Delayed contrast enhancement and perfusable tissue index in hypertrophic cardiomyopathy: comparison between cardiac

Paul Knaapen1, Willem G van Dockum, Olga Bondarenko

  • 1Department of Cardiology, 6D 120 VU University Medical Center, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands. p.knaapen@vumc.nl

Abstract

Insights

Delayed contrast enhancement (DCE) in hypertrophic cardiomyopathy (HCM) may not solely indicate fibrosis. Perfusable tissue index (PTI) measured by PET shows a positive correlation with DCE in HCM, unlike in myocardial infarction (MI).

Area of Science:

  • Cardiovascular Imaging
  • Cardiology
  • Medical Physics

Background:

  • Delayed contrast enhancement (DCE) on cardiac MRI (CMR) is common in hypertrophic cardiomyopathy (HCM), often attributed to myocardial fibrosis.
  • The exact pathophysiologic basis of this hyperenhancement in HCM remains unclear due to limited histologic data.

Purpose of the Study:

  • To compare DCE-CMR findings with perfusable tissue index (PTI) measured by Positron Emission Tomography (PET) as a marker of myocardial fibrosis in HCM patients.
  • To investigate the relationship between DCE and PTI in HCM and contrast it with findings in myocardial infarction (MI).

Main Methods:

  • Twenty-one HCM patients, 12 MI patients, and 6 healthy controls underwent DCE-CMR and PET.
  • PET utilized (15)O-labeled water and carbon monoxide to quantify PTI.

Main Results:

  • In healthy controls, PTI was normal and no hyperenhancement was observed.
  • In MI patients, hyperenhancement correlated inversely with decreased PTI (r = -0.65, P < 0.05).
  • In HCM, hyperenhancement (14% +/- 12%) was predominantly in the septum, but PTI in the hypertrophied septum was not reduced (1.12 +/- 0.13). A positive correlation was found between DCE extent and PTI in HCM (r = 0.45, P < 0.05).

Conclusions:

  • Hyperenhancement in the hypertrophied septum of HCM patients is not associated with reduced PTI.
  • The positive correlation between DCE and PTI in HCM suggests hyperenhancement may involve factors beyond fibrotic scarring.
  • Other pathological changes in HCM might contribute to gadolinium-diethylenetriaminepentaacetic acid (Gd-DTPA) enhancement observed on CMR.