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Late Gadolinium Enhancement in SarcoidosisLate Gadolinium Enhancement in Sarcoidosis: Ventricular Wall Stress Should Not Be Overlooked FREE TO VIEW

Peter Alter, MD; Claus F. Vogelmeier, MD; A. Rembert Koczulla, MD
Author and Funding Information

From the University of Marburg, Internal Medicine – Pneumology.

CORRESPONDENCE TO: Peter Alter, MD, University of Marburg, Internal Medicine – Pneumology, German Center for Lung Research, Baldingerstrasse, 35033 Marburg, Germany; e-mail: alter@uni-marburg.de


FINANCIAL/NONFINANCIAL DISCLOSURES: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;147(3):e118. doi:10.1378/chest.14-2740
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To the Editor:

With great interest, we read in CHEST (October 2014) the study by Nagai et al,1 who examined the occurrence of late gadolinium enhancement (LGE) by cardiovascular MRI (CMR) in patients with sarcoidosis. In sum, 13% of 61 patients exhibited perimyocardial, transmyocardial, or intramyocardial LGE. Noteworthy was that thinning of the interventricular septum, as measured by echocardiography, was revealed as an independent predictor of LGE. Thus, the question of the pathophysiologic rationale behind linking LGE to a thinned septum is addressed to the authors. Since no prognostic influences of LGE were found, the question on the morphologic or functional substrate also arises.

The appearance of LGE is caused by prolonged, interstitial contrast-agent deposition used for CMR image acquisition. LGE is known to accurately delineate scarring following myocardial infarction. In contrast, the diagnostic accuracy is less defined in other cardiac diseases. Intramyocardial, often distributed, spots of LGE are typically found in myocarditis, although the finding is neither obligatory nor specific. Additional sequences (eg, edema sensitive) are required for further classification.2 In dilated cardiomyopathy, LGE frequently occurs as a septal midwall pattern or at the hinge points of the septum. It has been deduced from postinfarct findings that LGE also would delineate fibrosis in dilated cardiomyopathy, which remains debatable. Studies on histology showed that the extent of myocardial fibrosis involves a gradient that increases from subepicardial to subendocardial layers not matching a midwall pattern. Due to the increased load of the affected regions, the question arises whether functional determinants are involved.

It was shown in 300 patients with cardiomyopathy that occurrence of LGE is associated with increased ventricular wall stress.3 Wall stress is predominantly determined by ventricular volumes, mass, and the transmural pressure gradient.4,5 In the study by Nagai et al,1 it was pointed out that thinning of the interventricular septum was an independent predictor of LGE. Thus, it can be assumed that septal thinning was associated with reduced myocardial mass, which leads to increased wall stress.

It is suggested that the authors1 provide CMR-based myocardial mass and calculate ventricular wall stress. It should be examined whether increased wall stress is related to LGE in sarcoidosis. Increased ventricular wall stress is associated with an increased arrhythmia risk by activation of stretch-associated ion channels, increased oxygen consumption, and unfavorable remodeling. Accordingly, it should be evaluated whether increased wall stress is a causative risk factor and associated with adverse events.

References

Nagai T, Kohsaka S, Okuda S, Anzai T, Asano K, Fukuda K. Incidence and prognostic significance of myocardial late gadolinium enhancement in patients with sarcoidosis without cardiac manifestation. Chest. 2014;146(4):1064-1072. [CrossRef] [PubMed]
 
Radunski UK, Lund GK, Stehning C, et al. CMR in patients with severe myocarditis: diagnostic value of quantitative tissue markers including extracellular volume imaging. JACC Cardiovasc Imaging. 2014;7(7):667-675. [CrossRef] [PubMed]
 
Alter P, Rupp H, Adams P, 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(9):937-944. [CrossRef] [PubMed]
 
Alter P, Rupp H, Rominger MB, Klose KJ, Maisch B. A new methodological approach to assess cardiac work by pressure-volume and stress-length relations in patients with aortic valve stenosis and dilated cardiomyopathy. Pflugers Archiv. 2008;455(4):627-636. [CrossRef] [PubMed]
 
Alter P, Rupp H, Stoll F, 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(2):233-238. [CrossRef] [PubMed]
 

Figures

Tables

References

Nagai T, Kohsaka S, Okuda S, Anzai T, Asano K, Fukuda K. Incidence and prognostic significance of myocardial late gadolinium enhancement in patients with sarcoidosis without cardiac manifestation. Chest. 2014;146(4):1064-1072. [CrossRef] [PubMed]
 
Radunski UK, Lund GK, Stehning C, et al. CMR in patients with severe myocarditis: diagnostic value of quantitative tissue markers including extracellular volume imaging. JACC Cardiovasc Imaging. 2014;7(7):667-675. [CrossRef] [PubMed]
 
Alter P, Rupp H, Adams P, 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(9):937-944. [CrossRef] [PubMed]
 
Alter P, Rupp H, Rominger MB, Klose KJ, Maisch B. A new methodological approach to assess cardiac work by pressure-volume and stress-length relations in patients with aortic valve stenosis and dilated cardiomyopathy. Pflugers Archiv. 2008;455(4):627-636. [CrossRef] [PubMed]
 
Alter P, Rupp H, Stoll F, 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(2):233-238. [CrossRef] [PubMed]
 
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