Early cardiac remodeling in aortic coarctation: insights from fetal and neonatal functional and structural assessment

Q: What are the key findings of this study?

Fetuses with aortic coarctation had an elongated left ventricle (median sphericity index 2.4 vs 1.8, P<0.001) that remodeled to become more globular postnatally (mean 1.5 vs 1.8, P<0.001).

Q: What is the clinical evidence from this study?

Study design: Case-Control. Population: Coarctation of the aorta (CoA) (n=90). Intervention: Coarctation of the aorta (CoA) vs. Gestational age-matched normal controls. Primary outcome: Fetal left ventricular midventricular sphericity index (p=<0.001).

Q: What does this research mean for the field?

Fetuses with aortic coarctation present with an abnormally elongated left ventricle that undergoes prompt postnatal remodeling into a more globular geometry following acute volume loading, with preserved systolic function. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

To investigate cardiovascular structural remodeling and dysfunction in fetuses with coarctation of the aorta and to evaluate their cardiac adaptation in early neonatal life.

I. Soveral; F. Crispi; Carin Walter; L. Guirado; Patricia García‐Canadilla; Andrew C. Cook; Anne Bonnin; Hector Dejea; C. Rovira‐Zurriaga; E. Gratacós; J. Martı́nez; Bart Bijnens; O. Gómez

doi:10.1002/uog.21970

January 7, 2020Ultrasound in Obstetrics and GynecologyOpen Access

Early cardiac remodeling in aortic coarctation: insights from fetal and neonatal functional and structural assessment

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Key result

Aortic coarctation links to elongated fetal left ventricles that remodel into more globular shapes postnatally.

P<0.001
n=90

Why the study?

Cardiac structure and function in fetal coarctation of the aorta (CoA) and cardiac adaptation to early neonatal life had not been described.

Does coarctation of the aorta cause fetal cardiovascular structural remodeling and dysfunction, and how does the heart adapt during the transition to early neonatal life?

Key Points

To investigate cardiovascular structural remodeling and dysfunction in fetuses with coarctation of the aorta and to evaluate their cardiac adaptation in early neonatal life.
Conducted a prospective observational case-control study between 2011 and 2018 at a single tertiary referral center, examining 30 fetuses with coarctation of the aorta (CoA) and 60 gestational age-matched controls using third-trimester echocardiography (32–36 weeks' gestation).
Evaluated 20 CoA neonates receiving PGE1 treatment and 44 controls postnatally between 48–96 hours after birth prior to coarctation surgery.
Assessed myocardial microstructure in one fetal CoA specimen (19 weeks) using synchrotron radiation-based X-ray phase-contrast microcomputed tomography and one neonatal CoA specimen (32 + 4 weeks) via histology.
Fetuses with CoA demonstrated left-to-right volume redistribution, right ventricular dominance, and an elongated left ventricle (LV midventricular sphericity index median [IQR], 2.4 [2.0–2.7] vs 1.8 [1.7–2.0]; P < 0.001) without hypertrophy, while maintaining preserved biventricular function and normal myocyte organization.
Postnatally, the LV remodeled rapidly to a more globular shape (sphericity index mean ± SD, 1.5 ± 0.3 vs 1.8 ± 0.2; P < 0.001) with preserved systolic output and increased right ventricular longitudinal function in the presence of a patent arterial duct.
Neonatal LV diastolic parameters were altered in CoA compared with controls (inflow peak velocity in early diastole, 97.8 ± 14.5 vs 56.5 ± 12.9 cm/s; inflow peak velocity in atrial contraction median [IQR], 70.5 [60.1–84.9] vs 47.0 [43.0–55.0] cm/s; peak myocardial velocity in atrial contraction, 5.1 ± 2.6 vs 6.3 ± 2.2 cm/s; P < 0.05).

Study Design

Type

Case-Control (n=90)

Multicenter

No

Structured PICO

Does coarctation of the aorta cause fetal cardiovascular structural remodeling and dysfunction, and how does the heart adapt during the transition to early neonatal life?

P

Population

90 fetuses (30 with postnatally confirmed aortic coarctation and 60 gestational age-matched controls) evaluated in the third trimester (32-36 weeks' gestation), with 64 neonates (20 CoA cases on prostaglandin-E1 and 44 controls) reassessed at 48-96 hours after birth.

E

Exposure

Coarctation of the aorta (CoA) evaluated via comprehensive third-trimester fetal and early postnatal (48-96 h) echocardiography, plus ex-vivo myocardial microstructural assessment (synchrotron X-ray phase-contrast microcomputed tomography in one 19-week fetal heart and histopathology in one preterm neonatal heart).

C

Comparator

Gestational age-matched healthy singleton controls from uncomplicated spontaneously conceived pregnancies without maternal or gestational conditions affecting cardiovascular remodeling (n=60 fetal, n=44 neonatal; plus one 19-week normal fetal heart specimen).

