depressed group. This study demonstrates that the psychological state of an individual can affect their individual risk of mortality following physical illness.
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PMID:Depression increases mortality and morbidity in acute life-threatening medical illness. 229 Jan 37

The classic electrocardiographic abnormalities observed in massive or submassive thromboembolism in the absence of preexistent cardiac or pulmonary disease are: S1Q3T3 pattern, right axis deviation, "pulmonary" P wave, ST segment depression or elevation, subepicardic ischemia and transient right bundle branch block. Left axis deviation due to pulmonary embolism was first described in 1949; this same finding and the presence of low voltage of the frontal plane owed to pulmonary embolism has been reported occasionally in the last decades, but it has had little diffusion. We report on a patient with no prior cardiac or pulmonary disease who suffered massive pulmonary thromboembolism. Electrocardiographically left axis deviation and low voltage of the horizontal plane attributed to pulmonary thromboembolism was observed. The mechanisms that originate this electrocardiographic changes in pulmonary embolism are unknown. Since the electrocardiogram is aspecific method for the diagnosis of this disorder, and the presence of the mentioned changes originate a greater difficulty in the diagnosis; we consider is important to publish it.
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PMID:[Massive pulmonary thromboembolism with left axis deviation and low voltage]. 296 Feb 86

Deep venous thromboses in the lower extremities were observed in three boys aged 8, 10, and 12 years. In one case, it must have originated from circulatory depression during diabetic ketoacidosis. In two children, osteomyelitis was detected in the proximity; they developed septic pulmonary embolism. Osteomyelitis and septic arthritis as possible cause or consequence should be actively looked for in septic thromboembolism.
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PMID:[Pelvic and femoral vein thrombosis in childhood]. 314 16

In a group of 245 patients with clinical suspicion of pulmonary embolism we analyzed the ECG for 22 signs that have been associated with this disease. Subsequently, the patients were divided into two groups: those with confirmed embolism and those in whom embolism was not confirmed. The occurrence of the ECG signs was assessed separately for the two groups. Furthermore, we related ECG features to severity of embolism as estimated at lung scan. Tachycardia and S-T depression were the commonest findings in both groups. P-R displacement, late R in a VR, S1Q3T3, S slurred and T inversion in V1-V2 were more frequent in embolic than in nonembolic patients (p less than 0.05 or less). All the above mentioned signs were more frequent at diagnosis than at recovery in embolic patients (p less than 0.05 or less), whereas only tachycardia was more frequent at diagnosis than at control in nonembolic patients (p less than 0.001). S-T depression and T inversion in V1-V2 were also associated to severity of embolism. Since some ECG signs are very frequent or specific in pulmonary embolism, this condition should always be suspected when they are found and, particularly, when previously absent in the same patients and/or not explained by other conditions.
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PMID:Routine electrocardiography in screening for pulmonary embolism. 382 34

Deoppilation of the pulmonary arteries by catheterization is infrequently used in severe pulmonary embolism. This technique can only be contemplated when conventional measures, such as injection of fibrinolytic agents or surgical removal of the emboli, cannot be applied. The catheter is introduced under local anaesthesia through the femoral vein or the internal jugular vein, and the emboli are aspirated by exerting a strong depression at the tip of the catheter. Satisfactory results can only be expected in cases with very recent (less than 72 hours), totally occlusive and proximal embolism. Three out of the authors' 6 attempts have been successful.
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PMID:[Nonsurgical pulmonary embolectomy using catheterization]. 623 93

Drug-addicts frequently suffer from pulmonary diseases, particularly those who practice self-injection of the drugs intravenously. Emphasis is at present laid on the various excipients which are thought to induce acute alveolitis with subsequent acute pulmonary oedema in heroin-addicts. It has also been suggested that the deep ventilatory depression that precedes pulmonary oedema may play a part and this is interesting since the depression can now be prevented with naloxone. Infectious lesions, such as septic pulmonary embolism or endocarditis, are easier to explain. The ever increasing use of tablets crushed for injection is responsible for peri-arteriolar granulomas of the lung with possibly severe sequelae. Finally, the almost generalized consumption of marihuana in the United-States has led to the discovery of new properties of this drug, including ventilatory stimulation and broncho-dilatation. However, this is mostly of theoretical interest. The psychotropic effects of marihuana and its irritant effect on the bronchi when inhaled make it unlikely that it will be ever be used for therapeutic purposes.
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PMID:[Pneumopathies in drug addicts]. 663 69

Five cases with recurrent pulmonary embolism (RPE), all having severe chronic cor pulmonale due to marked pulmonary hypertension, were reported. None of them had a history of thrombophlebitis of the legs. Dyspnea was the common symptom and signs of pulmonary hypertension were usual. Focal oligemia, cardiomegaly and plump pulmonary arteries on chest X-ray films, right axis deviation, clockwise rotation, ST-segment depression and T-wave inversion on electrocardiograms, and dilatations of the pulmonary arterial trunk, the right ventricle and the right atrium, and the posterior displacement of a small, compressed left ventricle on echocardiograms were the common findings. Gas exchange abnormalities were severe and they were considered the characteristic findings of this disease. Multiple perfusion defects were observed by a lung scan in all cases. Marked pulmonary hypertension with low cardiac output was the usual feature of RPE. Actual cutoffs or filling defects were demonstrated on a pulmonary angiogram. Deep vein of the legs were all intact and no thrombi were found. Pulmonary embolectomy was performed on one case. The importance of early diagnosis and early treatment of acute pulmonary embolism was emphasized for preventing the progress of this debilitating disease.
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PMID:Recurrent pulmonary embolism. 685 11


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