Parametric mapping techniques provide a non-invasive tool for quantifying tissue alterations in myocardial disease in those eligible for cardiovascular magnetic resonance (CMR). Parametric mapping with CMR now permits the routine spatial visualization and quantification of changes in myocardial composition based on changes in T1, T2, and T2*(star) relaxation times and extracellular volume (ECV). These changes include specific disease pathways related to mainly intracellular disturbances of the cardiomyocyte (e.g., iron overload, or glycosphingolipid accumulation in Anderson-Fabry disease); extracellular disturbances in the myocardial interstitium (e.g., myocardial fibrosis or cardiac amyloidosis from accumulation of collagen or amyloid proteins, respectively); or both (myocardial edema with increased intracellular and/or extracellular water). Parametric mapping promises improvements in patient care through advances in quantitative diagnostics, inter- and intra-patient comparability, and relatedly improvements in treatment. There is a multitude of technical approaches and potential applications. This document provides a summary of the existing evidence for the clinical value of parametric mapping in the heart as of mid 2017, and gives recommendations for practical use in different clinical scenarios for scientists, clinicians, and CMR manufacturers.

Rapid innovations in cardiovascular magnetic resonance (CMR) now permit the routine acquisition of quantitative measures of myocardial and blood T1 which are key tissue characteristics. These capabilities introduce a new frontier in cardiology, enabling the practitioner/investigator to quantify biologically important myocardial properties that otherwise can be difficult to ascertain clinically. CMR may be able to track biologically important changes in the myocardium by: a) native T1 that reflects myocardial disease involving the myocyte and interstitium without use of gadolinium based contrast agents (GBCA), or b) the extracellular volume fraction (ECV)–a direct GBCA-based measurement of the size of the extracellular space, reflecting interstitial disease. The latter technique attempts to dichotomize the myocardium into its cellular and interstitial components with estimates expressed as volume fractions. This document provides recommendations for clinical and research T1 and ECV measurement, based on published evidence when available and expert consensus when not. We address site preparation, scan type, scan planning and acquisition, quality control, visualisation and analysis, technical development. We also address controversies in the field. While ECV and native T1 mapping appear destined to affect clinical decision making, they lack multi-centre application and face significant challenges, which demand a community-wide approach among stakeholders. At present, ECV and native T1 mapping appear sufficiently robust for many diseases; yet more research is required before a large-scale application for clinical decision-making can be recommended.

Background Extracellular matrix (ECM) expansion may be a fundamental feature of adverse myocardial remodeling, appears to be treatable, and its measurement may improve risk stratification. Yet, the relationship between mortality and ECM is not clear due to difficulties with its measurement. To assess its relationship with outcomes, we used novel, validated cardiovascular magnetic resonance (CMR) techniques to quantify the full spectrum of ECM expansion not readily detectable by conventional CMR. Methods and Results We recruited 793 consecutive patients at the time of CMR without amyloidosis or hypertrophic cardiomyopathy as well as 9 healthy volunteers (ages 20–50). We measured the extracellular volume fraction (ECV) to quantify the extracellular matrix expansion in myocardium without myocardial infarction (MI). ECV employs gadolinium contrast (Gd) as an extracellular space marker based on T1 measures of blood and myocardium pre-/post-Gd and hematocrit measurement. In volunteers, ECV ranged from 21.7–26.2%, but in patients, it ranged from 21.0–45.8%, indicating considerable burden. There were 39 deaths over a median follow-up of 0.8 years (IQR 0.5–1.2 years), and 43 individuals who experienced the composite endpoint of death/cardiac transplant/left ventricular assist device (LVAD) implantation. In Cox regression models, ECV related to all-cause mortality and the composite endpoint (HR 1.55; 95% CI 1.27–1.88 and HR 1.48; 95% CI 1.23–1.78, respectively, for every 3% increase in ECV), adjusting for age, left ventricular ejection fraction, and MI size. Conclusions ECV measures of extracellular matrix expansion may predict mortality as well as other composite endpoints (death/cardiac transplant/LVAD).

Diabetes is associated with increased ECV. Extracellular volume fraction detects amelioration of ECM expansion associated with RAAS blockade, and is associated with mortality and/or incident hospitalization for heart failure in diabetic individuals. Extracellular matrix expansion may be an important intermediate phenotype in diabetic individuals that is detectable and treatable.