Abstract
Purpose of reviewThis review article discusses the evolution of extracellular volume (ECV) quantification using both cardiovascular magnetic resonance (CMR) and computed tomography (CT).Recent findingsVisualizing diffuse myocardial fibrosis is challenging and until recently, was restricted to the domain of the pathologist. CMR and CT both use extravascular, extracellular contrast agents, permitting ECV measurement. The evidence base around ECV quantification by CMR is growing rapidly and just starting in CT. In conditions with high ECV (amyloid, oedema and fibrosis), this technique is already being used clinically and as a surrogate endpoint. Non-invasive diffuse fibrosis quantification is also generating new biological insights into key cardiac diseases.SummaryCMR and CT can estimate ECV and in turn diffuse myocardial fibrosis, obviating the need for invasive endomyocardial biopsy. CT is an attractive alternative to CMR particularly in those individuals with contraindications to the latter. Further studies are needed, particularly in CT.
Highlights
Myocardial fibrosis is a frequently unwanted, common end point in the majority of pathological mechanisms affecting heart muscle
Resultant image quality is currently reduced, myocardial fibrosis can be assessed with cardiac computed tomography (CT)— both use an extracellular, extravascular contrast agent that lingers in extracellular water in areas of scar, due to a higher volume of distribution and slower kinetics
Bandula et al in the same year validated ECV imaging by cardiac CT (ECVCT) against the gold standard—invasive endomyocardial biopsy, as well as ECVCMR in 23 patients with severe aortic stenosis [34]. This time, they used an initial bolus of contrast agent, followed by a slow infusion to achieve equilibrium. They found that ECVCT showed significant correlation with both histological measures of fibrosis (r = 0.71, p < 0.001) and ECVCMR (r = 0.73) [34]
Summary
Myocardial fibrosis is a frequently unwanted, common end point in the majority of pathological mechanisms affecting heart muscle. It can occur as focal scarring due to replacement fibrosis following myocyte death (apoptosis, autophagy or necrosis) or as diffuse fibrosis due to expansion of the collagen fibre network around individual myocytes or myocyte
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