Cardiac malposition, redistribution of fetal cardiac output, and left heart hypoplasia reduce survival in neonates with congenital diaphragmatic hernia requiring extracorporeal membrane oxygenation

Baumgart, Stephen; Paul, James J.; Huhta, James C.; Katz, Aviva L.; Paul, Karen; Spettell, Claire M.; Spitzer, Alan R.

doi:10.1016/s0022-3476(98)70178-7

Cited by 77 publications

(61 citation statements)

References 26 publications

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“…14,20 Mechanical compression and impaired filling of the left ventricle occur in CDH. 21 Volume overload, ventricular dilation, and high-output failure are the hallmarks of the fetus with SCT. [5][6][7]22 The cardiovascular findings we observed during surgery reflect the summation of the effects of surgery, tocolytics, and anesthesia on the fetus, as well as any change in the primary lesion as a consequence of the operation.…”

Section: Discussionmentioning

confidence: 99%

“…This is because left ventricular filling volume is diminished in the fetus with CDH owing to compression of the left ventricle, impaired right-to-left shunting at the atrial level, and limited pulmonary venous return as a consequence of pulmonary hypoplasia. 21 Fetuses with SCT exhibit unique physiological changes at the time of surgery. Before surgery, the fetal heart is faced with the consequences of a giant arteriovenous malformation: increased preload and afterload that encompasses the combined vascular resistances of the fetal body, placenta, and low resistance mass.…”

Section: Discussionmentioning

confidence: 99%

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Acute Cardiovascular Effects of Fetal Surgery in the Human

et al. 2004

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Background-Prenatal surgery for congenital anomalies can prevent fetal demise or alter the course of organ development, resulting in a more favorable condition at birth. The indications for fetal surgery continue to expand, yet little is known about the acute sequelae of fetal surgery on the human cardiovascular system. Methods and Results-Echocardiography was used to evaluate the heart before, during, and early after fetal surgery for congenital anomalies, including repair of myelomeningocele (MMC, nϭ51), resection of intrathoracic masses (ITM, nϭ15), tracheal occlusion for congenital diaphragmatic hernia (CDH, nϭ13), and resection of sacrococcygeal teratoma (SCT, nϭ4). Fetuses with MMC all had normal cardiovascular systems entering into fetal surgery, whereas those with ITM, CDH, and SCT all exhibited secondary cardiovascular sequelae of the anomaly present. At fetal surgery, heart rate increased acutely, and combined cardiac output diminished at the time of fetal incision for all groups including those with MMC, which suggests diminished stroke volume. Ventricular dysfunction and valvular dysfunction were identified in all groups, as was acute constriction of the ductus arteriosus. Fetuses with ITM and SCT had the most significant changes at surgery. Conclusions-Acute cardiovascular changes take place during fetal surgery that are likely a consequence of the physiology of the anomaly and the general effects of surgical stress, tocolytic agents, and anesthesia. Echocardiographic monitoring during fetal surgery is an important adjunct in the management of these patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Acute Cardiovascular Effects of Fetal Surgery in the Human

et al. 2004

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“…In addition, associated anomalies-primarily cardiac anomaliesaccount for many of the deaths. The role of hypoplastic heart in the poor prognosis of patients with CDH has been recognized; therefore, hypoplastic heart has been used as an ultrasonographic predictor of poor prognosis in prenatally diagnosed fetuses [14][15][16] . The primary focus of the present study was to demonstrate whether the herniated viscera to the thorax produced compression over the developing heart and consequently promoted cardiac hypoplasia.…”

Section: Discussionmentioning

confidence: 99%

Heart hypoplasia in an animal model of congenital diaphragmatic hernia

Tannuri

2001

Rev. Hosp. Clin.

