title: Cardiac structural and functional abnormalities in end stage renal disease patients with elevated cardiac troponin T.
abstract: OBJECTIVE
  To identify in a prospective observational study the cardiac structural and functional abnormalities and mortality in patients with end stage renal disease (ESRD) with a raised cardiac troponin T (cTnT) concentration.
  
  
  METHODS
  126 renal transplant candidates were studied over a two year period. Clinical, biochemical, echocardiographic, coronary angiographic, and dobutamine stress echocardiographic (DSE) data were examined in comparison with cTnT concentrations dichotomised at cut off concentrations of < 0.04 microg/l and < 0.10 microg/l.
  
  
  RESULTS
  Left ventricular (LV) size and filling pressure were significantly raised and LV systolic and diastolic function parameters significantly impaired in patients with raised cTnT, irrespective of the cut off concentration. The proportions of patients with diabetes and on dialysis were higher in both groups with raised cTnT. With a cut off cTnT concentration of 0.04 microg/l but not 0.10 microg/l, significantly more patients had severe coronary artery disease and a positive DSE result. The total ischaemic burden during DSE was similar in cTnT positive and negative patients, irrespective of the cut off concentration used. LV end systolic diameter index and E:Ea ratio were independent predictors of cTnT rises > or = 0.04 microg/l and > or = 0.10 microg/l, respectively. Diabetes was independently associated with cTnT at both cut off concentrations. Mortality was higher in all patients with raised cTnT.
  
  
  CONCLUSIONS
  Patients with ESRD with raised cTnT concentrations have increased mortality. Raised concentrations are strongly associated with diabetes, LV dilatation, and impaired LV systolic and diastolic function, but not with severe coronary artery disease.
authors.affiliation: Department of Cardiology, St George's Hospital, London, UK. rajdoc.Sharma@tiscali.co.uk
authors.forename: R
authors.initials: R
authors.lastname: Sharma
authors.forename: D C
authors.initials: DC
authors.lastname: Gaze
authors.forename: D
authors.initials: D
authors.lastname: Pellerin
authors.forename: R L
authors.initials: RL
authors.lastname: Mehta
authors.forename: H
authors.initials: H
authors.lastname: Gregson
authors.forename: C P
authors.initials: CP
authors.lastname: Streather
authors.forename: P O
authors.initials: PO
authors.lastname: Collinson
authors.forename: S J D
authors.initials: SJ
authors.lastname: Brecker
mesh_terms: D002311:Cardiomyopathy, Dilated / Q000378:metabolism; D003925:Diabetic Angiopathies / Q000378:metabolism; D004452:Echocardiography; D025401:Echocardiography, Stress; D005260:Female; D006331:Heart Diseases / Q000401:mortality / Q000473:pathology* / Q000503:physiopathology*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000401:mortality; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000378:metabolism; D010446:Peptide Fragments / Q000378:metabolism; D011446:Prospective Studies; D020107:Troponin T / Q000378:metabolism*; D018487:Ventricular Dysfunction, Left / Q000378:metabolism
chemical_list: D010446:Peptide Fragments; D020107:Troponin T; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain