Association of Imaging Markers of Myocardial Fibrosis with Metabolic and Functional Disturbances in Early Diabetic Cardiomyopathy Jellis et al: Myocardial Fibrosis in Diabetes

Background Metabolic and vascular disturbances contribute to diabetic cardiomyopathy (DCM), but the role of interstitial fibrosis in early disease is unproven. We sought to assess the relationship between imaging markers of diffuse fibrosis with myocardial dysfunction, and to link this to possible etiologies of early DCM. Methods and Results Hemodynamic and metabolic data were measured in 67 subjects with T2DM (60±10 years) with no cardiac symptoms. Myocardial function was evaluated with standard echocardiography and myocardial deformation; ischemia was excluded by exercise echocardiography. Calibrated integrated backscatter (cIB) was calculated from parasternal long axis views. T1 mapping was performed post-contrast with a modified Look-Locker technique using saturation recovery images. Amino-terminal propeptides of pro-collagens type I and III (PIIINP), and the carboxy-terminal propeptide of pro-collagen type I, were assayed to determine collagen turnover. Subjects with abnormal early diastolic tissue velocity (Em) had shorter post-contrast T1 values (p=0.042) and higher cIB (p=0.007). They were heavier (p=0.003), had worse exercise capacity (p<0.001), lower insulin sensitivity (p=0.003) and blunted systolic tissue velocity (p=0.05). Post-contrast T1 was associated with diastolic dysfunction (Em r=0.28, p=0.020; E/Em r=-0.24, p=0.049), impaired exercise capacity (r=0.30, p=0.016), central adiposity (r=-0.26, p=0.046), blood pressure (systolic r=-0.30, p=0.012; diastolic r=-0.49, p<0.001) and insulin sensitivity (r=0.30, p=0.037). The association of T1 with E/Em ( =-0.31, p=0.017) was independent of blood pressure and metabolic disturbance. PIIINP was linked to diastolic dysfunction (Em r=-0.32, p=0.008) and cIB (r=0.30, p=0.015) but not T1 values. Conclusions The association between myocardial diastolic dysfunction, post-contrast T1 values and metabolic disturbance supports that diffuse myocardial fibrosis is an underlying contributor to early DCM.