title: Evaluation of diffuse myocardial fibrosis in heart failure with cardiac magnetic resonance contrast-enhanced T1 mapping.
abstract: OBJECTIVE
  The purpose of this study was to investigate a noninvasive method for quantifying diffuse myocardial fibrosis with cardiac magnetic resonance imaging (CMRI).
  
  
  BACKGROUND
  Diffuse myocardial fibrosis is a fundamental process in pathologic remodeling in cardiomyopathy and is postulated to cause increased cardiac stiffness and poor clinical outcomes. Although regional fibrosis is easily imaged with cardiac magnetic resonance, there is currently no noninvasive method for quantifying diffuse myocardial fibrosis.
  
  
  METHODS
  We performed CMRI on 45 subjects (25 patients with heart failure, 20 control patients), on a clinical 1.5-T CMRI scanner. A prototype T(1) mapping sequence was used to calculate the post-contrast myocardial T(1) time as an index of diffuse fibrosis; regional fibrosis was identified by delayed contrast enhancement. Regional and global systolic function was assessed by cine CMRI in standard short- and long-axis planes, with echocardiography used to evaluate diastology. An additional 9 subjects underwent CMRI and endomyocardial biopsy for histologic correlation.
  
  
  RESULTS
  Post-contrast myocardial T(1) times correlated histologically with fibrosis (R = -0.7, p = 0.03) and were shorter in heart failure subjects than controls (383 +/- 17 ms vs. 564 +/- 23 ms, p < 0.0001). The T(1) time of heart failure myocardium was shorter than that in controls even when excluding areas of regional fibrosis (429 +/- 22 ms vs. 564 +/- 23 ms, p < 0.0001). The post-contrast myocardial T(1) time shortened as diastolic function worsened (562 +/- 24 ms in normal diastolic function vs. 423 +/- 33 ms in impaired diastolic function vs. 368 +/- 20 ms in restrictive function, p < 0.001).
  
  
  CONCLUSIONS
  Contrast-enhanced CMRI T(1) mapping identifies changes in myocardial T(1) times in heart failure, which appear to reflect diffuse fibrosis.
authors.affiliation: Alfred Hospital and Baker IDI Heart and Diabetes Institute, Melbourne, Australia.
authors.forename: Leah
authors.initials: L
authors.lastname: Iles
authors.forename: Heinz
authors.initials: H
authors.lastname: Pfluger
authors.forename: Arintaya
authors.initials: A
authors.lastname: Phrommintikul
authors.forename: Joshi
authors.initials: J
authors.lastname: Cherayath
authors.forename: Pelin
authors.initials: P
authors.lastname: Aksit
authors.forename: Sandeep N
authors.initials: SN
authors.lastname: Gupta
authors.forename: David M
authors.initials: DM
authors.lastname: Kaye
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Taylor
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D018780:Body Surface Potential Mapping; D016022:Case-Control Studies; D005260:Female; D005355:Fibrosis / Q000175:diagnosis; D019786:Gadolinium DTPA; D006333:Heart Failure / Q000175:diagnosis*; D054144:Heart Failure, Diastolic / Q000175:diagnosis; D054143:Heart Failure, Systolic / Q000175:diagnosis; D006801:Humans; D007089:Image Enhancement / Q000379:methods*; D007091:Image Processing, Computer-Assisted; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D011336:Probability; D011446:Prospective Studies; D012016:Reference Values; D012720:Severity of Illness Index
chemical_list: D019786:Gadolinium DTPA