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Review
. 2024 Mar 31;13(4):234.
doi: 10.3390/biology13040234.

Hemodynamic Melody of Postnatal Cardiac and Pulmonary Development in Children with Congenital Heart Diseases

Sixie Zheng  1   2 , Lincai Ye  1   2
Affiliations
Review

Hemodynamic Melody of Postnatal Cardiac and Pulmonary Development in Children with Congenital Heart Diseases

Sixie Zheng et al. Biology (Basel). .

Abstract

Hemodynamics is the eternal theme of the circulatory system. Abnormal hemodynamics and cardiac and pulmonary development intertwine to form the most important features of children with congenital heart diseases (CHDs), thus determining these children's long-term quality of life. Here, we review the varieties of hemodynamic abnormalities that exist in children with CHDs, the recently developed neonatal rodent models of CHDs, and the inspirations these models have brought us in the areas of cardiomyocyte proliferation and maturation, as well as in alveolar development. Furthermore, current limitations, future directions, and clinical decision making based on these inspirations are highlighted. Understanding how CHD-associated hemodynamic scenarios shape postnatal heart and lung development may provide a novel path to improving the long-term quality of life of children with CHDs, transplantation of stem cell-derived cardiomyocytes, and cardiac regeneration.

Keywords: cardiomyocyte; maturation; pressure overload; proliferation; pulmonary alveolar dysplasia; pulmonary blood flow; volume overload.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Illustration of the three main characteristics that immature CMs require for development. (A) Neonatal and adult CMs have differences in sarcomere, metabolism, and electrophysiological functions. (B) Three main characteristics that immature CMs must develop, and the presumed key time points of these maturation events in rodents. Redrawn from [12]. (C) Summary of cardiomyocyte maturation factors that have been reported and those that remain unknown [67,68,69,70,71,72,73,74,75,76,77,78,81,82,83,84,85,86,87,88,89,90,91,92].
Figure 2
Figure 2
Differences between immature and mature lungs. (A) Five developmental stages of human lungs. Note that 90% of alveoli are formed at ages 0–7 years. (B) Different capillary network between immature and mature lungs. Redrawn from [101]. (C) Several pathways involved in lung maturation [99,100,101,102,103,104,105,106,107,108,109,110,111].
Figure 3
Figure 3
Neonatal surgical rodent models of CHDs. (A) nACF produces RA VO, RV VO, LA VO, LV VO, and IPF. (B) Surgical diagram of nACF. (C) nPAB produces RV PO and RPF, yellow arrow indicates the banding region. (D) Surgical diagram of nPAB. (E) nTAC produces LVPO. (F) Surgical diagram of nTAC. (G) nPVB produces PVS and IPF. (H) Surgical diagram of nPVB, red arrow indicates the banding region. IVC: inferior vena cava; PA: pulmonary artery; DA: ductus arteriosus; Ao: aorta; RPA: right pulmonary artery; PV: pulmonary vein; SVC: superior vena cava; RA: right atrium; MPA: main pulmonary artery. (A) was adopted ref. [23] under a Creative Commons Attribution-NonCommercial-NoDerivs License; (B) was adopted from ref. [115] under a Creative Commons Attribution-NonCommercial-NoDerivs License; (C) was adopted from ref. [30] with the permission of the publisher; (D) was adopted from ref. [116] with the permission of the publisher; (H) was adopted from ref. [28] under a Creative Commons Attribution-NonCommercial-NoDerivs License).
Figure 4
Figure 4
An alternative possibility for the increased percentage of polyploid cardiomyocytes in TOF children. (A) The four clinical features of TOF are RVOT obstruction, ventricular septal defect, thickened RV, and aortic riding, the most important of which is RVOT obstruction, which leads to RV PO and RV failure. (B) Illustration of the increased binuclear cardiomyocytes generated in TOF patients. Greater numbers of binuclear cardiomyocytes do not indicate a failure of cytokinesis. For example, in the beginning of a study, if both the control group and TOF group had 80 mononucleated and 20 binucleated cardiomyocytes (CMs), the proportion of binucleated CMs was 20%. Under PO conditions, both mononucleated and binucleated CMs in the TOF group increased by 10, and the proportion of binucleated CMs was 25%. Therefore, an increase in the proportion of binucleated CMs does not necessarily mean impaired cytokinesis and proliferation.
Figure 5
Figure 5
Omics information on postnatal cardiac development under of VO or PO.
See this image and copyright information in PMC

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