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Blunted myocardial oxygenation response during vasodilator stress in patients with hypertrophic cardiomyopathy

Theodoros D Karamitsos1, Sairia Dass, Joseph Suttie

  • 1University of Oxford Centre for Clinical Magnetic Resonance Research, Department of Cardiovascular Medicine, John Radcliffe Hospital, Oxford, United Kingdom. theo.karamitsos@cardiov.ox.ac.uk

Journal of the American College of Cardiology
|March 19, 2013
PubMed

Insights

Myocardial perfusion and oxygenation are impaired in patients with hypertrophic cardiomyopathy (HCM). However, HCM mutation carriers without left ventricular hypertrophy show only impaired oxygenation, suggesting a novel risk factor for HCM assessment.

Area of Science:

  • Cardiovascular Imaging
  • Cardiology
  • Biomedical Engineering

Background:

  • Myocardial perfusion impairment is known in hypertrophic cardiomyopathy (HCM) patients under vasodilator stress.
  • The association between impaired perfusion, myocardial oxygenation, and tissue ischemia in HCM is not fully understood.
  • The impact of vasodilator stress on perfusion and oxygenation in HCM mutation carriers without left ventricular hypertrophy (LVH) remains unclear.

Purpose of the Study:

  • To evaluate myocardial perfusion and tissue oxygenation during vasodilator stress in patients with overt HCM.
  • To compare these findings in HCM mutation carriers without LVH, athletes with comparable hypertrophy, and healthy controls.
  • To investigate potential novel risk factors in HCM using cardiovascular magnetic resonance (CMR).

Main Methods:

  • Cardiovascular magnetic resonance (CMR) scanning at 3-T was performed on 27 overt HCM patients, 10 HCM mutation carriers without LVH, 11 athletes, and 20 controls.
  • Adenosine stress was used to assess myocardial function, perfusion reserve index (MPRI), and blood-oxygen-level-dependent signal intensity (SI) change for oxygenation.
  • Quantitative analysis of perfusion and oxygenation responses was conducted for all groups.

Main Results:

  • MPRI was significantly reduced in overt HCM patients compared to controls and athletes.
  • HCM mutation carriers without LVH demonstrated normal MPRI but impaired oxygenation response to adenosine.
  • Overt HCM patients showed attenuated oxygenation response, while athletes had normal stress perfusion and oxygenation.

Conclusions:

  • Overt HCM is characterized by impaired myocardial perfusion and oxygenation during vasodilator stress.
  • HCM mutation carriers without LVH exhibit impaired myocardial oxygenation, but not perfusion.
  • CMR assessment of myocardial oxygenation shows promise as a novel risk factor for HCM.
Abstract

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