Cardiovascular magnetic resonance measurement of myocardial extracellular volume in health and disease
- Daniel M Sado1,2,
- Andrew S Flett1,2,
- Sanjay M Banypersad1,2,3,
- Steven K White1,2,
- Viviana Maestrini1,
- Giovanni Quarta1,
- Robin H Lachmann4,
- Elaine Murphy4,
- Atul Mehta5,
- Derralynn A Hughes5,
- William J McKenna1,2,
- Andrew M Taylor2,6,
- Derek J Hausenloy1,2,
- Philip N Hawkins3,
- Perry M Elliott1,2,
- James C Moon1,2
- 1The Heart Hospital, London, UK
- 2Institute of Cardiovascular Science, University College London, London, UK
- 3Centre for Amyloidosis and Acute Phase Proteins and National Amyloidosis Centre, University College London, London, UK
- 4The National Hospital for Neurology and Neurosurgery, Charles Dent Metabolic Unit, London, UK
- 5The Royal Free Hospital Lysosomal Storage Disorders Unit, Royal Free Hospital, London, UK
- 6Cardiovascular Unit, UCL Institute of Child Health, London, UK
- Correspondence to Dr James Moon, The Heart Hospital, 16–18 Westmoreland St, London W1G 8PH, UK; james.moon{at}uclh.nhs.uk
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Contributors DMS: led study and four patient groups; lead writer of manuscript. ASF, SMB, SKW: each contributed a patient group. VM, GQ: scanning, recruitment, analysis. RH, EM, AM, DAH, WJM, PME, DJH, PNH: clinicians advising and coordinating patient cohorts. AMT: senior CMR author; role in optimising the clinical and research CMR techniques used and then in the writing and formatting of the manuscript. JCM: concept and design of the study. All authors helped with writing, formatting and reviewing of manuscript.
- Accepted 14 June 2012
- Published Online First 30 August 2012
Abstract
Objective To measure and assess the significance of myocardial extracellular volume (ECV), determined non-invasively by equilibrium contrast cardiovascular magnetic resonance, as a clinical biomarker in health and a number of cardiac diseases of varying pathophysiology.
Design Prospective study.
Setting Tertiary referral cardiology centre in London, UK.
Patients 192 patients were mainly recruited from specialist clinics. We studied patients with Anderson–Fabry disease (AFD, n=17), dilated cardiomyopathy (DCM, n=31), hypertrophic cardiomyopathy (HCM, n=31), severe aortic stenosis (AS, n=66), cardiac AL amyloidosis (n=27) and myocardial infarction (MI, n=20). The results were compared with those for 81 normal subjects.
Results In normal subjects, ECV (mean (95% CI), measured in the septum) was slightly higher in women than men (0.273 (0.264 to 0.282 vs 0.233 (0.225 to 0.244), p<0.001), with no change with age. In disease, the ECV of AFD was the same as in normal subjects but higher in all other diseases (p<0.001). Mean ECV was the same in DCM, HCM and AS (0.280, 0.291, 0.276 respectively), but higher in cardiac AL amyloidosis and higher again in MI (0.466 and 0.585 respectively, each p<0.001). Where ECV was elevated, correlations were found with indexed left ventricular mass, end systolic volume, ejection fraction and left atrial area in apparent disease-specific patterns.
Conclusions Myocardial ECV, assessed non-invasively in the septum with equilibrium contrast cardiovascular magnetic resonance, shows gender differences in normal individuals and disease-specific variability. Therefore, ECV shows early potential to be a useful biomarker in health and disease.
- CMR
- gadolinium
- extracellular volume
- arrhythmias
- defibrillation
- cardiac function
- imaging and diagnostics
- MRI
- myocardial disease
- myocardial fibrosis
- myocardial ischaemia and infarction (IHD)
- sudden adult death syndrome
- cardiomyopathy hypertrophic
- arrhythmic right ventricular dysplasia
- congenital heart disease
- thoracic imaging
- cardiac anatomy
- paediatric cardiac function
- myocardial infarction
- myocytes
- apoptosis
- ischaemia reperfusion
- myocardial protection
- metabolic medicine
- diabetic heart disease
- cardiomyopathy
- cardiomyopathy apical
- cardiomyopathy restrictive
- hypertrophic cardiomyopathy
- cardiac imaging
- MRI
Footnotes
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Funding (1) British Heart Foundation; (2) Genzyme (for the Anderson–Fabry arm of the study).
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Competing interests RHL: received honoraria, consulting fees or grant funding from Genzyme, Shire and Amicus. DAH: travel, research support and honoraria for speaking and being on advisory boards from Shire, Genzyme and Glaxo SmithKline/Amicus. EM: unrestricted educational grants, travel expenses and honoraria from Shire and Genzyme. PME: consulting fees for Shire and Genzyme and speaker fees for Shire.
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Provenance and peer review Not commissioned; internally peer reviewed.
