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Interrogating congenital heart defects with noninvasive fetal echocardiography in a mouse forward genetic screen

  • Xiaoqin Liu
    ,
  • Richard Francis
    ,
  • Andrew J. Kim
    ,
  • Ricardo Ramirez
    ,
  • Guozhen Chen
    ,
  • Ramiah Subramanian
*Corresponding author for this work
  • University of Pittsburgh
    ,
  • ,
  • Jackson Laboratory
    ,
  • Children's National Medical Center
Scholary Output:
Contribution to journal
Article
Peer-review

Open access

Abstract

Background-Congenital heart disease (CHD) has a multifactorial pathogenesis, but a genetic contribution is indicated by heritability studies. To investigate the spectrum of CHD with a genetic pathogenesis, we conducted a forward genetic screen in inbred mice using fetal echocardiography to recover mutants with CHD. Mice are ideally suited for these studies given that they have the same four-chamber cardiac anatomy that is the substrate for CHD. Methods and Results-Ethylnitrosourea mutagenized mice were ultrasound-interrogated by fetal echocardiography using a clinical ultrasound system, and fetuses suspected to have cardiac abnormalities were further interrogated with an ultrahigh- frequency ultrasound biomicroscopy. Scanning of 46 270 fetuses revealed 1722 with cardiac anomalies, with 27.9% dying prenatally. Most of the structural heart defects can be diagnosed using ultrasound biomicroscopy but not with the clinical ultrasound system. Confirmation with analysis by necropsy and histopathology showed excellent diagnostic capability of ultrasound biomicroscopy for most CHDs. Ventricular septal defect was the most common CHD observed, whereas outflow tract and atrioventricular septal defects were the most prevalent complex CHD. Cardiac/visceral organ situs defects were observed at surprisingly high incidence. The rarest CHD found was hypoplastic left heart syndrome, a phenotype never seen in mice previously. Conclusions-We developed a high-throughput, 2-tier ultrasound phenotyping strategy for efficient recovery of even rare CHD phenotypes, including the first mouse models of hypoplastic left heart syndrome. Our findings support a genetic pathogenesis for a wide spectrum of CHDs and suggest that the disruption of left-right patterning may play an important role in CHD.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 31-42 (12 pages)

Journal (Volume, Issue Number)

Circulation: Cardiovascular Imaging (Volume 7, Issue 1)

Publication milestones

  • Published - 01/2014

Publication status

Published - 01/2014

ISSN

1941-9651

Publication IDs

  • Scopus: 84897019940
  • PubMed: 24319090

Publication metrics

Metrics

Scopus
citations
Fractional count
1
Fractional count
0.06
Fractional count
15
Fractional count
0.94
Fractional count
1
Fractional count
1
SciVal
FWCI
2.03
SciVal
Author count
16
SciVal
citations
25
SciVal
Paper percentile
85

PlumX, opens in new tab

Captures
42
Citation count
43

Funding Details

FunderFunding number
NHLBI
U01HL098180