title: Delayed contrast enhancement and perfusable tissue index in hypertrophic cardiomyopathy: comparison between cardiac MRI and PET.
abstract: Delayed contrast enhancement (DCE) visualized by cardiac MRI (CMR) is a common feature in patients with hypertrophic cardiomyopathy (HCM), presumed to be related to myocardial fibrosis. The pathophysiologic basis of hyperenhancement in this patient group, however, remains unclear as limited histologic comparisons are available. The present study compares the perfusable tissue index (PTI), an alternative marker of myocardial fibrosis obtained by PET, with DCE-CMR in HCM.
  
  
  METHODS
  Twenty-one patients with asymmetric septal HCM, 12 chronic myocardial infarction (MI) patients, and 6 age-matched healthy control subjects were studied with DCE-CMR and PET. PET was performed using (15)O-labeled water and carbon monoxide to obtain the PTI.
  
  
  RESULTS
  No hyperenhancement was observed in control subjects and the PTI was within normal limits (1.10 +/- 0.07 [mean +/- SD]). In MI patients, the extent of hyperenhancement (25% +/- 16% [mean +/- SD]) was inversely related to the decrease in the PTI (0.94 +/- 0.12; r = -0.65, P < 0.05). Average hyperenhancement in HCM was 14% +/- 12%, predominantly located in the interventricular septum. The PTI in the hypertrophied interventricular septum, however, was not reduced (1.12 +/- 0.13). Furthermore, in contrast to MI patients, there was a modest positive correlation between the extent of DCE and the PTI in HCM (r = 0.45, P < 0.05).
  
  
  CONCLUSIONS
  DCE in the hypertrophied septum of HCM patients is not accompanied by a decline in the PTI, and there is a positive correlation between the extent of DCE and the PTI. These results suggest that hyperenhancement may not be caused solely by fibrotic replacement scarring in this patient group. Other pathologic changes associated with HCM may also cause gadolinium-diethylenetriaminepentaacetic acid hyperenhancement.
authors.affiliation: Department of Cardiology, 6D 120 VU University Medical Center, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands. p.knaapen@vumc.nl
authors.forename: Paul
authors.initials: P
authors.lastname: Knaapen
authors.forename: Willem G
authors.initials: WG
authors.lastname: van Dockum
authors.forename: Olga
authors.initials: O
authors.lastname: Bondarenko
authors.forename: Wouter E M
authors.initials: WE
authors.lastname: Kok
authors.forename: Marco J W
authors.initials: MJ
authors.lastname: Götte
authors.forename: Ronald
authors.initials: R
authors.lastname: Boellaard
authors.forename: Aernout M
authors.initials: AM
authors.lastname: Beek
authors.forename: Cees A
authors.initials: CA
authors.lastname: Visser
authors.forename: Albert C
authors.initials: AC
authors.lastname: van Rossum
authors.forename: Adriaan A
authors.initials: AA
authors.lastname: Lammertsma
authors.forename: Frans C
authors.initials: FC
authors.lastname: Visser
mesh_terms: D000328:Adult; D000368:Aged; D002248:Carbon Monoxide / Q000737:chemistry; D002312:Cardiomyopathy, Hypertrophic / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology; D016022:Case-Control Studies; D002908:Chronic Disease; D005260:Female; D005355:Fibrosis; D019786:Gadolinium DTPA / Q000737:chemistry; D006346:Heart Septum / Q000000981:diagnostic imaging / Q000473:pathology; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D010104:Oxygen Radioisotopes / Q000737:chemistry; D049268:Positron-Emission Tomography; D019275:Radiopharmaceuticals / Q000737:chemistry; D014867:Water / Q000737:chemistry
chemical_list: D010104:Oxygen Radioisotopes; D019275:Radiopharmaceuticals; D014867:Water; D002248:Carbon Monoxide; D019786:Gadolinium DTPA