Volume 100, Issue 16
Linking left ventricular function and mural architecture: what does the clinician need to know?
John B Partridge1,
Morten H Smerup2,
Steffen E Petersen3,
Peter F Niederer4,
Robert H Anderson5
1Eurobodalla Unit, Rural Clinical School of the ANU College of Medicine, Biology & Environment, Batemans Bay, New South Wales, Australia
2Department of Cardiothoracic Surgery T, Aarhus University Hospital, Skejby, Denmark
3Cardiovascular Biomedical Research Unit at Barts, Centre for Advanced Cardiovascular Imaging, William Harvey Research Institute, National Institute for Health Research, The London Chest Hospital, London, UK
4Biomedical Engineering, Swiss Federal Institute of Technology, Zurich, Switzerland
5Institute for Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, UK
Correspondence to Dr John B Partridge, Eurobodalla Unit, Rural Clinical School of the ANU College of Medicine, Biology & Environment, PO Box 1221, Batemans Bay, NSW 2536, Australia; 101jbp{at}southernphone.com.au
http://dx.doi.org/10.1136/heartjnl-2013-304571
Cardiac Function
The myocardium has a unique architecture, which converts the linear pull of a striated but involuntary muscle into a constrictive action. The left ventricle has also to balance the need to restrict the diameter of its chamber, thereby minimising mural tension, while providing at the same time a wall thick enough to achieve systemic pressure within the cavity. The precise architectural arrangement of the cardiomyocytes that fulfils these requirements is currently a topic of considerable debate. There is a divide between proponents of a counter-wound, single myocardial band,1 and those who describe an arrangement of clefts around thinner lamellar units.2 ,3 In seeking to contribute to this debate, we present here a description of the changes that occur in surface geometry of the ventricle. We will show how the strain indexes of the wall, including mural thickening, are mathematically bound together by this geometry, irrespective of the internal architecture of the wall. We will then relate these indexes to demonstrable features of cardiomyocytic orientation and function.4 In so doing, we provide a relatively simple explanation for left ventricular (LV) twist that does not rely on the presence of a unique myocardial band. We will also reinforce the observation of MacIver and Townsend that hypertrophy of the left ventricle can falsely normalise its ejection fraction (EF) despite falling contractility.5 We conclude by addressing other significant aspects of mural architecture.
The volumes of the wall of the left ventricle and its cavity
Initially, we will regard the LV myocardium as a structure of fixed mass and so, at physiological pressures, of fixed volume. It envelops the cavity, and its surfaces are illustrated in figure 1. The magnitudes of changes in the inner and outer dimension of the wall, and of the distance between them, which is the mural thickness, are linked mathematically by the geometry of this very …
Contributors We can attest that all the authors of this paper have each contributed in these three areas: (1) making substantial contributions to conception and design, acquisition of data, or analysis and interpretation of data; (2) drafting the article or revising it critically for important intellectual content; and (3) giving final approval of the version to be published.
Funding This work forms part of the research areas contributing to the translational research portfolio of the Cardiovascular Biomedical Research Unit at Barts which is supported and funded by the National Institute for Health Research.
Competing interests In compliance with EBAC/EACCME guidelines, all authors participating in Education in Heart have disclosed potential conflicts of interest that might cause a bias in the article. SEP has undertaken consulting work for Circle Cardiovascular Imaging Inc. All other authors have no competing interests.
Provenance and peer review Commissioned; internally peer reviewed.
Heartbeat: Highlights from this issue
Catherine M Otto
Heart 2014; 100 1219-1220 Published Online First: 21 Jul 2014. doi: 10.1136/heartjnl-2014-306404