Cardiovascular Magnetic Resonance, Fibrosis, and Prognosis in Dilated Cardiomyopathy
Ravi G. Assomull, MRCP*, ,
Sanjay K. Prasad, MD, MRCP*,,
Jonathan Lyne, MRCP*,
Gillian Smith, MSc*,
Elizabeth D. Burman, MSc*,
Mohammed Khan, MSc, MPH ,
Mary N. Sheppard, MD, FRCPath ,
Philip A. Poole-Wilson, MD, FRCP and
Dudley J. Pennell, MD, FRCP, FESC, FACC*,,*
* Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital
National Heart and Lung Institute, Imperial College
Medical Statistics Unit, Royal Brompton Hospital
Pathology Department, Royal Brompton Hospital, London, United Kingdom
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Figure 1 Late gadolinium enhancement patterns in dilated cardiomyopathy in vertical long axis (A and C) and short axis (B and D). A patient without late enhancement is shown in A and B, and a patient with marked midwall enhancement is shown in C and D. The enhancement pattern (arrows) is distinct from that associated with coronary artery disease because of endocardial sparing and noncoronary territory distribution.
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Figure 2 (A) Macroscopic short-axis section of the right and left ventricle at a midventricular level from a patient with dilated cardiomyopathy showing midwall fibrosis (straight arrows), mainly in the inferior and lateral walls, but also in the lower and upper septum (curved arrows). (B) Microscopic section of the heart in which Sirius red staining confirms collagen (arrow) in areas of fibrosis seen macroscopically. Myocytes (stained yellow) are admixed with the collagen (red). (C) Premortem cardiovascular magnetic resonance of the same slice, with excellent accord between the areas of macroscopic fibrosis and areas of late gadolinium enhancement (matching arrows).
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Figure 3 (A) Kaplan-Meier survival estimates for the primary end point of all-cause mortality or hospitalization due to cardiovascular causes. (B) Same data adjusted for baseline differences in age, left ventricular (LV) end-systolic volume, LV end-diastolic volume, LV ejection fraction, right ventricular ejection fraction, and treatment with digoxin. LGE+ = patients with late gadolinium enhancement; LGE– = patients without late gadolinium enhancement.
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Figure 4 (A) Kaplan-Meier survival estimates for the secondary end point of sudden cardiac death or sustained ventricular tachycardia. (B) Same data adjusted for baseline differences in left ventricular ejection fraction. LGE+ = patients with late gadolinium enhancement; LGE– = patients without late gadolinium enhancement.
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Figure 5 (A) Binary logistic regression analysis comparing the extent of late enhancement (%LGE), left ventricular end-systolic volume (LVESV), left ventricular end-diastolic volume (LVEDV), and left ventricular ejection fraction (LVEF) as predictors of death or hospitalization. There was a strong association between %LGE and outcome, and %LGE was the sole significant predictor of the primary end point (odds ratio 1.12, 95% confidence interval 1.03 to 1.24, p = 0.02). (B) Kaplan-Meier subgroup analysis of the 35 patients in the LGE+ group divided into high and low LGE (division point 4.8% LGE). The analysis shows a trend (p = 0.07) toward a significant difference in outcome for the primary end point between the 2 subgroups. LGE+ = patients with late gadolinium enhancement; LGE– = patients without late gadolinium enhancement.
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