Author + information
- Received March 14, 2016
- Revision received July 14, 2016
- Accepted July 20, 2016
- Published online October 11, 2016.
- S0735109716348860-5ede3a7caf7e934681311bb77e5197e0Claire E. Raphael, MD, PhDa,∗ (, )
- S0735109716348860-f9bc368522d1fc510a785e97f4c3a048Robert Cooper, PhDb,
- S0735109716348860-7fce57ae8c8b0c194fc1dd312f34f18cKim H. Parker, PhDc,
- S0735109716348860-57d19e7b278d03b3b6edb7e6c041a6e2Julian Collinson, MDa,
- S0735109716348860-f98e69de2342684d88008afc838938b5Vassilis Vassiliou, MAa,
- S0735109716348860-219836a6f29d1b4b7dc6cf69b0cb9418Dudley J. Pennell, MDa,
- S0735109716348860-98531950c27932544363ff3da734a123Ranil de Silva, PhDa,
- S0735109716348860-080f5722f11a547e2706386571bd721bLi Yueh Hsu, PhDd,
- S0735109716348860-7f06cabf09ee5ac7cf2ad72caba26931Anders M. Greve, PhDd,
- S0735109716348860-8adfca8b8bcdc9405623e32caaca34e6Sukh Nijjer, PhDe,
- S0735109716348860-792b1a6bc582c348b3ec3b5dca324cedChris Broyd, PhDe,
- S0735109716348860-84029fd88f7726f4ef5deb2153464f86Aamir Ali, MDa,
- S0735109716348860-9a45a985905b64e5692a58a74936826eJennifer Keegan, PhDa,
- S0735109716348860-f66450e82c1dc89938244c98be158a5fDarrel P. Francis, MDe,
- S0735109716348860-26c8945ebd98c08f46bbc8090989a882Justin E. Davies, PhDe,
- S0735109716348860-610170a6e3dcdc0e629de3f25c787731Alun D. Hughes, PhDf,
- S0735109716348860-48dd67348991a01ee32d775bd4f4f4fdAndrew Arai, MDd,
- S0735109716348860-ab94c4b90dd4adc0bf529be98483f2ffMichael Frenneaux, PhDg,
- S0735109716348860-dbba8f7e7043d9cab0878fb399eb5172Rod H. Stables, MDb,
- S0735109716348860-01e2e73d6355d22b61fef7f3fda79eb8Carlo Di Mario, MD, PhDa and
- S0735109716348860-7024abed1c001d399b4c2fef5d82d19dSanjay K. Prasad, MDa
- aNIHR Cardiovascular Biomedical Research Unit, Royal Brompton Hospital, London, United Kingdom
- bInstitute of Cardiovascular Medicine and Science, Liverpool Heart and Chest Hospital, Liverpool, United Kingdom
- cDepartment of Bioengineering, Imperial College, London, United Kingdom
- dNational Institutes of Health, Bethesda, Maryland
- eInternational Centre for Circulatory Health, Imperial College, London, United Kingdom
- fUniversity College London, London, United Kingdom
- gDepartment of Cardiology, University of East Anglia, Norwich, United Kingdom
- ↵∗Reprint requests and correspondence:
Dr. Claire E. Raphael, NIHR Cardiovascular Biomedical Research Unit, Royal Brompton Hospital, Sydney Street, London SW3 6NP, United Kingdom.
Background Angina is common in hypertrophic cardiomyopathy (HCM) and is associated with abnormal myocardial perfusion. Wave intensity analysis improves the understanding of the mechanics of myocardial ischemia.
Objectives Wave intensity analysis was used to describe the mechanisms underlying perfusion abnormalities in patients with HCM.
Methods Simultaneous pressure and flow were measured in the proximal left anterior descending artery in 33 patients with HCM and 20 control patients at rest and during hyperemia, allowing calculation of wave intensity. Patients also underwent quantitative first-pass perfusion cardiac magnetic resonance to measure myocardial perfusion reserve.
Results Patients with HCM had a lower coronary flow reserve than control subjects (1.9 ± 0.8 vs. 2.7 ± 0.9; p = 0.01). Coronary hemodynamics in HCM were characterized by a very large backward compression wave during systole (38 ± 11% vs. 21 ± 6%; p < 0.001) and a proportionately smaller backward expansion wave (27% ± 8% vs. 33 ± 6%; p = 0.006) compared with control subjects. Patients with severe left ventricular outflow tract obstruction had a bisferiens pressure waveform resulting in an additional proximally originating deceleration wave during systole. The proportion of waves acting to accelerate coronary flow increased with hyperemia, and the magnitude of change was proportional to the myocardial perfusion reserve (rho = 0.53; p < 0.01).
Conclusions Coronary flow in patients with HCM is deranged. Distally, compressive deformation of intramyocardial blood vessels during systole results in an abnormally large backward compression wave, whereas proximally, severe left ventricular outflow tract obstruction is associated with an additional deceleration wave. Perfusion abnormalities in HCM are not simply a consequence of supply/demand mismatch or remodeling of the intramyocardial blood vessels; they represent a dynamic interaction with the mechanics of myocardial ischemia that may be amenable to treatment.
This study was funded by the British Heart Foundation (FS/14/13/30619), Rosetrees, and the NIHR Biomedical Research Unit. Dr. Raphael was funded by the British Heart Foundation (FS/14/13/30619), Rosetrees, and the Wellcome Trust. Dr. Prasad has received honoraria for talks for Bayer-Schering. Dr. Pennell has received consultancy fees from Siemens and Bayer-Schering; and is a director for and stockowner in Cardiovascular Imaging Solutions. Dr. Davies is a consultant to and receives research grants from Volcano-Philips. Dr. Arai has received research agreements with Siemens and Bayer. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received March 14, 2016.
- Revision received July 14, 2016.
- Accepted July 20, 2016.
- The Authors