Papillary fibroelastoma of the mitral valve with systemic embolization.
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Biomedical subjects
Publications and source records attributed to D Moraes.
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Pulmonary hypertension can be caused by an increase in pulmonary blood flow, an increase in left-heart impedance or an increase in pulmonary vascular resistance. Although there are many specific causes that have been identified, clinical presentation and natural history are common to all etiologies. Therapeutic options remain limited to correcting underlying causes whenever possible, as well as supplemental oxygen and, in the setting of severely reduced cardiac output, anticoagulation. Vasodilatory therapy with calcium channel blockers, intravenous epoprostenol or inhaled nitric oxide has also met with some success in patients with primary pulmonary hypertension. Lung or heart-lung transplantation remains the only viable therapeutic option for patients with severe pulmonary hypertension. There have been significant advances in our understanding of the pathobiology and treatment of this uncommon but serious class of disorders. Yet, much remains to be learned in our efforts to improve the lot of these unfortunate patients.
In order to describe the lethality predictors of patients with tuberculous meningoencephalitis, records of 231 patients were analysed. Ages ranged from less than 1 year to 68 years. Ninety-seven patients (42%) were four years old or less. Apart from 73.2% of patients whose diagnosis was performed by clinical and epidemiologic criteria associated with response to specific therapy, 26.8% had diagnostic confirmation through cerebrospinal fluid (culture, bacilloscopy, PCR) or necropsy. The lethality predictors were: less than 4 years of age, seizures, and severe alterations of consciousness.
Pulmonary hypertension comprises a family of disorders occurring as a primary disease or as a complication of a large number of respiratory and cardiac diseases. Pulmonary hypertension is present when pulmonary artery pressure or mean pressure exceeds 30 mmHg or 20 mmHg, respectively. Underlying the hemodynamic changes that result in pulmonary hypertension, whether from hypoxia, acidosis, increased pulmonary blood flow, increased shear stress, or idiopathic causes, is a dysfunctional vascular endothelium. In this review, the role of the history and physical examination in the initial assessment is emphasized. Newer diagnostic modalities, such as subselective pulmonary angiography and ultrafast computed tomography scanning, are reviewed. Low-flow oxygen, anticoagulation, and calcium-channel blockade are presented as accepted therapeutic modalities. Inhaled nitric oxide and prostacyclin infusion are presented as newer therapies that may be useful given the limited availability of donor organs for hear-lung transplantation. Future therapeutic strategies are likely to develop from advances in vascular biology.
A 52 year old man developed progressive painful swelling of both calves and difficulty walking. Physical examination showed asymmetrical localised swelling with induration and tenderness on palpation. Peripheral blood eosinophilia was noted. Biopsy of deep fascia and muscle showed typical features of eosinophilic fasciitis. He was treated with non-steroidal anti-inflammatory drugs and intensive physiotherapy. The clinical features had completely resolved six months later.
The principal aim of the study was to determine the degree of association between cerebrospinal fluid (CSF) that is positive for HTLV-1 and myelopathy in Salvador, Brazil. From the same hospital, twenty-eight cases of myelopathy and twenty-eight cases showing no neurological disorder were studied using blind selection matched 1:1 by age and sex. The twenty-eight pairs underwent HTLV-1 serology tests. In those with a positive result, anti-HTLV-1 antibodies were investigated in the CSF. The ELISA method was used, complemented by the Western-blot test. Myelopathy was considered associated with HTLV-1 only when the CSF was positive indicating neurotropism of the virus. The mean age of the cases was 44.6 +/- 15.6 years and the control group was 43.5 +/- 16.0 (p > 0.05). An OR of 9.0 was detected with a reliability interval (95%) of 1.652-48.866 and chi-square significant at the 0.02 level. Despite a strong degree of association and considering the low level of precision, there is a need for analytical studies with larger samples which besides improving the precision will allow for greater control of the confounding variables.
We report an audit of 786 oesophageal procedures, including 53 oesophagectomies, performed during 1990 in a specialist oesophageal unit. Apart from assessing morbidity and mortality, audit allows a review of cost efficiency and justification for certain practices with regard to patient management. The data reported here may provide a framework against which individual surgeons may assess their own results and compare costs of procedures with a similar outcome.
Two hundred and forty seven consecutive patients admitted to an acute general hospital were studied. The presence of an association between the ear lobe crease (ELC) and ischaemic heart disease, hypertension, hypercholesterolaemia, peripheral vascular disease, cerebrovascular disease and smoking was investigated. The association between an ELC and coronary heart disease was found to be significant. There was no significant difference between the prevalence of ear lobe creases in males versus females and no correlation between ear lobe creases and smoking, hypercholesterolaemia, hypertension, peripheral vascular disease or stroke was found. Despite having a low sensitivity the specificity of an ear lobe crease is 94% which suggests that it should be used as a physical sign predictive of the presence of coronary heart disease rather than a diagnostic test.
Forty six cadaveric lower limbs were examined to define the presence, site and shape of the tendinous interruption in semitendinosus. It was found to be: 1. Present in all limbs studied. 2. Single in all limbs studied. 3. V-shaped with a short lateral limb and a long medial limb measuring one fifth of the total muscle length. 4. Its apex is one third of the total muscle length from the origin of the muscle.