Abstract
Purpose: Interstitial fibrosis is believed to be one of several contributors to diabeticcardiomyopathy (DCM), manifesting as myocardial dysfunction in the absenceof ischemic heart disease in subjects with type 2 diabetes (T2DM). Myocardialultrasound reflectivity is proportionate to fibrosis, but use of the pericardiumas a frame of reference (calibrated integrated backscatter, cIB) may be limitedby signal saturation. Recently, diffuse fibrosis has been shown to be inverselyproportionate to T1 time on post-contrast T1 mapping using cardiac magneticresonance imaging. We sought to compare the association of cIB and T1 timewith DCM.Methods: Demographic, anthropometric, hemodynamic and biochemical datawere measured in 107 apparently healthy, asymptomatic subjects with T2DM (65men, 60±9 years). LV dysfunction (LVD) was sought on resting echo (early diastolictissue velocity [Em] < 1SD from mean for age). Ischemia was excludedby exercise echo. Standard 2D and color TDI measures (tissue velocity, strainand strain rate) were acquired in apical long axis views. Calibrated integratedbackscatter (cIB) was calculated from a parasternal long axis view. Tonometricaortic pulse wave velocity (APWV) was used to determine arterial stiffness. T1mapping was performed in those with LVD and matched controls.Results: LVD was identified in 23 subjects (28%) who also demonstrated significantlypoorer diabetic control (HbA1c 8.2±2.0 vs 7.3±1.4 mmol/L) but no relationshipwith cIB. T1 mapping was performed in 26 subjects (17 men, 60±10years) comprising 20 with LVD and 6 controls. Em was independently associatedwith age (β=-0.76 p<0.001), body mass index [BMI] (β=-0.65, p<0.001), strain(β=0.51, p=0.003) and post-contrast T1 time (β=0.36, p=0.04) [model R Square =0.63] but not cIB. Post-contrast T1 time was independently associated with insulinresistance (HOMA-IR β=-0.63, p=0.016) [model R Square = 0.38] but not withcIB, APWV, BMI or low density lipoprotein (LDL). The only independent correlateof cIB was APWV (β=0.59, p=0.009) [model R Square = 0.39] and not HOMA-IR,BMI or LDL.Conclusions: Quantitative tissue characterisation of fibrosis (T1 time) was independentlyassociated with subclinical DCM, in addition to systolic dysfunction(strain), age and BMI. The association of T1 mapping with insulin resistance contrastswith the link between cIB and arterial stiffness, suggesting potential differencesbetween fibrosis in DCM and hypertension.
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