Recurrence of atrial septal defect in three generations.

Beginning with a patient presenting with an atrial septal defect (ASD) of the secundum type, the genealogy was identified in four affected individuals who belonged to three successive generations of the same family. The defects were visually confirmed in all individuals and were found to be anatomically similar. No other congenital malformations were present in these individuals. The genealogy was identified in 1972, when ASD recurred in two generations, and it was concluded that the mechanism of transmission was autosomal recessive. The fifth individual, identified 21 years later, and having an anomaly identical to that of the others, was the child of a couple who had no consaguinity and whose mother was a member of the previously studied genealogy. Considering the absence of phenotype in the parents and the rarity of the ASD gene in the general population, the occurrence of the uniparental disomy for this family nucleus, and the same autosomal recessive mechanism of transmission by this affected individual is possible. This study reports the familial occurrence of ASD by genetic mechanisms of transmission, emphasizing the necessity for genetic-clinical studies in members of the familial nucleus in order to detect new carriers, who usually are asymptomatic, thereby allowing for early and adequate treatment of individuals who may be affected.

[Spironolactone protection from hydralazine-induced stress in the rat myocardium]. / Protecção pela espironolactona do estresse pela hidralazina em miocárdio de ratos.

OBJECTIVES: We wished to verify the possible protective action of spironolactone (SPIRO), through its blocking action of slow calcium channels, in what concerns behavioural, morphologic, histochemical and ultrastructural alterations caused by experimental exposure to hydralazine (HZ), due to the excess release of catecholamines and the cellular influx of calcium. MATERIAL AND METHODS: Forty-eight adult male Wistar rats [correction of mice] were divided into 4 groups. The control group (CON) was administered olive oil for 4 days and distilled water i.v. on the last day, the hydralazine group (HZ) was administered olive oil for 4 days and 40 mg/kg i.v. of hydralazine on the last day; the spironolactone group (SPIRO) was administered 20 mg/kg of spironolactone diluted in olive oil for 4 days and distilled water on the last day; and the hydralazine with spironolactone group (HZ + SPIRO) was administered 20 mg/kg of spironolactone diluted in olive oil for 4 days and 40 mg/kg i.v. of hydralazine on the last day. The rats [correction of mice] were dissected and fragments of the myocardium removed for electron microscopy, and suprarenal fragments removed for light microscopy. Mitochondrial alterations characterised by ridge edema, lysis and vacuolisation (Cristolysis rate = damaged mitochondria/total mitochondria) were considered in the ultrastructural study. RESULTS: Light microscopy of the HZ group showed intense depletion of lipids in the cortical region of the suprarenals. The HZ + SPIRO group did not present significant alterations and was similar in appearance to the CON group. The ultrastructural study of the myocardium revealed the following rates of Cristolysis: CON group = 5.8%, HZ group = 91.9%, SPIRO group = 10.9%, HZ + SPIRO group = 10.2%*. (* = p < 0.001 chi-square test). CONCLUSION: The use of spironolactone in a model of stress induced by hydralazine caused: 1. Myocardial protection shown by reduced lesion of cardiomyocytes; 2. Protection of the suprarenals.

[Myocardial protection against cold stress with pravastatin]. / Protecção miocárdica ao "estresse" do frio pela pravastatina.

The CARE study showed that the myocardial infarction recurrence rate in patients with moderate cholesterol blood level decreases early during pravastatin treatment. Our goal is to evaluate the possible role of pravastatin in preventing the myocardial lesions induced by cold stress. Twenty Wistar-EPM rats were divided into four groups: Control (CON); PR (Pravastatin) treated with 10 mg/kg/d for 15 days; S (Stress group) in which the rats were submitted to cold stress (-8 degrees C for four hours); and PR + S group treated with pravastatin like PR group and also submitted to the cold stress. The animals were sacrificed and heart fragments were removed for optic and electronic microscopic analysis. The variable considered was mitochondria abnormality (edema, lyses and vacuolization) that was interpreted as crystolyses indices (CI) (n degree of abnormal mitochondria/n degree total of mitochondria). The following crystolyses indices, were found for each group respectively: CON, 2.0%; S, 95.5%; PR, 19.9% and PR + S group, 27.7%*(*p < 0.01). In conclusion, pravastatin prevented myocardial lesions induced by cold stress significantly.

