Author + information
- Received April 9, 2018
- Revision received October 1, 2018
- Accepted October 10, 2018
- Published online August 5, 2019.
- Ankur Gulati, MDa,∗,
- Tevfik F. Ismail, PhDb,∗,
- Aamir Ali, MDa,c,
- Li-Yueh Hsu, DScd,
- Carla Gonçalves, MDa,
- Nizar A. Ismail, MDa,c,
- Kaushiga Krishnathasan, MDa,c,
- Natasha Davendralingam, MDa,c,
- Pedro Ferreira, PhDa,c,
- Brian P. Halliday, MDa,c,
- Daniel A. Jones, MD, PhDe,
- Ricardo Wage, DCRa,
- Simon Newsome, MScf,
- Peter Gatehouse, PhDa,c,
- David Firmin, PhDa,c,
- Andrew Jabbour, PhDa,
- Ravi G. Assomull, MDa,
- Anthony Mathur, MD, PhDe,
- Dudley J. Pennell, MDa,c,∗ (, )
- Andrew E. Arai, MD, PhDd,† and
- Sanjay K. Prasad, MDa,c,†
- aRoyal Brompton Hospital, London, United Kingdom
- bKing’s College London, London, United Kingdom
- cImperial College London, London, United Kingdom
- dNational Institutes of Health, Bethesda, Maryland
- eDepartment of Cardiology, Bart’s Health NHS Trust, London, United Kingdom
- fLondon School of Hygiene and Tropical Medicine, London, United Kingdom
- ↵∗Address for correspondence:
Prof. Dudley J. Pennell, Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital, Sydney Street, London SW3 6NP, United Kingdom.
Objectives This study sought to quantify myocardial blood flow (MBF) and myocardial perfusion reserve (MPR) in dilated cardiomyopathy (DCM) and examine the relationship between myocardial perfusion and adverse left ventricular (LV) remodeling.
Background Although regarded as a nonischemic condition, DCM has been associated with microvascular dysfunction, which is postulated to play a role in its pathogenesis. However, the relationship of the resulting perfusion abnormalities to myocardial fibrosis and the degree of LV remodeling is unclear.
Methods A total of 65 patients and 35 healthy control subjects underwent adenosine (140 μg/kg/min) stress perfusion cardiovascular magnetic resonance with late gadolinium enhancement imaging. Stress and rest MBF and MPR were derived using a modified Fermi-constrained deconvolution algorithm.
Results Patients had significantly higher global rest MBF compared with control subjects (1.73 ± 0.42 ml/g/min vs. 1.14 ± 0.42 ml/g/min; p < 0.001). In contrast, global stress MBF was significantly lower versus control subjects (3.07 ± 1.02 ml/g/min vs. 3.53 ± 0.79 ml/g/min; p = 0.02), resulting in impaired MPR in the DCM group (1.83 ± 0.58 vs. 3.50 ± 1.45; p < 0.001). Global stress MBF (2.70 ± 0.89 ml/g/min vs. 3.44 ± 1.03 ml/g/min; p = 0.017) and global MPR (1.67 ± 0.61 vs. 1.99 ± 0.50; p = 0.047) were significantly reduced in patients with DCM with LV ejection fraction ≤35% compared with those with LV ejection fraction >35%. Segments with fibrosis had lower rest MBF (mean difference: −0.12 ml/g/min; 95% confidence interval: −0.23 to −0.01 ml/g/min; p = 0.035) and lower stress MBF (mean difference: −0.15 ml/g/min; 95% confidence interval: −0.28 to −0.03 ml/g/min; p = 0.013).
Conclusions Patients with DCM exhibit microvascular dysfunction, the severity of which is associated with the degree of LV impairment. However, rest MBF is elevated rather than reduced in DCM. If microvascular dysfunction contributes to the pathogenesis of DCM, then the underlying mechanism is more likely to involve stress-induced repetitive stunning rather than chronic myocardial hypoperfusion.
- cardiovascular magnetic resonance imaging
- dilated cardiomyopathy
- microvascular dysfunction
- myocardial blood flow
- myocardial perfusion imaging
↵∗ Drs. Gulati and Ismail contributed equally to this work and are joint first authors.
↵† Drs. Arai and Prasad contributed equally to this work and are joint senior authors.
This work was supported by the National Institute for Health Research Cardiovascular Biomedical Research Unit at the Royal Brompton and Harefield NHS Foundation Trust and Imperial College, London, England. Drs. Arai and Hsu were funded by the Intramural Research Program of the National Heart, Lung, and Blood Institute, and National Institutes of Health (HL 006137–07). Dr. Gulati has received grant support from the National Institute for Health Research, CORDA, and Rosetrees Trust. Dr. Gatehouse has a research agreement with Siemens. Dr. Firmin has a research agreement with Siemens. Prof. Mathur received grant support from the Heart Cells Foundation and Barts and the London Charity. Prof. Pennell has received grant support from the National Institute for Health Research and the British Heart Foundation; has received research support from Siemens; served as a consultant to Siemens, Novartis, ApoPharma, AMAG, and Bayer; and served as the director and owns stock in Cardiovascular Imaging Solutions. Dr. Arai has a research agreement with Siemens and a clinical trial agreement with Bayer. Dr. Prasad has received grant support from the British Heart Foundation, CORDA, Rosetrees Trust, the Alexander Jansons Foundation, and the National Institute for Health Research; and has received speaking fees from Bayer Schering. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received April 9, 2018.
- Revision received October 1, 2018.
- Accepted October 10, 2018.
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