(Circulation. 2007;115:e430-e431.)
© 2007 American Heart Association, Inc.
Images in Cardiovascular Medicine |
From the Cardiovascular Magnetic Resonance and Computed Tomography Sector of Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil.
Correspondence to Carlos E. Rochitte, MD, PhD, Instituto do Coração, InCor, Setor de Ressonância Magnética e Tomografia Computadorizada Cardiovascular, Av. Dr. Enéas de Carvalho Aguiar, 44, Cerqueira César, São Paulo, SP Brazil 05403000. E-mail rochitte{at}incor.usp.br
A 35-year-old woman with a previous diagnosis of hypertrophic cardiomyopathy (HCM) was admitted to the Heart Institute of the University of São Paulo Medical School for recurrent palpitation and syncope. The patient had 2 brothers who already had been diagnosed with HCM, and her mother had died suddenly at the age of 38.
ECG revealed sinus-rhythm and leftbundle branch block. A tilt-table test was negative, and 24-hour Holter monitoring showed one isolated episode of nonsustained ventricular tachycardia with 3 beatings.
Echocardiography revealed hypertrophy of the septal (24 mm) and inferior walls (Movie I), with a maximum systolic gradient of 77 mm Hg. Left ventricular ejection fraction was estimated at 72%, and mass index was estimated at 268 g/m.2
Left ventricular hypertrophy was confirmed by cardiovascular magnetic resonance (CMR) and a 30-mm septum thickness was noted (Figure, A and D, and Movie II). Left ventricular ejection fraction was calculated (Simpson) at 77%, and mass index was calculated at 164 g/m2. Delayed enhancement by CMR demonstrated multiple foci of myocardial fibrosis, particularly in the septum and in its junctions with the right ventricular free wall, which has been correlated with the prevalence of risk factors for sudden death1 in HCM patients.
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The patient was then submitted to cardiac multidetector computed tomography (Aquilion 64, Toshiba Inc., Japan) 10 minutes after injection of 150 mL of iodine contrast (Iopamiron 370, Shering AG, Germany). Images by multidetector computed tomography showed multiple areas of delayed enhancement in the septum that precisely matched the CMR delayed-enhancement findings (Figure, B, C, E, and F).
On the basis of the overall risk factors and test results, the patient received an implantable cardioverterdefibrillator.
Recently, myocardial fibrosis has been identified in ischemic patients by multidetector computed tomography, demonstrating infarcted areas similarly to CMR.2,3
To our knowledge, this is the first demonstration of myocardial fibrosis by multidetector computed tomography in HCM patients. Such findings may be useful in the evaluation of HCM patients with contraindications for CMR (eg, pacemakers, implantable cardioverterdefibrillators, and claustrophobia).
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2. Gerber BL, Belge B, Legros GJ, Lim P, Poncelet A, Pasquet A, Gisellu G, Coche E, Vanoverschelde JLJ. Characterization of acute and chronic myocardial infarcts by multidetector computed tomography: comparison with contrast-enhanced magnetic resonance. Circulation. 2006; 113: 823833.
3. Lardo AC, Cordeiro MAS, Silva C, Amado LC, George RT, Saliaris AP, Schuleri KH, Fernandes VR, Zviman M, Nazarian S, Halperin HR, Wu KC, M. Hare JM, Lima JAC. Contrast-enhanced multidetector computed tomography viability imaging after myocardial infarction: characterization of myocyte death, microvascular obstruction, and chronic scar. Circulation. 2006; 113: 394404.
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