[Exercise test: abnormal ST segments restricted to recovery phase]. / Teste de esforço: alterações do segmento ST restritas à fase de recuperação.

PURPOSE: To determine the incidence of atherosclerotic coronary artery disease (CAD) and or myocardial ischemia in patients (pt) with abnormal ST segments restrict to recovery phase (RRAST) of exercise testing (ET). MATERIAL AND METHOD: Retrospective study in 19 non consecutive pt with RRAST, related to coronary arteriography or exercise planar scyntillography (18 men, 58 +/- 9 years, 18 asymptomatic). RESULTS: RRAST corresponded to ST segment depression from 1 to 4 mm, with T inversion during early recovery (2 pt); late (14 pt) or both (4 pt). It was documented CAD (14 pt and 9) with artery-by-pass surgery); hypertensive myocardiopathy with normal coronary (3 pt), and mitral prolapse valve (1 pt). In 13 pt with coronary arteriography or exercise scyntillography, within the first 6 months from exercise testing, myocardial ischemia was confirmed in 8 pt in 3 pt, successive exercise testing showed RRAST reproductive in 2 cases. CONCLUSION: The authors report the high incidence of CAD and or transitory hypoperfusion during myocardial scyntillography in symptomatic men with middle age with RRAST during exercise testing.

Teste de esforço: alteraçöes do segmento ST retritas à fase de recuperaçäo / Exercise testing: abnormal ST segments restrict to recovery phase

Objetivo. Determinar a incidência de doença coronária aterosclerótica (DCA) e/ou isquemia miocárdica em pacientes (pt) com alteraçoes do segmento ST restrita à fase de recuperaçao (ASTRR) do teste ergométrico. Casuística e Método. Estudo retrospectivo em 19 pacientes nao consecutivos com ASTRR, através da cinecoronariografia e/ou cintigrafia de esforço planar. Amostra de 18 homens, uma mulher, com idade de 58 + 9 anos, 18 sintomáticos. Resultados. ASTRR corresponderam a segmentos ST infra-desnivelados de 1 a 4 mm da linha de base, com inversao da onda T durante a recuperaçao precoce (2pt), tardia (14 pt). Foi documentada DCA em 14 pt (nove submetidos à cirurgia de revascularizaçao); miocardiopatia hipertensiva com coronárias normais em 3 pt e prolapso de válvula mitral em 1 pt. Em 13 casos a cinecoronariografia eóu cintilografia de esforço foram realizados dentro de seis meses do Teste Ergométrico, sendo a presença de DCA e ou isquemia miocárdica detectada em 8 pt. Em 3 pt, testes ergométricos sucessivos mostraram ASTRR reprodutíveis em dois casos. Conlusao. Os autores relatam a elevada prevalência de DCA e ou hipoperfusao transitória na cintigrafia de esforço em homens sintomáticos de meia idade com ASTRR no teste de esforço.

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.

Coração de atleta em desportistas deficientes de elite / Athlete's heart elite disable athletes

OBJETIVO - Verificar a prevalência de sinais de "coração de atleta" em desportistas deficientes para-olímpicos. MÉTODOS - Avaliação clínica, eletrocardiográfica, ecocardiográfica, vetocardiográfica, ergométrica em 75 atletas, 27ñ6,7 anos, 56 homens, várias modalidades; com deficiência física (47), visual (12) e paralisia cerebral (16). RESULTADOS - Sinais de coração de atleta ocorreram em 33 'por cento' dos exames clínicos (sopros e estalidos), em 55 'por cento' dos eletrocardiogramas (bradicardia, bloqueio incompleto de ramo direito, sobrecargas, alteraçöes de onda T), em 15 'por cento' dos vetocardiogramas (sobrecargas), em 5 'por cento' dos ecocardiogramas (dimensöes cavitárias acima do habitual). Os sinais ocorreram em 51 'por cento' dos atletas, sendo que em 46 'por cento' dos casos havia 2 ou mais sinais e, em 12 'por cento', 4 ou mais sinais. O TE foi normal em 77 'por cento' dos atletas; não houve ST isquêmico. Em 23 'por cento' dos casos houve bloqueio divisional direito. CONCLUSÄO - Foram encontrados dois ou mais sinais de coração de atleta em 46 'por cento' dos atletas deficientes para-olímpicos.

