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Evidence for microvascular dysfunction in hypertrophic cardiomyopathy: new insights from multiparametric magnetic

Steffen E Petersen1, Michael Jerosch-Herold, Lucy E Hudsmith

  • 1University of Oxford Centre for Clinical Magnetic Resonance Research, Department of Cardiovascular Medicine, John Radcliffe Hospital, Oxford, OX3 9DU, UK. steffen.petersen@cardiov.ox.ac.uk

Circulation
|April 25, 2007
PubMed

Insights

In hypertrophic cardiomyopathy (HCM), reduced blood flow reserve is linked to greater heart muscle thickness and fibrosis. This microvascular dysfunction may increase sudden cardiac death risk in HCM patients.

Area of Science:

  • Cardiology
  • Cardiovascular Imaging
  • Myocardial Perfusion

Background:

  • Microvascular dysfunction in hypertrophic cardiomyopathy (HCM) may contribute to sudden cardiac death.
  • The relationship between the degree of cardiac hypertrophy and impaired perfusion reserve in HCM is not well understood.
  • Multiparametric imaging is needed to explore hypertrophy, perfusion, and fibrosis for risk stratification.

Purpose of the Study:

  • To investigate the association between the extent of left ventricular hypertrophy and myocardial perfusion reserve in HCM patients.
  • To compare myocardial blood flow (MBF) and fibrosis in HCM patients versus healthy controls.
  • To determine if hypertrophy magnitude correlates with reduced perfusion reserve and increased fibrosis.

Main Methods:

  • Magnetic resonance imaging (MRI) was used to assess hypertrophy, resting and hyperemic myocardial blood flow (hMBF), and fibrosis in 35 HCM patients and 14 controls.
  • The American Heart Association 16-segment model of the left ventricle was utilized.
  • Statistical analyses adjusted for multiple variables, including end-diastolic wall thickness.

Main Results:

  • HCM patients exhibited significantly lower hMBF compared to controls, independent of wall thickness.
  • In HCM patients, hMBF decreased proportionally with increasing end-diastolic wall thickness, particularly in the endocardial layer.
  • Increased wall thickness correlated with a higher frequency of endocardial hMBF falling below epicardial hMBF and a greater incidence of myocardial fibrosis.

Conclusions:

  • Hypertrophic cardiomyopathy is characterized by a reduced vasodilator response, especially in the endocardium, which is proportional to the degree of hypertrophy.
  • Microvascular dysfunction and resulting ischemia are likely significant contributors to the risk of sudden cardiac death in HCM.
  • These findings suggest that multiparametric MRI assessment of hypertrophy, perfusion, and fibrosis could enhance risk stratification in HCM.
Abstract

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