Biventricular structural and functional responses to aortic constriction in a rabbit model of chronic right ventricular pressure overload

Objectives: Chronic right ventricular (RV) pressure overload results in pathologic RV hypertrophy and diminished RV function. Although aortic constriction has been shown to improve systolic function in acute RV failure, its effect on RV responses to chronic pressure overload is unknown. Methods: Adjustable vascular banding devices were placed on the main pulmonary artery and descending aorta. In 5 animals (sham group), neither band was inflated. In 9 animals (PAB group), only the pulmonary arterial band was inflated, with adjustments on a weekly basis to generate systemic or suprasystemic RV pressure at 28 days. In 9 animals, both pulmonary arterial and aortic devices were inflated (PAB+AO group), the pulmonary arterial band as for the PAB group and the aortic band adjusted to increase proximal systolic blood pressure by approximately 20 mm Hg. Effects on the functional performance were assessed 5 weeks after surgery by conductance catheters, followed by histologic and molecular assessment. Results: Contractile performance was significantly improved in the PAB+AO group versus the PAB group for both ventricles. Relative to sham-operated animals, both banding groups showed significant differences in myocardial histologic and molecular responses. Relative to the PAB group, the PAB+AO group showed significantly decreased RV cardiomyocyte diameter, decreased RV collagen content, and reduced RV expression of endothelin receptor type B, matrix metalloproteinase 9, and transforming growth factor beta genes. Conclusions: Aortic constriction in an experimental model of chronic RV pressure overload not only resulted in improved biventricular systolic function but also improved myocardial remodeling. These data suggest that chronically increased left ventricular afterload leads to a more physiologically hypertrophic response in the pressure-overloaded RV. (J Thorac Cardiovasc Surg 2012;144:1494-501)Deutsche Herzstiftung e.V., Frankfurt, German

Tolerância da placenta à parada circulatória umbilical normotérmica Tolerance of placenta to normothermic umbilical circulatory arrest

O aumento da resistência vascular placentáriae distúrbios de trocas gasosas freqüentemente ocorrem após a circulação extracorpórea (CEC) fetal. A utilização de um circuito convencional de CEC que exclua a placenta da circulação através do clampeamento temporário do cordão umbilical pode proteger a vasculatura placentária dos estímulos que levam ao aumento da resistência vascular. Para avaliar a tolerância placentária à parada normotérmica do fluxo sangüíneo umbílico-placentário, 9 placentas de ovelhas isoladas in-situ, foram colocadas em CEC através da canulação dos vasos umbilicais, com fluxo médio de artéria umbilical de 214 ml/min/kg. Após 30 minutos de estabelecimento da CEC, a circulação placentária foi interrompida por 30 minutos, simulando o clapeamento do cordão umbilical durante a CEC fetal total. Posteriormente, a circulação placentária foi restabelecida aos valores basais. A troca de gases placentária, o fluxo sangüíneo e a resistência vascular materno-placentários foram avaliados antes e depois da parada circulatória. Não houve diferença estatisticamente significante entre os gradientes transplacentários de pO2 e pCO2, indicando que a interrupção do fluxo sangüíneo placentário por 30 minutos, em condições normotérmicas, não afeta a função placentária. Este modelo sugere um método alternativo para a aplicação clínica da CEC fetal, através da exclusão da circulação umbílico-placentária durante a CEC fetal, eliminandose, assim, os efeitos deletérios da CEC nas trocas gasosas placentárias.<br>Elevation of placental vascular resistance (PVR) and depression of fetal gas exchange occurs after fetal cardiopulmonary bypass (CPB). Excluding the placenta from the CPB circuit may protect the placental vasculature from the unwanted stimuli which lead to elevated PVR. To evaluate this approach, 9 isolated in-situ sheep placentas were placed on CPB by cannulating the umbilical vessels, with a mean umbilical artery flow of 214 ml/min/kg. After 30 minutes of stable flow, placental circulation was arrested for 30 minutes, simulating the umbilical vessel clamp time during whole body fetal CPB. Placental circulation was then restored to baseline values. Placental gas exchange and maternal placental blood flow were evaluated before and after arrest. Interruption of blood flow to the placenta for 30 minutes under normothermic conditions does not affect placental function or maternal placental blood flow. It may be possible to exclude the placenta from the circulation during fetal CPB as a mean of eliminating the detrimental effects of CPB on placental gas exchange. This model suggests an alternative way of designing a scheme for clinical fetal CPB which may avoid the negatives effects of CPB on the placenta

