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Abnormal myocardial perfusion in hypertrophic cardiomyopathy: preliminary findings of a cardiovascular MRI study


Reduced myocardial perfusion has been speculated as a potential mechanism for the development and/or propagation of myocardial fibrosis in hypertrophic cardiomyopathy (HCM). This study aims to evaluate the prevalence, distribution and extent of stress-induced perfusion abnormalities and their relationship to underlying fibrosis in patients with HCM using magnetic resonance imaging.


15 patients with echocardiographically diagnosed HCM have been enrolled. Cine imaging, first-pass stress perfusion imaging using vasodilator stress (Dipyridamole), and delayed gadolinium enhancement imaging were performed. Stress hypoperfusion and delayed enhancement images were assessed both quantitatively and visually using a 16-segment model. Conversion of segmental visual scoring to % of LV by volume was achieved for both hypoperfusion (HP) and late enhancement (LE) using a standardized scoring system. For quantitative assessment prospectively defined cut-offs for LE and HP were used.


Maximal wall thickness ranged from 13 to 22 mm (mean 17 ± 2.6 mm). Non-ischemic pattern LE was present in 70% of patients. Perfusion abnormalities were identified on stress perfusion images in 80% of patients using visual analysis and 87% of patients using quantitative analysis. Perfusion abnormalities were predominantly subendocardial, and were regionally associated with segments containing LE (p < 0.01). Mean percent HP and mean percent LE were 17 ± 8.4% and 10 ± 9.3%, respectively by visual estimation and 20.0 ± 12.1% and 14.0 ± 7.4%, respectively by quantitative assessment. Figure 1.

Figure 1

Short axis cine (top) , delayed contrast (middle row) and stress perfusion (bottom row) images in a patient with apical hypertrophic cardiomyopathy. Stress perfusion abnormalities seen corresponding to (white arrows) and distinct from (yellow arrows) established fibrosis.


These preliminary results suggest that patients with HCM have a high prevalence of stress-induced myocardial hypoperfusion as represented by reduced first-pass gadolinium enhancement during vasodilator stress. This hypoperfusion appears to extend beyond regions of established LE suggesting a potential contribution of ischemia in the development and/or propagation of myocardial fibrosis in patients with HCM.

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Correspondence to James A White.

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Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution 2.0 International License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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White, J.A., Armstrong, S., Al-Admawi, M. et al. Abnormal myocardial perfusion in hypertrophic cardiomyopathy: preliminary findings of a cardiovascular MRI study. J Cardiovasc Magn Reson 11, P55 (2009).

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  • Myocardial Perfusion
  • Hypertrophic Cardiomyopathy
  • Myocardial Fibrosis
  • Perfusion Abnormality
  • Stress Perfusion