title: Effects of prior intensive versus conventional therapy and history of glycemia on cardiac function in type 1 diabetes in the DCCT/EDIC.
abstract: Intensive diabetes therapy reduces the prevalence of coronary calcification and progression of atherosclerosis and the risk of cardiovascular disease (CVD) events in the Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Interventions and Complications (EDIC) study. The effects of intensive therapy on measures of cardiac function and structure and their association with glycemia have not been explored in type 1 diabetes (T1DM). We assess whether intensive treatment compared with conventional treatment during the DCCT led to differences in these parameters during EDIC. After 6.5 years of intensive versus conventional therapy in the DCCT, and 15 years of additional follow-up in EDIC, left ventricular (LV) indices were measured by cardiac magnetic resonance (CMR) imaging in 1,017 of the 1,371 members of the DCCT cohort. There were no differences between the DCCT intensive versus conventional treatment in end diastolic volume (EDV), end systolic volume, stroke volume (SV), cardiac output (CO), LV mass, ejection fraction, LV mass/EDV, or aortic distensibility (AD). Mean DCCT/EDIC HbA1c over time was associated with EDV, SV, CO, LV mass, LV mass/EDV, and AD. These associations persisted after adjustment for CVD risk factors. Cardiac function and remodeling in T1DM assessed by CMR in the EDIC cohort was associated with prior glycemic exposure, but there was no effect of intensive versus conventional treatment during the DCCT on cardiac parameters.
authors.affiliation: Case Western Reserve University, Cleveland, Ohio.
authors.forename: Saul M
authors.initials: SM
authors.lastname: Genuth
authors.forename: Jye-Yu C
authors.initials: JY
authors.lastname: Backlund
authors.forename: Margaret
authors.initials: M
authors.lastname: Bayless
authors.forename: David A
authors.initials: DA
authors.lastname: Bluemke
authors.forename: Patricia A
authors.initials: PA
authors.lastname: Cleary
authors.forename: Jill
authors.initials: J
authors.lastname: Crandall
authors.forename: John M
authors.initials: JM
authors.lastname: Lachin
authors.forename: Joao A C
authors.initials: JA
authors.lastname: Lima
authors.forename: Culian
authors.initials: C
authors.lastname: Miao
authors.forename: Evrim B
authors.initials: EB
authors.lastname: Turkbey
mesh_terms: D000293:Adolescent; D000328:Adult; D050197:Atherosclerosis / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D001786:Blood Glucose / Q000187:drug effects; D001794:Blood Pressure; D002302:Cardiac Output; D003922:Diabetes Mellitus, Type 1 / Q000150:complications* / Q000188:drug therapy* / Q000503:physiopathology; D003925:Diabetic Angiopathies / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D003928:Diabetic Nephropathies / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D003971:Diastole; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006442:Glycated Hemoglobin; D006801:Humans; D006943:Hyperglycemia / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D008297:Male; D012307:Risk Factors; D013318:Stroke Volume; D013599:Systole; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D020257:Ventricular Remodeling
chemical_list: D001786:Blood Glucose; D006442:Glycated Hemoglobin; C517652:hemoglobin A1c protein, human