O

Outcome

Fetal and early neonatal biventricular cardiac morphometry and function, specifically left ventricular (LV) midventricular sphericity index, ventricular dimensions, stroke volume, cardiac output, and systolic/diastolic functional parameters.surrogate

Main Result

Absolute Event Rate: 2.4% vs 1.8%

p-value: p=<0.001

This study demonstrates that fetuses with aortic coarctation have an underfilled, elongated left ventricle with normal intrinsic myocardial organization and function that undergoes acute volume loading, globular remodeling, and diastolic alteration immediately after birth.

Limitations

Single tertiary referral center study
Small sample size (30 CoA cases prenatally and 20 postnatally)
Microstructural and histological assessment limited to only one fetal and one neonatal CoA specimen
Single-center study
Relatively small sample size (30 fetal CoA cases, 20 neonatal CoA cases)
Postnatal attrition (10 CoA cases and 16 controls excluded from postnatal analysis due to prematurity, no PGE1, or incomplete/out-of-window scans)
Microstructural and histological analysis limited to a single fetal and a single neonatal CoA specimen

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Implication

Anticipate acute postnatal LV remodeling in aortic coarctation; extends fetal adaptation data but leaves open prognostic value.

Abstract

OBJECTIVES: Coarctation of the aorta (CoA) is associated with left ventricular (LV) dysfunction in neonates and adults. Cardiac structure and function in fetal CoA and cardiac adaptation to early neonatal life have not been described. We aimed to investigate the presence of cardiovascular structural remodeling and dysfunction in fetuses with CoA and their early postnatal cardiac adaptation. METHODS: This was a prospective observational case-control study, conducted between 2011 and 2018 in a single tertiary referral center, of fetuses with CoA and gestational age-matched normal controls. All fetuses/neonates underwent comprehensive echocardiographic evaluation in the third trimester of pregnancy and after birth. Additionally, myocardial microstructure was assessed in one fetal and one neonatal CoA-affected heart specimen, using synchrotron radiation-based X-ray phase-contrast microcomputed tomography and histology, respectively. RESULTS: We included 30 fetuses with CoA and 60 gestational age-matched controls. Of these, 20 CoA neonates and 44 controls were also evaluated postnatally. Fetuses with CoA showed significant left-to-right volume redistribution, with right ventricular (RV) size and output dominance and significant geometry alterations with an abnormally elongated LV, compared with controls (LV midventricular sphericity index (median (interquartile range; IQR), 2.4 (2.0-2.7) vs 1.8 (1.7-2.0); P < 0.001). Biventricular function was preserved and no ventricular hypertrophy was observed. Synchrotron tomography and histological assessment revealed normal myocyte organization in the fetal and neonatal specimens, respectively. Postnatally, the LV in CoA cases showed prompt remodeling, becoming more globular (LV midventricular sphericity index (mean ± SD), 1.5 ± 0.3 in CoA vs 1.8 ± 0.2 in controls; P < 0.001) with preserved systolic and normalized output, but altered diastolic, parameters compared with controls (LV inflow peak velocity in early diastole (mean ± SD), 97.8 ± 14.5 vs 56.5 ± 12.9 cm/s; LV inflow peak velocity in atrial contraction (median (IQR), 70.5 (60.1-84.9) vs 47.0 (43.0-55.0) cm/s; LV peak myocardial velocity in atrial contraction (mean ± SD), 5.1 ± 2.6 vs 6.3 ± 2.2 cm/s; P < 0.05). The neonatal RV showed increased longitudinal function in the presence of a patent arterial duct. CONCLUSIONS: Our results suggest unique fetal cardiac remodeling in CoA, in which the LV stays smaller from the decreased growth stimulus of reduced volume load. Postnatally, the LV is acutely volume-loaded, resulting in an overall geometry change with higher filling velocities and preserved systolic function. These findings improve our understanding of the evolution of CoA from fetal to neonatal life.

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Cite This Study

Soveral et al. (2020) conducted a case-control in Coarctation of the aorta (CoA) (n=90). Coarctation of the aorta (CoA) vs. Gestational age-matched normal controls was evaluated on Fetal left ventricular midventricular sphericity index (p=<0.001). Fetuses with aortic coarctation had an elongated left ventricle (median sphericity index 2.4 vs 1.8, P<0.001) that remodeled to become more globular postnatally (mean 1.5 vs 1.8, P<0.001).

synapsesocial.com/papers/6a81d38c28bb6950eb610493 https://doi.org/10.1002/uog.21970

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Early cardiac remodeling in aortic coarctation: insights from fetal and neonatal functional and structural assessment

Key Points

Study Design

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Early cardiac remodeling in aortic coarctation: insights from fetal and neonatal functional and structural assessment

Key Points

Study Design

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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