Volume 11 Supplement 1

Abstracts of the 12th Annual SCMR Scientific Sessions – 2009

Open Access

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

  • James A White1,
  • Sarah Armstrong2,
  • Mohammed Al-Admawi2,
  • Sherryn Rambihar2,
  • Gerald Wisenberg2,
  • Ivonna Verschuur1,
  • Anna MacDonald2,
  • Cyndi Harper-Little3,
  • Aaron So3,
  • Ting-Yim Lee4,
  • Frank Prato4 and
  • Terry Thomspon4
Journal of Cardiovascular Magnetic Resonance200911(Suppl 1):P55

https://doi.org/10.1186/1532-429X-11-S1-P55

Published: 28 January 2009

Background

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.

Methods

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.

Results

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.

Conclusion

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.

Authors’ Affiliations

(1)
Dept. of Medicine and Lawson Health Research Institute and Robarts Research Institute, University of Western Ontario
(2)
Dept. of Medicine, University of Western Ontario
(3)
Robarts Research Institute, University of Western Ontario
(4)
Lawson Health Research Institute, University of Western Ontario

Copyright

© White et al; licensee BioMed Central Ltd. 2009

This article is published under license to BioMed Central Ltd.

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