Developmental biology of the vertebrate heart

Icardo, José M.

doi:10.1002/(sici)1097-010x(19960601/15)275:2/3<144::aid-jez7>3.0.co;2-d

Cited by 60 publications

(33 citation statements)

References 133 publications

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“…Most of the heart morphogenesis processes occur under blood flow conditions, implying an intrinsic interaction between cardiac development and hemodynamics (Oppenheimer-Dekker et al, 1981; Icardo, 1996; Manner, 2000; Hove et al, 2003; Martinsen, 2005). In this review, we describe the initial heart tube morphogenesis into the four-chambered mature heart focusing on the developmental processes that are influenced by hemodynamics.…”

Section: Normal Heart Formationmentioning

confidence: 99%

“…The early heart tube is composed of three tissue layers: the outer myocardium layer, the inner monolayer of endocardium, and a thick middle layer of largely extracellular matrix, also known as the cardiac jelly. Looping begins at HH9-10, where the initially straight cardiac tube bulges, rotates to the right, and wrap into a loop (De La Cruz et al, 1989; Icardo, 1996; Manner, 2000). After the primitive ventricular region forms a bend in the c-shaped loop at HH11–12, three morphologically distinct cardiac regions emerge: the primitive atrium, the primitive ventricle, and the primitive outflow tract (Manner, 2000).…”

Section: Normal Heart Formationmentioning

confidence: 99%

“…Correct looping is essential for normal cardiac septation. Septation occurs via combinations of merging and fusion of endocardial cushions, compaction of trabeculae, and ballooning of the ventricles (Icardo, 1996; Lamers and Moorman, 2002; Gittenberger-De Groot et al, 2005; Van Den Berg and Moorman, 2009). …”

Section: Normal Heart Formationmentioning

confidence: 99%

“…Numerous studies have shown that surgically altered blood flow conditions in embryos result in a spectrum of cardiac defects that resemble those found in human babies with congenital heart disease (Rychter, 1962; Oscar, 1965; Harh et al, 1973; Clark and Rosenquist, 1978; Clark et al, 1984; Icardo, 1996; Hogers et al, 1997, 1999; Broekhuizen et al, 1999; Sedmera et al, 1999, 2002; Tobita and Keller, 2000; Tobita et al, 2005; Dealmeida et al, 2007; Hu et al, 2009). During normal development, cardiac performance progressively improves to meet the rising metabolic demands of the growing embryo under increased hemodynamic loading conditions (Hu and Clark, 1989).…”

Section: Introductionmentioning

confidence: 99%

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Congenital heart malformations induced by hemodynamic altering surgical interventions

Midgett

Rugonyi

2014

Front. Physiol.

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Embryonic heart formation results from a dynamic interplay between genetic and environmental factors. Blood flow during early embryonic stages plays a critical role in heart development, as interactions between flow and cardiac tissues generate biomechanical forces that modulate cardiac growth and remodeling. Normal hemodynamic conditions are essential for proper cardiac development, while altered blood flow induced by surgical manipulations in animal models result in heart defects similar to those seen in humans with congenital heart disease. This review compares the altered hemodynamics, changes in tissue properties, and cardiac defects reported after common surgical interventions that alter hemodynamics in the early chick embryo, and shows that interventions produce a wide spectrum of cardiac defects. Vitelline vein ligation and left atrial ligation decrease blood pressure and flow; and outflow tract banding increases blood pressure and flow velocities. These three surgical interventions result in many of the same cardiac defects, which indicate that the altered hemodynamics interfere with common looping, septation and valve formation processes that occur after intervention and that shape the four-chambered heart. While many similar defects develop after the interventions, the varying degrees of hemodynamic load alteration among the three interventions also result in varying incidence and severity of cardiac defects, indicating that the hemodynamic modulation of cardiac developmental processes is strongly dependent on hemodynamic load.

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Section: Normal Heart Formationmentioning

confidence: 99%

Section: Normal Heart Formationmentioning

confidence: 99%

Section: Normal Heart Formationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Congenital heart malformations induced by hemodynamic altering surgical interventions

Midgett

Rugonyi

2014

Front. Physiol.

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“…The heart consists of a primitive atrium and primitive ventricle, and the heart outflow tract (OFT) connects the ventricle to the arterial system. We further focused on the OFT portion of the embryonic heart as major congenital heart defects are known to develop from this region (Bartelings and Gittenberger-de Groot 1991; Icardo 1996; van den Hoff et al 1999; Hove et al 2003; Gittenberger-de Groot et al 2005). …”

Section: Introductionmentioning

confidence: 99%

4D subject-specific inverse modeling of the chick embryonic heart outflow tract hemodynamics

Goenezen

Chivukula

Midgett

et al. 2015

Biomech Model Mechanobiol

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Blood flow plays a critical role in regulating embryonic cardiac growth and development, with altered flow leading to congenital heart disease. Progress in the field, however, is hindered by a lack of quantification of hemodynamic conditions in the developing heart. In this study, we present a methodology to quantify blood flow dynamics in the embryonic heart using subject-specific computational fluid dynamics (CFD) models. While the methodology is general, we focused on a model of the chick embryonic heart outflow tract (OFT), which distally connects the heart to the arterial system, and is the region of origin of many congenital cardiac defects. Using structural and Doppler velocity data collected from optical coherence tomography (OCT), we generated 4D (3D + time) embryo-specific CFD models of the heart OFT. To replicate the blood flow dynamics over time during the cardiac cycle, we developed an iterative inverse-method optimization algorithm, which determines the CFD model boundary conditions such that differences between computed velocities and measured velocities at one point within the OFT lumen are minimized. Results from our developed CFD model agree with previously measured hemodynamics in the OFT. Further, computed velocities and measured velocities differ by less than 15% at locations that were not used in the optimization, validating the model. The presented methodology can be used in quantifications of embryonic cardiac hemodynamics under normal and altered blood flow conditions, enabling an in depth quantitative study of how blood flow influences cardiac development.

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Role of vitamin A in the formation of congenital heart defects

Sinning

1998

Anat. Rec.

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Retinoic acid, the biologically active form of vitamin A, is a critical player in normal development. The concentration of retinoic acid is highly regulated by the embryo to prevent either a deficit or an excess of this molecule, conditions that have been shown to produce cardiac defects that vary depending on the severity and the timing of the insult. The vast majority of these defects are associated with the valves or the membranous septa of the heart, suggesting a problem with the formation of the cardiac mesenchyme from both within and outside the heart. While the exact role of retinoic acid in cardiac development is not known, it is believed that retinoic acid influences development by up-or down-regulating cardiac specific genes. This review briefly discusses the role of cardiac mesenchyme and cardiac neural crest in septation of the heart. This is followed by a discussion of vitamin A metabolism and the cardiac defects associated with abnormal levels of retinoic acid. Finally, a mechanism is proposed concerning the ways abnormal levels of retinoic acid lead to similar cardiac defects by disrupting the production of the extracellular matrix. Anat. Rec.(New Anat.) 253:147-153, 1998.

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Developmental biology of the vertebrate heart

Cited by 60 publications

References 133 publications

Congenital heart malformations induced by hemodynamic altering surgical interventions

Congenital heart malformations induced by hemodynamic altering surgical interventions

4D subject-specific inverse modeling of the chick embryonic heart outflow tract hemodynamics

Role of vitamin A in the formation of congenital heart defects

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