Relation of coronary microvascular dysfunction in hypertrophic cardiomyopathy to contractile dysfunction independent

Stefan A J Timmer1, Tjeerd Germans, Marco J W Götte

  • 1Department of Cardiology, VU University Medical Center, Amsterdam, The Netherlands.

Insights

Hypertrophic cardiomyopathy (HC) impairs hyperemic myocardial blood flow (hMBF) and contractile function, independent of tissue alterations. Delayed contrast enhancement (DCE) indicates disease progression with reduced perfusion and function.

Area of Science:

  • Cardiology
  • Medical Imaging
  • Physiology

Background:

  • Hypertrophic cardiomyopathy (HC) is a complex disease affecting myocardial structure and function.
  • Understanding the interplay between blood flow, contractility, and tissue changes is crucial for managing HC.

Purpose of the Study:

  • To investigate the spatial relationships among hyperemic myocardial blood flow (hMBF), contractile function (E(cc)), and morphologic tissue alterations (delayed contrast enhancement - DCE) in patients with HC.
  • To compare these parameters between HC patients and healthy controls.

Main Methods:

  • Utilized oxygen-15 water positron emission tomography (PET) for assessing myocardial perfusion at rest and during adenosine stress.
  • Employed cardiovascular magnetic resonance (CMR) with tissue tagging to calculate E(cc) and derive DCE images.
  • Included 19 HC patients and 11 healthy controls in the study.

Main Results:

  • HC patients exhibited significantly reduced hMBF and E(cc) compared to controls.
  • DCE was observed exclusively in HC patients, indicating myocardial scarring or fibrosis.
  • Impaired hMBF and E(cc) were noted in segments with DCE, suggesting a link between perfusion deficits, dysfunction, and tissue damage.
  • Multivariate analysis confirmed E(cc) was independently related to both hMBF and DCE.

Conclusions:

  • In HC, hMBF is impaired and linked to contractile dysfunction, irrespective of DCE presence.
  • DCE in HC signifies a more advanced disease state, characterized by increased perfusion deficits and worsened contractile function.

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