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Purpose:In previous papers, we described a new experimental model of congenital diaphragmatic hernia in rabbits, and we also reported noninvasive therapeutic strategies for prevention of the functional and structural immaturity of the lungs associated with this defect. In addition to lung hypoplasia, pulmonary hypertension, biochemical, and structural immaturity of the lungs, the hemodynamics of infants and animals with congenital diaphragmatic hernia are markedly altered. Hence, cardiac hypoplasia has been implicated as a possible cause of death in patients with congenital diaphragmatic hernia, and it is hypothesized to be a probable consequence of fetal mediastinal compression by the herniated viscera. Cardiac hypoplasia has also been reported in lamb and rat models of congenital diaphragmatic hernia. The purpose of the present experiment was to verify the occurrence of heart hypoplasia in our new model of surgically produced congenital diaphragmatic hernia in fetal rabbits.Methods: Twelve pregnant New Zealand rabbits underwent surgery on gestational day 24 or 25 (normal full gestational time -31 to 32 days) to create left-sided diaphragmatic hernias in 1 or 2 fetuses per each doe. On gestational day 30, all does again underwent surgery, and the delivered fetuses were weighed and divided into 2 groups: control (non-surgically treated fetuses) (n = 12) and congenital diaphragmatic hernia (n = 9). The hearts were collected, weighed, and submitted for histologic and histomorphometric studies.Results: During necropsy, it was noted that in all congenital diaphragmatic hernia fetuses, the left lobe of the liver herniated throughout the surgically created defect and occupied the left side of the thorax, with the deviation of the heart to the right side, compressing the left lung; consequently, this lung was smaller than the right one. The body weights of the animals were not altered by congenital diaphragmatic hernia, but heart weights were decreased in comparison to control fetuses. The histomorphometric analysis demonstrated that congenital diaphragmatic hernia promoted a significant decrease in the ventricular wall thickness and an increase in the interventricular septum thickness.Conclusion: Heart hypoplasia occurs in a rabbit experimental model of congenital diaphragmatic hernia. This model may be utilized for investigations in therapeutic strategies that aim towards the prevention or the treatment of heart hypoplasia caused by congenital diaphragmatic hernia. DESCRIPTORS: Congenital diaphragmatic hernia. Heart. Hypoplasia. Fetus.In previous papers, we have described a new experimental model of congenital diaphragmatic hernia (CDH) in rabbits, and we also have reported on studies of noninvasive therapeutic strategies for prevention of functional and structural immaturity of lungs associated with this defect. These strategies consist of prenatal intra-amniotic administration of porcine surfactant or dexamethasone and prenatal tracheal ligation (TL), an invasive method that effectively treats or prevents pulmonary...

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“…Secondary diminution of chamber growth, particularly of the left heart, has been documented in human CDH fetuses. In particular, when left-sided cardiac underdevelopment is detected prenatally, this is considered a poor prognostic factor since at delivery the heart is less compliant and unable to maintain normal cardiac function [8, 34, 35]. Additionally, in animal models [4] and human CDH [5], histological and immunohistochemical alterations support structural cardiac impairment.…”

Section: Discussionmentioning

confidence: 99%

Effects of Simvastatin on Fetal Cardiac Impairment in the Diaphragmatic Experimental Hernia Model

Pelizzo¹,

Bussani

Mazzon

et al. 2018

Fetal Diagn Ther

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Background: Statins and sildenafil have been shown to exert beneficial effects in cardiac injury. We hypothesized that antenatal maternal administration of simvastatin and/or sildenafil might also promote benefits in cardiac remodeling of congenital diaphragmatic hernia (CDH). Therefore, we performed micro-CT image analysis and histology of the heart after antennal treatment in experimental nitrofen-induced CDH. Methods: At 9.5 days post conception (dpc), pregnant rats were exposed to nitrofen. At 16 and 20 dpc fetuses were treated with simvastatin and/or sildenafil. At 21 dpc postmortem micro-CT and autopsy were performed. Results: All nitrofen-treated fetuses had a lower birth weight compared to controls; in the simvastatin-treated group, a significant improvement in CDH was noted. Impairment of the lung and liver was also noted in CDH. Compared to controls, CDH rats showed lower ventricular mass, with greater left ventricular thickness; simvastatin decreased the ventricular mass and improved wall thickness. CDH rats exhibited myocardial hypotrophy, severe vascular depression in the left ventricle, and intense interstitial edema compared to controls and nitrofen-exposed animals without CDH. In CDH, the cardiac morphology appeared deformed with left ventricular wall verticalization. Simvastatin improved cardiac myocyte appearance and heart morphology. Conclusion: The potential to treat CDH with antenatal simvastatin may improve the management of this malformation.

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Cardiac malposition, redistribution of fetal cardiac output, and left heart hypoplasia reduce survival in neonates with congenital diaphragmatic hernia requiring extracorporeal membrane oxygenation

Cited by 77 publications

References 26 publications

Acute Cardiovascular Effects of Fetal Surgery in the Human

Acute Cardiovascular Effects of Fetal Surgery in the Human

Heart hypoplasia in an animal model of congenital diaphragmatic hernia

Effects of Simvastatin on Fetal Cardiac Impairment in the Diaphragmatic Experimental Hernia Model

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