Pathological processes cause myocardial structural modifications including extracellular matrix alterations, such as interstitial fibrosis, myocyte hypertrophy, and microcirculation impairment. The fibrotic extracellular matrix causes increased myocardial stiffness and induces pathologic signaling within cardiomyocytes ultimately resulting in progressive cardiac failure. Furthermore, fibrosis impairs the mechanoelectrical coupling of cardiomyocytes and increases the incidence of arrhythmias. Early detection of myocardial fibrosis using CMRI could be clinically relevant to assess patient prognosis, to select the most appropriate therapy, and to monitor its efficacy.

MYOCARDIAL FIBROSIS occurs in two forms: diffuse interstitial fibrosis and replacement fibrosis (myocardial scar). Detection of replacement fibrosis due to myocardial infarct is well established in vivo using late gadolinium-enhanced T1-weighted MRI. Diffuse interstitial fibrosis is the main pathologic process in several cardiomyopathies, Quantitative myocardial T1 mapping before and after gadolinium chelate injection is used for assessing diffuse fibrosis.

MYOCARDIAL EDEMA and AREAS AT RISK can be assessed by T2 mapping using a threshold signal intensity > 2SD greater than remote.