Anika Afroz

Evelyn M Horn

Jiwon Kim

Jonathan D Kochav

Jonathan W Weinsaft

Maya M Petashnick

Parag Goyal

Peter M Okin

Richard B Devereux

Sergey Gurevich

Journal of Cardiovascular Magnetic Resonance

PubMed

Springer - Publisher Connector

ORAL PRESENTATION Open Access
Mid-wall fibrosis on delayed enhancement
CMR - a marker for adverse left ventricular
chamber remodeling independent of
cardiomyopathic etiology
Jiwon Kim2*, Jonathan D Kochav1, Sergey Gurevich1, Evelyn M Horn1, Parag Goyal1, Maya M Petashnick1,
Anika Afroz1, Peter M Okin1, Richard B Devereux1, Jonathan W Weinsaft1,2
From 17th Annual SCMR Scientific Sessions
New Orleans, LA, USA. 16-19 January 2014
Background
Mid-wall fibrosis (MWF) is a hallmark of non-ischemic
cardiomyopathy (NICM) that confers increased risk for
sudden cardiac death and mortality. The relationship
between MWF and left ventricular (LV) remodeling is
unknown.
Methods
The population comprised patients with advanced systo-
lic dysfunction (LVEF ≤ 40%) undergoing CMR (1.5T,
General Electric Signa). Ischemic vs. NICM etiology was
classified in accordance with established convention
based on obstructive CAD on invasive angiography.
Delayed enhancement CMR (IR-GRE acquired 10-30
minutes post gadolinium [0.2 mmol/kg]) was used to
identify MWF, defined as hyperenhancement confined
to the mid-myocardial or epicardial aspect of the inter-
ventricular septum. LV mass and chamber volume were
quantified by planimetry of contiguous SSFP cine-CMR
short axis slices, with ejection fraction (EF) calculated as
the proportional difference between end-diastolic (EDV)
and end-systolic (ESV) volumes.
Results
523 patients (61 ± 14 yo, 72% M, 66% ischemic CM)
were studied: MWF was present in 16%, and was 6-fold
more common in patients with angiographically classified
NICM (37% vs. 6%; p < 0.001). Regarding LV remodeling,
MWF was associated with higher EDV (134 ± 39 ml vs.
114 ± 34 ml; p < 0.001) and LV mass (102 ± 24 vs. 96 ±
28 gm; p < 0.001) and lower LVEF (26 ± 8% vs. 30 ± 8%;
p ≤ 0.05). MWF was nearly 3-fold more common among
patients in the highest tertile of EDV vs. the remainder of
the population (29% vs. 10%; p < 0.001). Multivariate
regression analysis was performed to further assess mar-
kers for MWF: Restricted to imaging indices, results
(Table 1A) demonstrated EF and EDV to be indepen-
dently associated with MWF (OR = 1.46, CI 1.03-2.10; p
< 0.05, OR = 1.13, CI 1.04-1.20; p < 0.05, respectively)
after controlling for mass (OR = 0.95, CI 0.85-1.00;
p = 0.29). Regarding clinical variables, results (Table 1B)
confirmed a strong association with NICM (OR = 8.4, CI
4.78-14.72; p < 0.001), independent of other clinical
indices. A combined model incorporating both clinical
and imaging variables demonstrated both NICM and LV
volume to be independently associated with MWF even
after controlling for EF (Table 1C). Overall strength of
the combined clinical/imaging (c2 = 91.2; p < 0.001)
model for MWF was higher than that of isolated clinical
(c2 = 76.7; p < 0.001) and imaging (c2 = 26.0; p < 0.001)
models.
Conclusions
Among patients with advanced cardiomyopathy, MWF
is associated with advanced LV chamber dilation inde-
pendent of severity of LV dysfunction and cardiomyo-
pathic etiology.
2Medicine, Memorial Sloan Kettering Cancer Center, New York, New York,
USA
Full list of author information is available at the end of the article
Kim et al. Journal of Cardiovascular Magnetic
Resonance 2014, 16(Suppl 1):O23
http://www.jcmr-online.com/content/16/S1/O23
© 2014 Kim et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in
any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://
creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Funding
National Institutes of Health (K23 HL102249-01).
Authors’ details
1Medicine, Weill Cornell Medical College, New York, New York, USA.
2Medicine, Memorial Sloan Kettering Cancer Center, New York, New York,
USA.
Published: 16 January 2014
doi:10.1186/1532-429X-16-S1-O23
Cite this article as: Kim et al.: Mid-wall fibrosis on delayed enhancement
CMR - a marker for adverse left ventricular chamber remodeling
independent of cardiomyopathic etiology. Journal of Cardiovascular
Magnetic Resonance 2014 16(Suppl 1):O23.
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Table 1 Multivariate Regression for Prediction of LV MWF
1A. Imaging (Model c2 = 26.0, p < 0.001)
Variable Odds Ratio 95% Confidence Interval P
LV Ejection Fraction (per 10% decrement) 1.46 1.03-2.10 < 0.05
LV End-Diastolic Volume (per 10 ml/m2) 1.13 1.04-1.20 < 0.05
Myocardial Mass (per 10 gm/m2) 0.95 0.85-1.00 0.29
1B. Clinical (Model c2 = 76.7, p < 0.001)
Variable Odds Ratio 95% Confidence Interval P
Hypertension 0.10 0.36 - 1.10 0.10
Hypercholesterolemia 0.94 0.59 - 1.78 0.94
Age (years) 0.70 0.99 - 1.00 0.70
Non-Ischemic Etiology 8.4 4.78- 14.72 < 0.001
1C. Integrated Clinical/Imaging (Model c2 = 91.2, p < 0.001)
Variable Odds Ratio 95% Confidence Interval P
LV Ejection Fraction (per 10% decrement) 1.22 0.84- 1.78 0.29
LV End-Diastolic Volume (10 ml/m2) 1.11 1.03 - 1.20 < 0.05
Non-Ischemic Etiology 8.22 4.75 - 14.2 < 0.001
Kim et al. Journal of Cardiovascular Magnetic
Resonance 2014, 16(Suppl 1):O23
http://www.jcmr-online.com/content/16/S1/O23
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Mid-wall fibrosis on delayed enhancement CMR - a marker for adverse left ventricular chamber remodeling independent of cardiomyopathic etiology

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Mid-wall fibrosis on delayed enhancement CMR - a marker for adverse left ventricular chamber remodeling independent of cardiomyopathic etiology

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