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Thus, our data suggests that wall thickness is not a determinant factor for RA or RAA rupture in blunt trauma.

Objective: Mitral valve insufficiency must be treated by repair whenever as prossible as it provides better resultsespecially within the pediatric population in order to avoid valve replacement incovenients. The aim of this study is to describe mitral valve repair technique based on an anatomical and functional approach.Methods: During a 13 months period, eight children (age ranged from 2 and 12 years old 6.37 +\3.66) with mitral valve insufficiency underwent intermittent anterior and posterior annuloplasty associated with Alfieri's repair -performed by placing a stitch between the anterior and posterior leaflets in the point of maximal regurgitation thus creating a double orificial mitral valve.Results: There were no surgical deaths. All patients underwent postoperative echocardiography. Three patients showed mild insufficiency and five patients showed no insufficiency. The time in intensive care unit ranged from 2 to 4 days (2.5 + 0.75), and the time of stay in hospital ranged from 5 to 8 days (6.37 + 1.06).Conclusion: In spite of the little sample size, the proposed technique proved itself to be simple and effective in the treatment of single mitral valve insufficiency within the pediatric population. In addition, it also yielded satisfactory immediate results. Long-term follow-up is nevertheless necessary in order to evaluate long-term results.Descriptors: Heart defects,congenital. Child. Mitral valve. ResumoObjetivo: A insuficiência mitral com indicação cirúrgica na faixa etária pediátrica deve ser tratada por meio de plastia sempre que possível, evitando-se os inconvenientes da substituição valvar. O objetivo deste trabalho é propor técnica de plastia mitral baseada em abordagem funcional e anatômica.

OBJETIVO: Avaliar a eficácia da proteção miocárdica obtida com o acréscimo da lidocaína à solução sangüínea hipercalêmica normotérmica. MÉTODO: Foram estudados 26 cães, divididos em dois grupos de dez animais e um grupo de seis, de forma aleatória, conforme a solução cardioplégica de indução que receberam. O grupo I recebeu a solução composta por lidocaína 5mg/kg, cloreto de potássio 41,6mEq/l em 180ml de sangue normotérmico. O grupo II recebeu a solução anterior sem lidocaína e o grupo III recebeu somente os 180ml de sangue. A solução de manutenção foi a mesma para os 3 grupos composta por 120ml de sangue normotérmico, reinfundidos a cada 20min. Os animais foram submetidos à circulação extracorpórea, a duas horas de isquemia miocárdica e três horas de reperfusão. Foram avaliados mortalidade operatória, dosagens seriadas de troponina I, creatina quinase e lactado, débito cardíaco, fração de ejeção e fração de área das mitocôndrias. A análise estatística foi através dos testes exato de Fisher e a análise de variância de duplo fator complementada com o teste de Bonferroni. RESULTADO: O grupo I apresentou menor mortalidade (p=0,08), menor liberação da creatina quinase (p<0,05) e menor comprometimento mitocondrial (p=0,036). Não houve diferença entre os grupos quanto à liberação de troponina I, lactato e avaliação hemodinâmica. CONCLUSÃO: Pode-se concluir que a lidocaína conferiu efeito protetor adicional ao miocárdio isquêmico e que os animais dos grupos I e II apresentaram alterações significativas, sugestivas de dano celular, com repercussões funcionais, para todos os parâmetros avaliados no decorrer do tempo.
OBJECTIVE: The purpose of this research is to evaluate the efficacy of the lidocaine in myocardial protection with normothermic antegrade blood cardioplegia. METHOD: Twenty six dogs were studied divided at random into two groups of ten and one group of six, depending on which cardioplegic solution they had received. Group I received a cardioplegic solution induction of lidocaine 5mg/kg, 41,6mEq/l of KCl and 180ml of normothermic blood. Group II received the same solution except for the lidocaine and group III received only 180ml of blood. Every 20min 120ml of normothermic blood was reinfused. All dogs underwent cardiopulmonary bypass, two hours of myocardial ischemia and three hours of reperfusion. These dogs were evaluated through operative mortality, myocardial enzymes such as cardiac troponin I and creatine kinase, lactate production, hemodynamic performance measured by ejection fraction and cardiac output, and morphometrics mitochondrial ultrastructural changes. Statistical analysis tests used to compare the results were the Fisher exact test and the two-way Anova. RESULTS: The results have shown that the animals from group I in comparison to those of group II, had no mortality (p=0,08), a lower production of creatine kinase (p<0,05), lower mitochondrial ultrastructural changes (p=0,036) and had no difference with cardiac troponin I production, lactate production and hemodynamic performance. CONCLUSIO...

IntroductionIdiopathic dilated cardiomyopathy causes great impact but many aspects of its pathophysiology remain unknown.ObjectiveTo evaluate anatomical and histological aspects of hearts with idiopathic dilated cardiomyopathy and compare them to a control group, evaluating the behavior of the perimeters of the atrioventricular rings and ventricles and to compare the percentage of collagen and elastic fibers of the atrioventricular rings.MethodsThirteen hearts with cardiomyopathy and 13 normal hearts were analysed. They were dissected keeping the ventricular mass and atrioventricular rings, with lamination of segments 20%, 50% and 80% of the distance between the atrioventricular groove and the ventricular apex. The sections were subjected to photo scanning, with measurement of perimeters. The atrioventricular rings were dissected and measured digitally to evaluate their perimeters, later being sent to the pathology laboratory, and stained by hematoxylin-eosin, picrosirius and oxidized resorcin fuccin.ResultsRegarding to ventricles, dilation occurs in all segments in the pathological group, and the right atrioventricular ring measurement was higher in idiopathic dilated cardiomyopathy group, with no difference in the left side. With respect to collagen, both sides had lower percentage of fibers in the pathological group. With respect to the elastic fibers, there was no difference between the groups.ConclusionThere is a change in ventricular geometry in cardiomyopathy group. The left atrioventricular ring does not dilate, in spite of the fact that in both ventricles there is lowering of collagen.