CLINICAL RESEARCH
Toward clinical risk assessment inhypertrophic cardiomyopathy withgadolinium cardiovascular magnetic resonance
James C. C. Moon, MB, BCh*,
William J. McKenna, FACC, FESC ,
Jane A. McCrohon, FRACP, PhD*,
Perry M. Elliott, MD, MRCP, FACC,
Gillian C. Smith, BSc* and
Dudley J. Pennell, MD, FRCP, FESC, FACC*,*
* Centre for Advanced Magnetic Resonance in Cardiology (CAMRIC), Royal Brompton Hospital, London, United Kingdom
Department of Cardiological Sciences, St. George’s Hospital Medical School, London, United Kingdom
Manuscript received May 20, 2002;
revised manuscript received September 25, 2002,
accepted October 4, 2002.
* Reprint requests and correspondence: Dr. Dudley J. Pennell, Professor of Cardiology, CMR Unit, Royal Brompton Hospital, Sydney Street, London SW3 6NP, United Kingdom.
d.pennell{at}ic.ac.uk
OBJECTIVES: We sought to assess whether hyperenhancement by gadolinium cardiovascular magnetic resonance (CMR) occurs in hypertrophic cardiomyopathy (HCM) and correlates with the risk of heart failure and sudden death.
BACKGROUND: The myocardial interstitium is abnormal in HCM at post-mortem. Focally increased interstitial myocardial space appears as hyperenhancement with gadolinium CMR.
METHODS: In a blinded, prospective study, HCM patients were selected for the presence (n = 23) or absence (n = 30) of an increased clinical risk of sudden death and/or progressive adverse left ventricular (LV) remodeling. Gadolinium-enhanced CMR was performed.
RESULTS: Myocardial hyperenhancement was found in 42 patients (79%), affecting 10.9% (range 0% to 48%) of the LV mass. There was a greater extent of hyperenhancement in patients with progressive disease (28.5% vs. 8.7%, p < 0.001) and in patients with two or more risk factors for sudden death (15.7% vs. 8.6%, p = 0.02). Improved discrimination was seen in patients >40 years old (29.6% vs. 6.7%, p < 0.001) for progressive disease and for patients <40 years old for risk factors for sudden death (15.7% vs. 2.1%, p = 0.002). Patients with diffuse rather than confluent enhancement had two or more risk factors for sudden death (87% vs. 33%, p = 0.01).
CONCLUSIONS: Gadolinium CMR reveals myocardial hyperenhancement in HCM. The extent of hyperenhancement is associated with progressive ventricular dilation and markers of sudden death.
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Abbreviations and Acronyms
| | CMR | = cardiovascular magnetic resonance | | DTPA | = diethylenetriaminepentaacetic acid | | FISP | = fast imaging with steady-state precession | | HCM | = hypertrophic cardiomyopathy | | LV | = left ventricle/ventricular | | LVH | = left ventricular hypertrophy |
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H. P. Kuhl
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A. S. Flett, M. A. Westwood, L. C. Davies, A. Mathur, and J. C. Moon
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A. Grace
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A Esposito, F De Cobelli, G Perseghin, and A D. Maschio
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A. Attili, G. C. Mueller, and S. M. Day
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S. Nazarian, D. A. Bluemke, and H. R. Halperin
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A. Rudolph, H. Abdel-Aty, S. Bohl, P. Boye, A. Zagrosek, R. Dietz, and J. Schulz-Menger
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M. L. Chuang and W. J. Manning
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S. Sen-Chowdhry, P. Syrris, S. K. Prasad, S. E. Hughes, R. Merrifield, D. Ward, D. J. Pennell, and W. J. McKenna
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E. Belloni, F. De Cobelli, A. Esposito, R. Mellone, G. Perseghin, T. Canu, and A. Del Maschio
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W P Bandettini and A E Arai
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M. S. Maron, J. J. Finley, J. M. Bos, T. H. Hauser, W. J. Manning, T. S. Haas, J. R. Lesser, J. E. Udelson, M. J. Ackerman, and B. J. Maron
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P Elliott and P Spirito
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T. H. Marwick and M. Schwaiger
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M. S. Maron, E. Appelbaum, C. J. Harrigan, J. Buros, C. M. Gibson, C. Hanna, J. R. Lesser, J. E. Udelson, W. J. Manning, and B. J. Maron
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J. Schulz-Menger, H. Abdel-Aty, A. Rudolph, T. Elgeti, D. Messroghli, W. Utz, P. Boye, S. Bohl, A. Busjahn, B. Hamm, et al.
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N. Reichek and D. Gupta
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T. D. Henry, J. R. Lesser, and D. Satran
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B. J. Schietinger, G. M. Brammer, H. Wang, J. M. Christopher, K. W. Kwon, A. J. Mangrum, J. M. Mangrum, and C. M. Kramer
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S. Sen-Chowdhry and W. J. McKenna
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B. Sotgia, R. Sciagra, I. Olivotto, G. Casolo, L. Rega, I. Betti, A. Pupi, P. G. Camici, and F. Cecchi
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I. S. Syed, S. R. Ommen, J. F. Breen, and A. J. Tajik
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A. S. Adabag, B. J. Maron, E. Appelbaum, C. J. Harrigan, J. L. Buros, C. M. Gibson, J. R. Lesser, C. A. Hanna, J. E. Udelson, W. J. Manning, et al.
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T. Germans and A. C van Rossum
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M. W. Hansen and N. Merchant
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M. W. Hansen and N. Merchant
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R. G Assomull, D. J Pennell, and S. K Prasad
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S. E. Petersen, M. Jerosch-Herold, L. E. Hudsmith, M. D. Robson, J. M. Francis, H. A. Doll, J. B. Selvanayagam, S. Neubauer, and H. Watkins
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