Resolving the natural myocardial remodelling brought upon by cardiac contraction; a porcine ex-vivo cardiovascular magnetic resonance study of the left and right ventricle.


Journal

Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance
ISSN: 1532-429X
Titre abrégé: J Cardiovasc Magn Reson
Pays: England
ID NLM: 9815616

Informations de publication

Date de publication:
01 07 2019
Historique:
received: 14 01 2019
accepted: 29 05 2019
entrez: 2 7 2019
pubmed: 2 7 2019
medline: 29 1 2020
Statut: epublish

Résumé

The three-dimensional rearrangement of the right ventricular (RV) myocardium during cardiac deformation is unknown. Previous in-vivo studies have shown that myocardial left ventricular (LV) deformation is driven by rearrangement of aggregations of cardiomyocytes that can be characterised by changes in the so-called E3-angle. Ex-vivo imaging offers superior spatial resolution compared with in-vivo measurements, and can thus provide novel insight into the deformation of the myocardial microstructure in both ventricles. This study sought to describe the dynamic changes of the orientations of the cardiomyocytes in both ventricles brought upon by cardiac contraction, with particular interest in the thin-walled RV, which has not previously been described in terms of its micro-architecture. The hearts of 14 healthy 20 kg swine were excised and preserved in either a relaxed state or a contracted state. Myocardial architecture was assessed and compared between the two contractional states by quantification of the helical, transmural and E3-angles of the cardiomyocytes using high-resolution diffusion tensor imaging. The differences between the two states of contraction were most pronounced in the endocardium where the E3-angle decreased from 78.6° to 24.8° in the LV and from 82.6° to 68.6° in the RV. No significant change in neither the helical nor the transmural angle was found in the cardiomyocytes of the RV. In the endocardium of the LV, however, the helical angle increased from 35.4° to 47.8° and the transmural angle increased from 3.1° to 10.4°. The entire myocardium rearranges through the cardiac cycle with the change in the orientation of the aggregations of cardiomyocytes being the predominant mediator of myocardial wall thickening. Interestingly, differences also exist between the RV and LV, which helps in the explanation of the different physiological capabilities of the ventricles.

Sections du résumé

BACKGROUND
The three-dimensional rearrangement of the right ventricular (RV) myocardium during cardiac deformation is unknown. Previous in-vivo studies have shown that myocardial left ventricular (LV) deformation is driven by rearrangement of aggregations of cardiomyocytes that can be characterised by changes in the so-called E3-angle. Ex-vivo imaging offers superior spatial resolution compared with in-vivo measurements, and can thus provide novel insight into the deformation of the myocardial microstructure in both ventricles. This study sought to describe the dynamic changes of the orientations of the cardiomyocytes in both ventricles brought upon by cardiac contraction, with particular interest in the thin-walled RV, which has not previously been described in terms of its micro-architecture.
METHODS
The hearts of 14 healthy 20 kg swine were excised and preserved in either a relaxed state or a contracted state. Myocardial architecture was assessed and compared between the two contractional states by quantification of the helical, transmural and E3-angles of the cardiomyocytes using high-resolution diffusion tensor imaging.
RESULTS
The differences between the two states of contraction were most pronounced in the endocardium where the E3-angle decreased from 78.6° to 24.8° in the LV and from 82.6° to 68.6° in the RV. No significant change in neither the helical nor the transmural angle was found in the cardiomyocytes of the RV. In the endocardium of the LV, however, the helical angle increased from 35.4° to 47.8° and the transmural angle increased from 3.1° to 10.4°.
CONCLUSION
The entire myocardium rearranges through the cardiac cycle with the change in the orientation of the aggregations of cardiomyocytes being the predominant mediator of myocardial wall thickening. Interestingly, differences also exist between the RV and LV, which helps in the explanation of the different physiological capabilities of the ventricles.

Identifiants

pubmed: 31256759
doi: 10.1186/s12968-019-0547-2
pii: 10.1186/s12968-019-0547-2
pmc: PMC6600899
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