[Enalaprilat in the prevention of left ventricular hypertrophy induced by isoproterenol]. / Enalaprilato na prevenção da hipertrofia ventricular esquerda induzida pelo isoproterenol.

PURPOSE: To evaluate whether the enalaprilat, angiotensin I enzyme conversion inhibitor, could prevent the left ventricular hypertrophy (LVH) induced by isoproterenol. METHODS: Seventy two adult Wistar-EPM rats were divided into four groups: CON, control; ENA, treated with enalaprilat (1 mg/kg via subcutaneous (s.c.) for 8 days); ISO, treated with isoproterenol (0.3 mg via s.c. for 8 days) e ENA + ISO, treated with both drugs simultaneously. Each group had the arterial blood pressure, cardiac rate and the left ventricle (LV) weight determined in 10 animals. In 8 animals from each group a small sample was taken from the LV and stained with hematoxyline-eosine and picrosirius for morphometric and ultra-structural studies with optic and transmission electronic microscopy. RESULTS: The ISO group showed that the LV weight increased 47% in comparison with control. On the other hand the ENA + ISO group showed only 22.1% increase (p < or = 0.05). The morphometric and ultra-structural analyses revealed that isoproterenol induced cardiomyocite hypertrophy and augmented the content of the type I collagen in the cardiac interstitium. CONCLUSION: Enalaprilat inhibited the isoproterenol action on the cardiomyocite, avoiding partially the LVH and decreasing the content of collagen fibers.

[Organophosphate poisoning and myocardial necrosis]. / Intoxicação por órgano-fosforado e necrose miocárdica.

A man (46 years-old) was admitted to the intensive care unit (ICU) with a history that eight hours before he had voluntarily drank 100 ml of malathion. He complained of a burning pain on the anterior thorax and was confused. His cardiovascular evaluation was normal and his breathing was heavy with some rales on the pulmonary auscultation. He was treated with atropine and contrathion and rapidly evolved into coma. Electrocardiogram showed subendocardial lesion in the inferior wall with diffuse ly altered ventricular repolarization and increase QT interval. During the ICU period his cardiac enzyme levels also raised. The patient died in the 8th day after admission. The pathological evaluation of the heart revealed foci of myocardial necrosis. This is the 1st case of medical literature with histological confirmation of myocardial necrosis from organophosphate intoxication.

Intoxicaçäo por órgano-fosforado e necrose miocárdica / Organophosphate Intoxication and Myocardial Necrosis

Paciente masculino, de 46 anos, foi internado no centro de terapia com quadro de ingestäo voluntária de 100ml há 8h. Queixava-se de ardor na face anterior do tórax. Estava torporoso. O exame cardiovascular era normal e a ventilaçäo espontânea com muitos roncos na ausculta pulmonar. Foi medicado com atropina e cotrathion, evoluindo para o coma. O eletrocardiograma apresentou lesäo subendocárdica em parede inferior, alteraçöes difusas da repolarizaçäo ventricular e aumento do intervalo QT. As enzimas cardíacas se elevaram. No 8§ dia o paciente foi a óbito e a análise anatomopatológica do coraçäo revelou: artérias coronárias normais em toda a extensäo, e focos difusos de necrose niocárdica comprovada por anatomopatológico em intoxicaçäo por órgano-fosforado. A necrose miocárdica difusa pode ser a responsável pelas alteraçöes cardíacas comumente encontradas.

Spreading depression in isolated spinal cord.

