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Circulation. 2003;108:e1-e3
doi: 10.1161/01.CIR.0000069947.13421.2E
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(Circulation. 2003;108:e1.)
© 2003 American Heart Association, Inc.


Images in Cardiovascular Medicine

Echocardiographic Description of Recurrent Idiopathic Giant-Cell Myocarditis in Cardiac Allograft

Przemyslaw Palka, MD; Aleksandra Lange, MD; Belinda Clarke, MD; Edwina Duhig, MD; Andrew Galbraith, MD

From the Departments of Cardiology (A.G.) and Pathology (B.C., E.D.), The Prince Charles Hospital and St Andrew’s Heart Institute (P.P., A.L.), Brisbane, Australia.

Correspondence to Dr P. Palka, St Andrew’s Heart Institute, St Andrew’s Place, Level 5, Suite 335, 33 North St, Spring Hill, Brisbane, QLD 4004, Australia. E-mail ppalka{at}hotmail.com

A 23-year-old woman with a cardiac allograft transplanted for giant-cell myocarditis 4 years earlier presented with exertional dyspnea. Her chest x-ray showed a normal cardiothoracic ratio and mild pulmonary venous congestion. An ECG demonstrated sinus rhythm with partial right bundle branch block. Conventional echocardiogram was essentially normal with only the interventricular septum being severely hypokinetic. The left ventricle (LV) was of normal size with low-normal systolic function (Figure 1). The right ventricle was of normal size and function. There was mild tricuspid regurgitation with a right ventricular systolic pressure of 31 mm Hg. There was no significant pericardial effusion. Doppler mitral inflow and pulmonary venous flow indices showed abnormal LV relaxation and elevated LV end- diastolic filling pressure. Color M-mode Doppler tissue echocardiography (DTE) showed an abnormally positive myocardial velocity gradient (MVG) across the LV posterior wall during isovolumic relaxation and a reduction during rapid ventricular filling indicating impaired myocardial relaxation (Figure 2). There was a reduction of early diastolic tricuspid annulus velocities and a virtual lack of medial annulus velocities with normal lateral mitral annulus velocities by pulsed-wave DTE (Figure 3). Described abnormalities in MVG and annular velocities were consistent with the features of an allograft rejection. Right ventricular endocardial biopsy showed giant-cell myocarditis in the transplanted heart (Figure 4). The patient was given high-dose immunosuppressive therapy and made a full recovery.



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Figure 1. M-mode echocardiogram of the LV; parasternal long-axis view. Note normal LV dimensions and LV fractional shortening (37%) and upper normal limit of the LV posterior wall thickness. IVS indicates interventricular septum; RV, right ventricle; and PW, posterior wall.



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Figure 2. Top, Color M-mode DTE of the LV posterior wall with the quantification of MVG and mean myocardial velocities (MMV); parasternal long-axis view. Bottom, Corresponding LV filling pattern on Doppler mitral inflow (E-wave deceleration time, 138 ms). Note that during isovolumic relaxation (IVR), MVG is abnormally positive at 2.9 s-1 (normal range, -2.3 to 1.4 s-1). Also, during rapid ventricular filling (RVF), just after the opening of the mitral valve, MVG is significantly reduced to 2.8 s-1 (normal range, 5.9 to 18.1 s-1). PCG indicates phonocardiogram. Dotted vertical lines show isovolumic relaxation time.



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Figure 3. Pulsed-wave DTE of the atrioventricular annulus motion; shown is apical 4-chamber view. A, Tricuspid (lateral); B, medial (septum); C, mitral (lateral). Note that early diastolic velocities, both tricuspid (Elt=8 cm/s) and medial (Em<1 cm/s), were significantly reduced (normal ranges, 13 to 29 and 7 to 26 cm/s, respectively). Early diastolic mitral velocities (Elm=18 cm/s) were within the normal range (9 to 39 cm/s). Elt indicates tricuspid (lateral) early diastolic velocity; Em, medial (septal) early diastolic velocity; and Elm, mitral (lateral) early diastolic velocity.



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Figure 4. Right ventricular endocardial biopsy showing an extensive interstitial inflammatory infiltrate within the myocardium comprising lymphocytes, plasma cells, eosinophils, and numerous multinucleated giant cells (arrows). This was associated with myofiber loss and active injury. Hematoxylin-eosin, original magnification x200).

Footnotes

The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke’s Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.

Circulation encourages readers to submit cardiovascular images to the Circulation Editorial Office, St Luke’s Episcopal Hospital/Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.





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Right arrow Other heart failure
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Right arrow CV surgery: transplantation, ventricular assistance, cardiomyopathy