Korean J Radiol. 2016 Jan-Feb;17(1):171-172. English.
Published online Jan 06, 2016.
Copyright © 2016 The Korean Society of Radiology
letter

RE: Relation of Late Gadolinium Enhancement to Increased Ventricular Wall Stress in Dilated Cardiomyopathy

Peter Alter, Prof, MD, PhD, FESC
    • Department of Medicine, Pulmonary and Critical Care Medicine, University Medical Center Giessen and Marburg, Philipps-University Marburg, Marburg 35033, Germany.
Received September 16, 2015; Accepted October 01, 2015.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Keywords
Dilated cardiomyopathy; Ventricular wall stress; Late gadolinium enhancement; Wall stress index; Cardiac magnetic resonance imaging; Heart failure

With great interest, we read the study by Yoon et al. (1) confirming the previously reported relationship between late gadolinium enhancement (LGE) and increased left ventricular (LV) wall stress (2). Assessment of postcontrast T1 values by cardiac magnetic resonance imaging (CMR) using look-locker sequences is related to myocardial tissue characteristics of LV remodeling, LV compliance and increased N-terminal pro-B-type natriuretic peptide, a marker of increased ventricular distending forces and wall stress (3). Interestingly, the findings are independent of LGE.

Causes and consequences of LGE in dilated cardiomyopathy are still controversial (4). Since LGE delineates myocardial postinfarct scar accurately, it was assumed that LGE also represents fibrosis in dilated cardiomyopathy. However, morphology, type and extent of LGE varies markedly between different etiologies (5). In dilated cardiomyopathy, LGE typically occurs in a streak-like midwall pattern and at the septal hinge points. In contrast, the extent of fibrosis, as shown by histology, increases from the right to left side of the interventricular septum and from the subepicardial to subendocardial myocardial layers of the free wall, which does not match a midwall pattern (6).

We defined the wall stress index to calculate LV wall stress based on LV cavity size and myocardial mass/volume as assessed by CMR (7). Increased wall stress is reportedly associated with LGE in dilated cardiomyopathy (2). However, in dilated cardiomyopathy, the synonymous use of the terms LGE and fibrosis is not recommended (4).

It is unclear whether LGE is reversible after load reduction, assuming functional causes. Support comes from the finding of increased ventricular wall stress in transient apical ballooning, i.e., Takotsubo syndrome, which is frequently associated with temporary LGE emergence (8). Underlying fibrosis appears unlikely, since the short-term reversibility within few days is not in line with the usual collagen turnover rate (9).

The present study (1) substantially contributes to the understanding and interpretation of LGE. In particular, the results indicated that LGE cannot provide sufficient information on the degree of interstitial fibrosis. Current pre- and post-contrast T1 mapping techniques appear to be helpful for further characterization.

References

    1. Yoon JH, Son JW, Chung H, Park CH, Kim YJ, Chang HJ, et al. Relationship between myocardial extracellular space expansion estimated with post-contrast T1 mapping MRI and left ventricular remodeling and neurohormonal activation in patients with dilated cardiomyopathy. Korean J Radiol 2015;16:1153–1162.
    1. Alter P, Rupp H, Adams P, Stoll F, Figiel JH, Klose KJ, et al. Occurrence of late gadolinium enhancement is associated with increased left ventricular wall stress and mass in patients with non-ischaemic dilated cardiomyopathy. Eur J Heart Fail 2011;13:937–944.
    1. Alter P, Rupp H, Rominger MB, Vollrath A, Czerny F, Klose KJ, et al. Relation of B-type natriuretic peptide to left ventricular wall stress as assessed by cardiac magnetic resonance imaging in patients with dilated cardiomyopathy. Can J Physiol Pharmacol 2007;85:790–799.
    1. Alter P, Figiel JH. Prognostic value of late gadolinium enhancement in cardiomyopathy: causative risk factor or surrogate marker? Int J Cardiol 2015;180:111–113.
    1. Alter P, Rupp H. Late gadolinium enhancement and higher risk of arrhythmias: fibrosis or increased ventricular wall stress? J Am Coll Cardiol 2011;58:1194, author reply 1194-1195.
    1. Unverferth DV, Baker PB, Swift SE, Chaffee R, Fetters JK, Uretsky BF, et al. Extent of myocardial fibrosis and cellular hypertrophy in dilated cardiomyopathy. Am J Cardiol 1986;57:816–820.
    1. Alter P, Rupp H, Stoll F, Adams P, Figiel JH, Klose KJ, et al. Increased end diastolic wall stress precedes left ventricular hypertrophy in dilative heart failure--use of the volume-based wall stress index. Int J Cardiol 2012;157:233–238.
    1. Alter P. Increased ventricular wall stress and late gadolinium enhancement in Takotsubo cardiomyopathy. Int J Cardiol 2014;174:804–805.
    1. Alter P, Rupp H. Occurrence of late gadolinium enhancement in ventricular ballooning or Tako-Tsubo syndrome: increased wall stress should not be overlooked. Eur Heart J 2009;30:2948–2949. author reply 2949.

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