New electrode for pacing fetuses with complete heart block Novo eletrodo para implante de marcapasso em fetos com bloqueio atrioventricular total

OBJECTIVE: As fetal complete heart block with hydrops carries a poor prognosis, intrauterine pacing appears the most logical treatment. However, premature labor following hysterotomy remains a major obstacle to open procedures. Therefore, we developed a new lead for fetal pacing that avoids the need for intrauterine open surgical procedures. METHODS We successfully implanted a new T-bar-shaped lead into the myocardium of a fetus at 25 weeks gestation presenting with complete heart block (heart rate = 47 beats per minute), hydrops, and structural heart defects. The procedure was performed under ultrasound guidance, and the lead was introduced through the tip of a specially designed, 18G needle. The new lead was then connected to a Biotronik Actros pulse generator, which was implanted subcutaneously in the maternal abdominal wall. RESULTS: The stimulation resistance was 357 omega, and the sensed fetal R wave was 6.4 mV. The voltage strength-duration curve remained relatively constant at pulse widths > 0.6 msec. An echocardiogram on the first postoperative day revealed a mild pericardial effusion. The fetal heart rate was sTable , with low stimulation thresholds and no stimulation failures. No uterine contractions were observed during the postoperative period. However, the fetus died 36 hours after the procedure, probably due to cardiac tamponade. CONCLUSION: To our knowledge, this is the first documentation of voltage strength-duration curves for the acute myocardial stimulation threshold of a human fetus that survived 36 hours after intrauterine pacemaker implantation. This case emphasizes that percutaneous fetal pacing with the new lead is feasible and may minimize the chances of premature labor.OBJETIVO: O bloqueio atrioventricular total (BAVT) fetal apresenta mau prognóstico quando associado à hidropsia. O implante de marcapasso no feto a céu aberto pode desencadear o trabalho de parto prematuro e suas conseqüências. Por isso, desenvolvemos um novo eletrodo para implante de marcapasso em fetos, que evitaria a operação intra-uterina a céu aberto. MÉTODO: Um novo eletrodo em formato de "T" foi implantado no miocárdio de um feto com 25 semanas de gestação, BAVT (FC= 47 bpm), hidropsia e cardiopatia congênita associada. O procedimento foi realizado com ajuda de ultra-som, sendo o eletrodo veiculado através da ponta de uma agulha 18-G. Após o implante, o eletrodo foi conectado ao analisador de pulsos para avaliação dos limiares e, posteriormente, ao gerador de pulsos Biotronik Actros. RESULTADOS: A resistência foi de 357 ômega e a onda R foi de 6,4 mV. A curva do limiar de estimulação permaneceu relativamente constante para larguras de pulso acima de 0,6 mseg. O ecocardiograma no 1º P.O. revelou derrame pericárdico discreto. A freqüência cardíaca fetal permaneceu estável, com baixos limiares de estimulação e sem perda de comando. Não foram observadas contrações uterinas durante o pós-operatório. Entretanto, o feto foi a óbito 36 horas após o procedimento, provavelmente por tamponamento cardíaco. CONCLUSÕES: Este caso representa a primeira documentação de limiares agudos de estimulação de um feto humano que sobreviveu 36 horas ao implante de marcapasso intra-uterino. Este caso enfatiza que o implante de marcapasso fetal percutâneo é factível e pode minimizar as chances de trabalho de parto prematuro