title: Determinants of subclinical diabetic heart disease.
abstract: OBJECTIVE
  Subclinical left ventricular (LV) dysfunction has been shown by tissue Doppler and strain imaging in diabetic patients in the absence of coronary disease or LV hypertrophy, but the prevalence and aetiology of this finding remain unclear. This study sought to identify the prevalence and the determinants of subclinical diabetic heart disease.
  
  
  METHODS
  A group of 219 unselected patients with type 2 diabetes without known cardiac disease underwent resting and stress echocardiography. After exclusion of coronary artery disease or LV hypertrophy, the remaining 120 patients (age 57+/-10 years, 73 male) were studied with tissue Doppler imaging. Peak systolic strain of each wall and systolic (Sm) and diastolic (Em) velocity of each basal segment were measured from the three apical views and averaged for each patient. Significant subclinical LV dysfunction was identified according to Sm and Em normal ranges adjusted by age and sex. Strain and Em were correlated with clinical, therapeutic, echocardiographic and biochemical variables, and significant independent associations were sought using a multiple linear regression model.
  
  
  RESULTS
  Significant subclinical LV dysfunction was present in 27% diabetic patients. Myocardial systolic dysfunction by peak strain was independently associated with glycosylated haemoglobin level (p<0.001) and lack of angiotensin-converting enzyme inhibitor treatment (p=0.003). Myocardial diastolic function (Em) was independently predicted by age (p=0.013), hypertension (p=0.001), insulin (p=0.008) and metformin (p=0.01) treatment.
  
  
  CONCLUSIONS
  In patients with diabetes mellitus, subclinical LV dysfunction is common and associated with poor diabetic control, advancing age, hypertension and metformin treatment; ACE inhibitor and insulin therapies appear to be protective.
authors.affiliation: University of Queensland, Brisbane, Australia.
authors.forename: Z Y
authors.initials: ZY
authors.lastname: Fang
authors.forename: R
authors.initials: R
authors.lastname: Schull-Meade
authors.forename: M
authors.initials: M
authors.lastname: Downey
authors.forename: J
authors.initials: J
authors.lastname: Prins
authors.forename: T H
authors.initials: TH
authors.lastname: Marwick
mesh_terms: D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D048909:Diabetes Complications / Q000175:diagnosis*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D003925:Diabetic Angiopathies / Q000175:diagnosis* / Q000188:drug therapy / Q000453:epidemiology; D003971:Diastole; D004452:Echocardiography; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006331:Heart Diseases / Q000175:diagnosis*; D006339:Heart Rate; D006801:Humans; D006973:Hypertension; D007328:Insulin / Q000627:therapeutic use; D008297:Male; D008687:Metformin / Q000627:therapeutic use; D008875:Middle Aged; D013599:Systole; D018487:Ventricular Dysfunction, Left / Q000453:epidemiology*; D016277:Ventricular Function, Left / Q000502:physiology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D001786:Blood Glucose; D006442:Glycated Hemoglobin; D007328:Insulin; D008687:Metformin