LGE is seen in 40% in a subepicardial or mid myocardial distribution in the anterior and anterolateral LV segments (occasionally subendocardial or transmural), more commonly in scans taken >7 days after the acute phase [84]. High T1 and T2 values and EGE are also seen in the acute stages [103]. Patients with LGE showed higher decompensation and did not regain LVEF [84]. Muscular dystrophies may present with ventricular dilation, and mid myocardial/subepicardial pattern of LGE, with occasional noncompacted myocardium. LGE may be present when echocardiography is still normal [104] and is an adverse prognostic determinant [84]. A higher amount of LGE is associated with lower LVEF, but LGE has a variable association with arrhythmia [104]. With longer duration of steroid treatment, lower increase in fibrosis burden was seen over time [105]. T1 and ECV values are also abnormal, which were associated with arrhythmia. Strain imaging shows abnormalities in earlier stages, before onset of overt HF, shows better serial decline in LV function, and provides reliable monitoring of progression of dystrophy [106]. LGE is also seen in mutation carriers [104]. Nonischemic Myocardial Disease used MRI diagnostic criteria for noncompaction, indicating that these criteria have poor specificity. This may, therefore, represent a variant anatomical phenotype than cardiomyopathy [112,113]. MRI in stress-induced cardiomyopathy shows reversible global systolic dysfunction and LV apical ballooning with normal or hyperkinetic basal segments and akinetic/hypokinetic apical segments. There are also reverse and mid ventricular variants. RV is involved in 40% of cases, which is associated with a worse prognosis [114]. Myocardial edema may be present, leading to a high signal in T2-weighted images, high native T1, and high T2 values, typically confined to the abnormal segment [115].
Nonischemic Myocardial Disease with Clinical Manifestations Ischemic Cardiomyopathy Already Excluded . LGE is seen in 40% in a subepicardial or mid myocardial distribution in the anterior and anterolateral LV segments (occasionally subendocardial or transmural), more commonly in scans taken >7 days after the acute phase [84]. High T1 and T2 values and EGE are also seen in the acute stages [103]. Patients with LGE showed higher decompensation and did not regain LVEF [84]. Muscular dystrophies may present with ventricular dilation, and mid myocardial/subepicardial pattern of LGE, with occasional noncompacted myocardium. LGE may be present when echocardiography is still normal [104] and is an adverse prognostic determinant [84]. A higher amount of LGE is associated with lower LVEF, but LGE has a variable association with arrhythmia [104]. With longer duration of steroid treatment, lower increase in fibrosis burden was seen over time [105]. T1 and ECV values are also abnormal, which were associated with arrhythmia. Strain imaging shows abnormalities in earlier stages, before onset of overt HF, shows better serial decline in LV function, and provides reliable monitoring of progression of dystrophy [106]. LGE is also seen in mutation carriers [104]. Nonischemic Myocardial Disease used MRI diagnostic criteria for noncompaction, indicating that these criteria have poor specificity. This may, therefore, represent a variant anatomical phenotype than cardiomyopathy [112,113]. MRI in stress-induced cardiomyopathy shows reversible global systolic dysfunction and LV apical ballooning with normal or hyperkinetic basal segments and akinetic/hypokinetic apical segments. There are also reverse and mid ventricular variants. RV is involved in 40% of cases, which is associated with a worse prognosis [114]. Myocardial edema may be present, leading to a high signal in T2-weighted images, high native T1, and high T2 values, typically confined to the abnormal segment [115].