35

Références

Chest. 2009 Mar;135(3):794-804
pubmed: 19265089
J Cardiovasc Magn Reson. 2017 Nov 27;19(1):93
pubmed: 29178894
Technol Health Care. 2013;21(1):63-79
pubmed: 23358060
Circ Res. 1969 Mar;24(3):339-47
pubmed: 5766515
J Am Coll Cardiol. 2017 Feb 14;69(6):661-676
pubmed: 28183509
Am J Cardiol. 2000 Aug 1;86(3):319-23
pubmed: 10922441
Anat Rec (Hoboken). 2009 Jan;292(1):1-11
pubmed: 19051244
Clin Anat. 2016 Apr;29(3):316-32
pubmed: 26478993
Am J Physiol. 1998 Dec;275(6):H2308-18
pubmed: 9843833
Am J Physiol Heart Circ Physiol. 2009 Feb;296(2):H413-20
pubmed: 19098113
Am J Physiol. 1995 Aug;269(2 Pt 2):H571-82
pubmed: 7653621
Magn Reson Med. 2000 Jul;44(1):157-61
pubmed: 10893534
Pediatr Res. 2016 Apr;79(4):565-74
pubmed: 26679151
Am J Physiol Heart Circ Physiol. 2005 Nov;289(5):H1898-907
pubmed: 16219812
J Cardiovasc Magn Reson. 2017 Mar 10;19(1):31
pubmed: 28279178
Int J Cardiol. 2012 Jan 26;154(2):102-10
pubmed: 21696836
Am J Physiol Heart Circ Physiol. 2002 Jul;283(1):H139-45
pubmed: 12063284
Circulation. 2014 Mar 4;129(9):1033-44
pubmed: 24589696
Anat Rec (Hoboken). 2013 Nov;296(11):1724-34
pubmed: 24591128
Circ Res. 1995 Jul;77(1):182-93
pubmed: 7788876
Eur J Cardiothorac Surg. 2005 Oct;28(4):517-25
pubmed: 16179192
Circ Res. 1975 Sep;37(3):299-308
pubmed: 1157219
Clin Anat. 2009 Jan;22(1):64-76
pubmed: 18567009
J Cardiovasc Magn Reson. 2014 Nov 12;16:87
pubmed: 25388867
J Am Coll Cardiol. 2017 Feb 14;69(6):677-678
pubmed: 28183510
Anat Rec A Discov Mol Cell Evol Biol. 2006 Jun;288(6):565-78
pubmed: 16705738
Circulation. 2008 Apr 1;117(13):1717-31
pubmed: 18378625
Heart. 2014 Aug;100(16):1289-98
pubmed: 24310520
Circ Res. 2004 Aug 6;95(3):261-8
pubmed: 15217909
Prog Biophys Mol Biol. 2012 Oct-Nov;110(2-3):319-30
pubmed: 23043978
Eur J Cardiothorac Surg. 2018 Apr 1;53(4):714-723
pubmed: 29136124
Curr Opin Pediatr. 2015 Oct;27(5):563-8
pubmed: 26262580
Heart. 2006 Apr;92 Suppl 1:i27-38
pubmed: 16543599
Heart. 2008 Nov;94(11):1510-5
pubmed: 18931164
Br Heart J. 1981 Mar;45(3):248-63
pubmed: 7008815

Auteurs

Camilla Omann (C)

Department of Cardiothoracic & Vascular Surgery, Aarhus University Hospital, Skejby, Denmark. camillaomann@clin.au.dk.
Department of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark. camillaomann@clin.au.dk.

Peter Agger (P)

Department of Cardiothoracic & Vascular Surgery, Aarhus University Hospital, Skejby, Denmark.
Department of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark.
Comparative Medicine Lab, Aarhus University Hospital, Skejby, Denmark.

Nikolaj Bøgh (N)

Department of Cardiothoracic & Vascular Surgery, Aarhus University Hospital, Skejby, Denmark.
Department of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark.

Christoffer Laustsen (C)

Department of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark.
MR Research Centre, Aarhus University, Aarhus, Denmark.

Steffen Ringgaard (S)

MR Research Centre, Aarhus University, Aarhus, Denmark.

Robert S Stephenson (RS)

Department of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark.
Comparative Medicine Lab, Aarhus University Hospital, Skejby, Denmark.
Institute of Clinical Sciences, College of Medical and Dental Sciences, The University of Birmingham, Birmingham, UK.

Robert H Anderson (RH)

Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, UK.

Vibeke E Hjortdal (VE)

Department of Cardiothoracic & Vascular Surgery, Aarhus University Hospital, Skejby, Denmark.
Department of Clinical Medicine, Aarhus University, Palle Juul-Jensens Boulevard 99, 8200, Aarhus N, Denmark.

Morten Smerup (M)

Department of Cardiothoracic & Vascular Surgery, Aarhus University Hospital, Skejby, Denmark.

Articles similaires

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male
Humans Meals Time Factors Female Adult

Classifications MeSH