Author + information
- Received September 5, 2012
- Revision received November 10, 2012
- Accepted December 9, 2012
- Published online March 19, 2013.
- Theodoros D. Karamitsos, MD, PhD⁎,⁎ (, )
- Sairia Dass, DPhil⁎,
- Joseph Suttie, DPhil⁎,
- Emily Sever⁎,
- Jacqueline Birks, MA, MSc†,
- Cameron J. Holloway, DPhil⁎,
- Matthew D. Robson, PhD⁎,
- Michael Jerosch-Herold, PhD‡,
- Hugh Watkins, MD, PhD, FMedSci⁎ and
- Stefan Neubauer, MD, FMedSci⁎
- ↵⁎Reprint requests and correspondence:
Dr. Theodoros D. Karamitsos, Department of Cardiovascular Medicine, John Radcliffe Hospital, Headley Way, OX3 9DU Oxford, United Kingdom
Objectives This study sought to assess myocardial perfusion and tissue oxygenation during vasodilator stress in patients with overt hypertrophic cardiomyopathy (HCM), as well as in HCM mutation carriers without left ventricular (LV) hypertrophy, and to compare findings to those in athletes with comparable hypertrophy and normal controls.
Background Myocardial perfusion under vasodilator stress is impaired in patients with HCM. Whether this is associated with impaired myocardial oxygenation and tissue ischemia is unknown. Furthermore, it is not known whether perfusion and oxygenation are impaired in HCM mutation carriers without left ventricular hypertrophy (LVH).
Methods A total of 27 patients with overt HCM, 10 HCM mutation carriers without LVH, 11 athletes, and 20 healthy controls underwent cardiovascular magnetic resonance (CMR) scanning at 3-T. Myocardial function, perfusion (perfusion reserve index [MPRI]), and oxygenation (blood-oxygen level dependent signal intensity [SI] change) under adenosine stress were assessed.
Results MPRI was significantly reduced in HCM (1.3 ± 0.1) compared to controls (1.8 ± 0.1, p < 0.001) and athletes (2.0 ± 0.1, p < 0.001), but remained normal in HCM mutation carriers without LVH (1.7 ± 0.1; p = 0.61 vs. controls, p = 0.02 vs. overt HCM). Oxygenation response was attenuated in overt HCM (SI change 6.9 ± 1.4%) compared to controls (18.9 ± 1.4%, p < 0.0001) and athletes (18.7 ± 2.0%, p < 0.001). Interestingly, HCM mutation carriers without LVH also showed an impaired oxygenation response to adenosine (10.4 ± 2.0%; p = 0.001 vs. controls, p = 0.16 vs. overt HCM, p = 0.003 vs. athletes).
Conclusions In overt HCM, both perfusion and oxygenation are impaired during vasodilator stress. However, in HCM mutation carriers without LVH, only oxygenation is impaired. In athletes, stress perfusion and oxygenation are normal. CMR assessment of myocardial oxygenation has the potential to become a novel risk factor in HCM.
A patent application was filed on September 19, 2011 (Application Number GB1116140.3) by Dr. Karamitsos, Dr. Dass, Prof. Watkins, and Prof. Neubauer in conjunction with ISIS Innovation Ltd., claiming BOLD CMR as a method of detecting hypertrophic cardiomyopathy or the presence of a gene mutation for hypertrophic cardiomyopathy. This work was supported by a British Heart Foundation project grant (PG/08/101/26126). The authors acknowledge support from the National Institute for Health Research Oxford Biomedical Research Centre Programme. Stefan Neubauer and Hugh Watkins also acknowledge support from the Oxford British Heart Foundation Centre for Research Excellence. Dr. Neubauer is a consultant for Novartis, the topic of which is not related to the findings of this paper. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Drs. Karamitsos and Dass contributed equally to this work.
- Received September 5, 2012.
- Revision received November 10, 2012.
- Accepted December 9, 2012.
- American College of Cardiology Foundation