: Fibrosis, in general, is a scarring process, which is characterized by fibroblast accumulation and excess deposition of extracellular matrix (ECM) proteins, which leads to distorted organ architecture and function. The contribution of fibrogenesis to impaired cardiac function is increasingly recognized. The fibrotic ECM causes increased stiffness and induces pathological signaling within cardiomyocytes resulting in progressive cardiac failure. Also, the excessive ECM impairs mechano-electric coupling of cardiomyocytes and increases the risk of arrhythmias. But today patient treatment and prognosis is based on ejection fraction quantification, QRS duration, and symptoms.

Hypothesis: the increased level of fibrosis quantified using T1 mapping technique, compared with normal value, is of prognostic value in patient with dilated cardiomyopathies under optimal treatment.

Methods: 330 patients are planned to be included and followed for 2 years

Inclusion Criteria:

• patient with dilated cardiomyopathy and typical symptoms of cardiac insufficiency at the time of the diagnosis: oedemas of lower limbs, dyspnoea, asthenia.
• and of a reduction in the fraction of ventricular ejection left (awkward) 45 % measured in echocardiography ( modified Simpson biplane) and associated with a volume télédiastolic volume superior to the normal in echocardiography: > 90ml / m2 ( modified Simpson biplane).

Exclusion Criteria:

• Patients to whom the dysfunction VG is secondary or in a secondary overload of pressures in a HTA or a severe valvulopathie is in a coronary infringement(achievement), proved by histories of infarct or gestures(movements) of revascularisation (bypass(decking), stent) and or coronary hurts at least bi tronculaires significant the severity of which can explain the ventriculaire failure.