title: Relationship between coronary microvascular dysfunction and cardiac energetics impairment in type 1 diabetes mellitus.
abstract: BACKGROUND
  Asymptomatic subjects with diabetes mellitus have an impaired cardiac energetics status that may play a significant role in the development of heart failure. In the present study, we assessed the role of microvascular dysfunction in the development of impaired cardiac energetics in subjects with type 1 diabetes mellitus.
  
  
  RESULTS
  Twenty-five asymptomatic subjects with type 1 diabetes mellitus (mean age +/-1 SD 33+/-8 years) and 26 age-, sex-, and body mass index-matched healthy control subjects (32+/-8 years old) were recruited into the study. The type 1 diabetes mellitus subjects were divided into 2 age-matched groups (newly diagnosed [<5 years] and longer-duration [>10 years] diabetes) to assess the impact of microvascular disease. All subjects had an echocardiogram and an exercise ECG performed, followed by magnetic resonance spectroscopy and stress magnetic resonance imaging. Compared with healthy control subjects, the phosphocreatine/gamma-ATP ratio was reduced significantly both in subjects with longer-term (2.1+/-0.5 versus 1.5+/-0.4, P<0.000) and newly diagnosed (2.1+/-0.5 versus 1.6+/-0.2, P<0.000) diabetes. The phosphocreatine/gamma-ATP ratio was similar in newly diagnosed diabetes subjects and those with longer-term disease (1.6+/-0.2 versus 1.5+/-0.4, P=0.32). The mean myocardial perfusion reserve index in the longer-term type 1 diabetes mellitus subjects was significantly lower than in healthy control subjects (1.7+/-0.6 versus 2.3+/-0.4, P=0.005). On univariate analysis, there was no significant correlation of phosphocreatine/gamma-ATP ratio with myocardial perfusion reserve index (r=0.21, P=0.26).
  
  
  CONCLUSIONS
  We demonstrate that young subjects with uncomplicated type 1 diabetes mellitus have impaired myocardial energetics irrespective of the duration of diabetes and that the impaired cardiac energetics status is independent of coronary microvascular function. We postulate that impairment of cardiac energetics in these subjects primarily results from metabolic dysfunction rather than microvascular impairment.
authors.affiliation: Department of Cardiovascular Medicine, University of Birmingham, Edgbaston, Birmingham, UK. drgani23@gmail.com
authors.forename: G Nallur
authors.initials: GN
authors.lastname: Shivu
authors.forename: T T
authors.initials: TT
authors.lastname: Phan
authors.forename: K
authors.initials: K
authors.lastname: Abozguia
authors.forename: I
authors.initials: I
authors.lastname: Ahmed
authors.forename: A
authors.initials: A
authors.lastname: Wagenmakers
authors.forename: A
authors.initials: A
authors.lastname: Henning
authors.forename: P
authors.initials: P
authors.lastname: Narendran
authors.forename: M
authors.initials: M
authors.lastname: Stevens
authors.forename: M
authors.initials: M
authors.lastname: Frenneaux
mesh_terms: D000328:Adult; D003331:Coronary Vessels / Q000503:physiopathology*; D003922:Diabetes Mellitus, Type 1 / Q000150:complications* / Q000503:physiopathology; D004734:Energy Metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D006333:Heart Failure / Q000209:etiology*; D006801:Humans; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009206:Myocardium / Q000378:metabolism*
chemical_list: D005230:Fatty Acids, Nonesterified