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JACC Cardiovasc Imaging. 2014 Aug;7(8):762-70. doi: 10.1016/j.jcmg.2014.03.012. Epub 2014 Jul 16.

Coronary vessel wall contrast enhancement imaging as a potential direct marker of coronary involvement: integration of findings from CAD and SLE patients.

Author information

1
Cardiovascular Imaging Department, Division of Imaging Sciences and Biomedical Engineering, King's College London, London, United Kingdom.
2
The Lupus Unit, Rayne's Institute, King's College London, London, United Kingdom.
3
Department of Medical Physics and Bioengineering, Division of Imaging Sciences and Biomedical Engineering, King's College London, London, United Kingdom.
4
Cardiovascular Division, King's College London, London, United Kingdom.
5
Cardiovascular Imaging Department, Division of Imaging Sciences and Biomedical Engineering, King's College London, London, United Kingdom. Electronic address: v.puntmann@kcl.ac.uk.

Abstract

OBJECTIVES:

This study investigated the feasibility of visual and quantitative assessment of coronary vessel wall contrast enhancement (CE) for detection of symptomatic atherosclerotic coronary artery disease (CAD) and subclinical coronary vasculitis in autoimmune inflammatory disease (systemic lupus erythematosus [SLE]), as well as the association with aortic stiffness, an established marker of risk.

BACKGROUND:

Coronary CE by cardiac magnetic resonance (CMR) is a novel noninvasive approach to visualize gadolinium contrast uptake within the coronary artery vessel wall.

METHODS:

A total of 75 subjects (CAD: n = 25; SLE: n = 27; control: n = 23) underwent CMR imaging using a 3-T clinical scanner. Coronary arteries were visualized by a T2-prepared steady state free precession technique. Coronary wall CE was visualized using inversion-recovery T1 weighted gradient echo sequence 40 min after administration of 0.2 mmol/kg gadobutrol. Proximal coronary segments were visually examined for distribution of CE and quantified for contrast-to-noise ratio (CNR) and total CE area.

RESULTS:

Coronary CE was prevalent in patients (93%, n = 42) with a diffuse pattern for SLE and a patchy/regional distribution in CAD patients. Compared with control subjects, CNR values and total CE area in patients with CAD and SLE were significantly higher (mean CNR: 3.9 ± 2.5 vs. 6.9 ± 2.5 vs. 6.8 ± 2.0, respectively; p < 0.001; total CE area: median 0.8 [interquartile range (IQR): 0.6 to 1.2] vs. 3.2 [IQR: 2.6 to 4.0] vs. 3.3 [IQR: 1.9 to 4.5], respectively; p < 0.001). Both measures were positively associated with aortic stiffness (CNR: r = 0.61, p < 0.01; total CE area: 0.36, p = 0.03), hypercholesterolemia (r = 0.68, p < 0.001; r = 0.61, p < 0.001) and hypertension (r = 0.40, p < 0.01; r = 0.32, p < 0.05).

CONCLUSIONS:

We demonstrate that quantification of coronary CE by CNR and total CE area is feasible for detection of subclinical and clinical uptake of gadolinium within the coronary vessel wall. Coronary vessel wall CE may become an instrumental novel direct marker of vessel wall injury and remodeling in subpopulations at risk.

KEYWORDS:

cardiac magnetic resonance; contrast-to-noise ratio; coronary enhancement; vessel wall remodeling

PMID:
25051945
PMCID:
PMC4136741
DOI:
10.1016/j.jcmg.2014.03.012
[Indexed for MEDLINE]
Free PMC Article

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