Abstract 3194: The Role of Coronary Microvascular Function and Rotational Deformation Delay in the Development of Increased Left Ventricular Torsion in Uncomplicated Type 1 Diabetes
BACKGROUND: Heart failure is a common cause of morbidity and mortality in diabetes. The early manifestations of diabetic cardiomyopathy are however not well established. Left ventricular (LV) torsion followed by untwisting during diastole is an important component that affects LV filling. We used speckle tracking echocardiography to study the early changes in LV torsion in patients with uncomplicated type 1 diabetes (T1DM) and used stress magnetic resonance imaging (MRI) to assess its interrelationships with coronary microangiopathy.
METHODS: 33 asymptomatic T1DM subjects (age 32.9±8.4 y) and 32 age-matched healthy controls (HC) (age 30.8±8.0 y) were recruited into the study. The T1DM subjects were divided into newly diagnosed and longer duration diabetes to assess impact of microvascular disease. All subjects underwent history, clinical examination, 12-lead electrocardiogram, echocardiogram and metabolic exercise testing to exclude heart failure and ischaemic heart disease. Stress MRI was performed in 30 subjects (8 healthy volunteers) to compute myocardial perfusion reserve index (MPRI), a measure of coronary microvascular function. LV rotation and strain measurements were made using a commercially available speckle tracking system (ECHOPAC workstation).
RESULTS: Peak LV torsion was significantly increased in the T1DM as compared to HC (1.9±0.6 vs 1.4±0.7, P<0.01). A significant increase in LV torsion (2±0.7 °/cm vs 1.4±0.7 °/cm, P<0.05) was identified in longer term and retinopathy (+) T1DM subjects (1.9±0.7 °/cm vs 1.4±0.7 °/cm, P<0.05) as compared to HC. Peak LV torsion rate and peak untwisting rate were not significantly increased in T1DM. Linear regression analysis demonstrated that rotational deformation delay and MPRI were independent predictors of LV torsion.
CONCLUSION: We demonstrate for the first time using speckle tracking that despite normal ejection fraction, LV torsion is increased in young patients with uncomplicated T1DM. This may represent a myocardial compensatory mechanism to maintain ejection fraction during the early stages of diabetic cardiomyopathy. MPRI predicted LV torsion in T1DM subjects implicating a role for microvascular disease in the development of increased torsion in these individuals.