SAT-620 Left Ventricular Myocardial Deformation in T2DM Is Associated with Chronic Hyperglycemia but Not Myocardial Perfusion: A Study Based on Magnetic Resonance Imaging

Background: Diabetic cardiomyopathy is accompanied by left ventricular diastolic dysfunction. Abnormal glucose metabolism plays an important role in the pathogenesis of diabetic cardiomyopathy. However, it’s still not clear whether the influence of hyperglycemia on LV dysfunction is directly affects cardiomyocytes or is related to impaired myocardial perfusion. In this work, we focus on investigating the association between HbA1c and myocardial dysfunction, and if it is independent of myocardial perfusion reserve. Materials and Methods: 64 type 2 diabetic patients were recruited at the endocrine clinic. They are divided into two group, well blood glucose-controlled group (HbA1c<7) and poor glucose-controlled group (HbA1c≥7) T2DM group, according to their HbA1c level. All of the T2DM patients and age-matched healthy volunteers (normal glucose metabolism group, NGM group) underwent CMR to acquire normal values for myocardial strain and perfusion reserve. Results: Well blood glucose-controlled group owned lower global circumferential PSSR than NGM group (p=0.037). Global circumferential PS (p=0.011), global longitudinal PS (p=0.004), global radial PDSR (p=0.005), circumferential PDSR (p=0.001), longitudinal PDSR (p=0.001), global circumferential PSSR (p=0.049), longitudinal PSSR (p=0.041) were significantly lower in the poor glucose-controlled group compared to the NGM group. In the multivariable linear regression analysis, HbA1c existed in all equations except the global circumferential PSSR equation and p<0.05, and Slope, Max SI and Tpeak did not show dependent association with longitudinal and circumferential strain parameters. Conclusion: In subclinical cardiac dysfunction T2DM patients, diastolic dysfunction is more common, but systolic dysfunction is still exist. Poor blood glucose control which is defined as HbA1c ≥ 7% is an independent risk factor for LV deformation for T2DM patients. Subclinical myocardial dysfunction is not triggered by myocardial perfusion reserve.