Rational utilization of diagnostic tests in cardiology.
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Biomedical subjects
Publications and source records attributed to B Luna Filho.
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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.
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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.
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.
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.
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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.
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.
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.
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.
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PURPOSE: To assess the role of pulsed Doppler echocardiography (PDE) in the indirect assessment of pulmonary artery (PA) pressure (P), analysing the pulmonary velocity blood flow curves (PVBFC) profile. PATIENTS AND METHODS: Sixty-one adults with several kinds of heart disease were submitted to heart catheterization to obtain PAP (systolic, diastolic, mean), and other hemodynamic variables. A PDE examination was performed in all to obtain the PVBFC at the level of the pulmonic annulus. Qualitative features of the curve were analysed (morphological pattern, presence of pulmonic regurgitation) as well as quantitative data (acceleration time = AT, right ventricle ejection time = RVET index, AT/RVET index AT corrected for heart rate = ATC), which were compared to the invasive measurements. RESULTS: An abnormal rapid acceleration of the PVBFC, with triangular configuration, was noted in patient with pulmonary hypertension (PH), in contrast to the dome-like shape of the PVBFC in normal PAP. Pulmonary regurgitation was more frequent (p < 0.05) in patients with severe PH (mean PAP > or = 40 mmHg), comparing with patients with PAP < 40 mmHg. Inverse linear correlations were observed between AT and mean PAP, particularly when sinus rhythm was present (r = 0.89; p < 0.05) excluding patients with atrial fibrillation (19 cases). CONCLUSION: PDE is an useful and noninvasive method for indirect evaluation of PAP in adults, especially during stable sinus rhythm, in heart rate range from 60 to 115 bpm.
PURPOSE: To assess the role of pulsed Doppler echocardiography (PDE) in the indirect assessment of pulmonary artery (PA) pressure (P), analysing the pulmonary velocity blood flow curves (PVBFC) profile. PATIENTS AND METHODS: Sixty-one adults with several kinds of heart disease were submitted to heart catheterization to obtain PAP (systolic, diastolic, mean), and other hemodynamic variables. A PDE examination was performed in all to obtain the PVBFC at the level of the pulmonic annulus. Qualitative features of the curve were analysed (morphological pattern, presence of pulmonic regurgitation) as well as quantitative data (acceleration time = AT, right ventricle ejection time = RVET index, AT/RVET index AT corrected for heart rate = ATC), which were compared to the invasive measurements. RESULTS: An abnormal rapid acceleration of the PVBFC, with triangular configuration, was noted in patient with pulmonary hypertension (PH), in contrast to the dome-like shape of the PVBFC in normal PAP. Pulmonary regurgitation was more frequent (p less than 0.05) in patients with severe PH (mean PAP greater than or equal to 40 mmHg), comparing with patients with PAP less than 40 mmHg. Inverse linear correlations were observed between AT and mean PAP, particularly when sinus rhythm was present (r = 0.89; p less than 0.05) excluding patients with atrial fibrilation (19 cases). CONCLUSION: PDE is an useful and noninvasive method for indirect evaluation of PAP in adults, especially during stable sinus rhythm, in heart rate range from 60 to 115 bpm.