[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.

[Athlete's heart in elite disabled athletes]. / Coração de atleta em desportistas deficientes de elite.

PURPOSE: To assess the prevalence of the athlete's, heart syndrome in elite disabled Brazilians athletes. METHODS: Seventy-five athletes, age 27.8 +/- 6.7 years, 56 men, with various disabilities (47 physical, 12 visual and 16 cerebral paralysis) underwent clinical, electrocardiographic, vectorcardiographic, ergometric and echocardiographic evaluations. RESULTS: Athlete's heart signs occurred in 33% of the clinical evaluations, in 55% of the electrocardiograms, in 15% of the vectorcardiograms, and in 5% of the echocardiograms. At least one of these signs was presented in 51% of the athletes. There were 2 or more abnormalities in 46% of the athletes and 4 or more signs in 12%. Exercise test was considered not ischemic in 77% of the subjects. There was right bundle branch block in 23% of the tests. CONCLUSION: There were two or more athlete's heart syndrome signs in 46% of Brazilian disabled athletes.

[Effect of enalaprilat on cardiotoxicity induced by doxorubicin]. / Efeito do enalaprilato na cardiotoxidade induzida pela doxorubicina.

PURPOSE: To evaluate whether the enalaprilat, an angiotensin converting enzyme inhibitor, was able to prevent the myocardial damage induced by doxorubicin (DOX). METHODS: Four groups composed of 10 Wistar rats each were followed for seven weeks: control (CONT); treated with enalaprilat (ENA, 1mg/kg/d/sc) treated with doxorubicin (DOX, 25 mg/kg/d/sc), and treated with doxorubicin plus enalaprilat (DOX+ENA). In eight animals of each group, the left ventricle (LV) was prepared for morphometric study and stained with HE and picro-sírius for identifying muscle fibers and collagen. In each group three fragments of the LV were examined with electronic microscopy (EM). For statistical analysis: the one-way analysis of variance was performed and was followed by multiple comparisons test when the difference between groups were detected p values < or = 0.05 were considered significant. RESULTS: Light microscopy-it was not found any significant difference among the groups for muscle fibers patterns and proportion of collagen fibers of left ventricle. Electronic microscopy-the cristolysis index (proportion between normal and damage mitochondria) demonstrated significant difference between DOX and DOX+ENA groups (30.1 vs 11.6, p < or = 0.01). CONCLUSION: ENA prevented cardiotoxic alterations induced by DOX minimizing the aggression to the mitochondria and these findings, if confirmed in anima nobilis, may open a new clinical use for this type of drug.

[Effect of verapamil on left ventricular hypertrophy induced by isoproterenol]. / Efeito do verapamil na hipertrofia ventricular esquerda induzida pelo isoproterenol.

PURPOSE: We evaluated whether verapamil (VERA) has a protective effect on left ventricular hypertrophy (LVH) induced by Isoproterenol (ISO) in rat. METHODS: Seventy two male adult rats were divided in four groups and treated accordingly during eight days: Control (CON), VERA (10 mg/kg), ISO (0.3 mg/kg) and VERA + ISO. It was measured in 10 animals from each group heart rate, blood pressure, left ventricle dry weight and ratio between left ventricular weight (LVW) and rat weight. Samples were taken from the left ventricle to be examined by light microscopy. RESULTS: LVW of the CON group was 0.145 g, of VERA was 0.144 g, of ISO with 0.201 g, and of VERA + ISO was 0.148 g. The difference between ISO group and others was statistically significant (P < 0.05). The LVW/W ratio also showed similar result. The myocardial pattern induced by ISO was left hypertrophy and collagen content increase. In VERA + ISO group it was found a protective effect to hypertrophy (ISO group 97% vs VERA + ISO 87%; p < 0.001) and increased collagen content. CONCLUSION: VERA prevents the deleterious effects of ISO in the myocardium. Probably this action is due to prevention the myocardial hypertrophy and proliferation of collagen tissue.