1. Isolated spinal cord of amphibians is able to express Leão's spreading depression (SD). 2. SD can be evoked when the spinal cord is in an appropriated medium. There are two conditions that favor its elicitation: hypotonicity and low [Cl-] levels in the extracellular microenvironment. 3. Spinal cord SD is accompanied by a stereotyped negative extracellular voltage transient of 17.3 +/- 4.9 (standard deviation) mV amplitude and 1.2 +/- 0.5 min duration concomitantly with a reversible [K+]o increase up to 21.1 +/- 4.6 mM in the extracellular fluid. 4. Potassium salt solution can trigger SD waves that spread at 12 +/- 4.7 mm/min. 5. SD waves occur "spontaneously" in preparations superfused by Ringer solutions with very low [Cl-] (< 20 mM). The frequency of these waves decreases, and they may stop if [Mg2+] is increased.

[Enalapril and myocardial protection from stress by cold]. / Enalapril e proteção do miocárdio ao estresse pelo frio.

PURPOSE: To evaluate the myocardial protective effect of enalaprilat in rats submitted to stress by cold. METHODS: Fifteen adults, male rats were studied. They were allocated into four groups: group A received unrestricted diet + intraperitoneal (IP) diluent; group B: unrestricted diet + IP enalaprilat 1.0 mg/kg; group C: high salt diet (HD) for seven days + IP indomethacin 1.0 mg/kg and group D received high salt diet for seven days + IP indomethacin 1.0 mg/kg + IP enalaprilat 1.0 mg/kg. Three animals were the control group. The animals of the groups A, B, C and D were then submitted to stress by cold. Fragments of the left ventricle were obtained for electron microscopy and the occurrence of mitochondrial lysis or preservation of the mitochondrial ultrastructure were considered as parameter for myocardial protective effect evaluation. RESULTS: Crystolysis (partial or total) was observed in 16.2% group A; 19.5% of group C; 3.2% of group B and in 8.8% of group D. CONCLUSION: Enalaprilat protects the cardiomyocyte from the stress by cold.

[Acute pulmonary edema secondary to pheochromocytoma. A case report]. / Edema agudo de pulmáo secundário a feocromocitoma. Relato de caso.

Authors report a case of a patient with abdominal pheochromocytoma who presented recurrent episodes of acute pulmonary edema. No cardiopathy was detected either by clinical examination or by electrocardiogram, echograms or invasive cineventricleangiograma. They concluded that a non cardiogenic etiology is possible for the referred clinical manifestations.

Endocardite infecciosa por listeria monocytogenes em prótese valvar. Relato de um caso / Infective endocartites due to listeria monocytogenes in valvar prosthesis. Report of a case

Os autores relatam o caso de um paciente portador de protese biologica em posicao mitral, que apresentou endocardite infecciosa por Listeria monocytogenes. Apos remitral, que apresentou endocardite infecvisao da literatura, ressaltam a raridade desta associacao e as particularidades clinicas de endocardite por esse agente etiologico

Recorrência de infarto do miocárdio no lupus eritematoso sistêmico. Apresentação de um caso e revisão da literatura / Recurrence of myocardial infarction in systemic lupus erythematosus. Report of a case an review of the literature

Os autores relatam o caso de uma paciente jovem com lupus eritematoso sistemico, que apresentou 2 episodios de infarto agudo do miocardio no intervalo de 5 meses. No primeiro episodio, as provas laboratoriais foram compativeis com atividade lupica e no episodio seguinte nao se demonstrou atividade. Na cinecoronarioventriculografia as arterias coronarias eram normais, constatando-se a presenca de aneurisma apical importante. Os testes para pesquisa de espasmo coronario, pela prova de gelo, e a perfusao do miocardio, inferida pela dosagem do lactato no seio coronario, foram normais. A controversia dos achados clinicos e laboratoriais observados no presente relato motivaram a revisao da literatura pertinente

Mixoma atrial esquerdo. Diagnóstico por angiografia digital. Relato de caso / Left atrial myxoma. Diagnosis by digital angiography. A case report

Portador de volumoso mixoma, localizado no atrio esquerdo, apresentava febre sintomas de descompensacao cardiaca e a propedeutica simulava estenose mitral pura. Foi submetido a diferentes exames laboratoriais, entre os quais venticulografia com pirofosfato de tecnecio, ecocardiografia e angiografia digital. Os tres metodos demonstraram o mixoma, contudo, de modo preciso a ecocardiografia e angiografia digital