Premium
Coronary Anomalies in Mice With Congenital Heart Defects
Author(s) -
Tomanek Robert J.,
Yu Qing,
Lo Cecilia W.
Publication year - 2015
Publication title -
the anatomical record
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.23056
Subject(s) - coronary arteries , great arteries , tunica media , left coronary artery , medicine , ventricle , cardiology , double outlet right ventricle , anatomy , artery , cardiac muscle , pulmonary artery , transposition of the great vessels , truncus arteriosus , smooth muscle , heart disease , tetralogy of fallot
Background: Coronary anomalies are frequently associated with congenital cardiac defects. Accordingly, we tested the hypothesis that the development of the tunica media of coronary arteries/arterioles is compromised in mice with cardiac defects of the outflow tract (persistent truncus arteriosus, double outlet right ventricle and transposition of the great arteries) by studying hearts of G7‐9 generation mice bred from mutagenized mice caused by N‐ethyl‐N‐nitrosourea. Mice were studied at embryonic days E16.5, E17.5, and postnatal days 1 and 11. Data were based on immunohistochemistry of serial sections. Results: In 21 of 24 mice with outflow tract defects, the development of smooth muscle in arteries and arterioles was retarded; most commonly arterioles had an incomplete layer of smooth muscle or in a few instances, lacked a tunica media. In this model, an absence of a coronary ostium occurred in only 2 mice, indicating that the mechanisms underlying the formation of coronary ostia and the recruitment and differentiation of vascular smooth muscle differ. Coronary fistulas were present in 20% and dilated vessels in 30% of the hearts with cardiac defects. Conclusions: The data suggest that vascular smooth muscle recruitment and differentiation are not necessarily linked to other coronary anomalies, such as absence of a main coronary artery or branching patterns. Anat Rec, 298:408–417, 2015. © 2014 Wiley Periodicals, Inc.