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Cardiac sarcoidosis or giant cell myocarditis? On treatment improvement of fulminant myocarditis as demonstrated by cardiovascular magnetic resonance imaging.

Bogabathina H, Olson P, Rathi VK, Biederman RW - Case Rep Cardiol (2011)

Bottom Line: Giant cell myocarditis, but not cardiac sarcoidosis, is known to cause fulminant myocarditis resulting in severe heart failure.This patient was treated with cyclosporine and prednisone and recovered well.This case we believe challenges our current understanding of these intertwined conditions.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiovascular Magnetic Resonance Imaging, Gerald McGinnis Cardiovascular Institute, Allegheny General Hospital, 320 East North Avenue, Pittsburgh, PA 15212, USA.

ABSTRACT
Giant cell myocarditis, but not cardiac sarcoidosis, is known to cause fulminant myocarditis resulting in severe heart failure. However, giant cell myocarditis and cardiac sarcoidosis are pathologically similar, and attempts at pathological differentiation between the two remain difficult. We are presenting a case of fulminant myocarditis that has pathological features suggestive of cardiac sarcoidosis, but clinically mimicking giant cell myocarditis. This patient was treated with cyclosporine and prednisone and recovered well. This case we believe challenges our current understanding of these intertwined conditions. By obtaining a sense of severity of cardiac involvement via delayed hyperenhancement of cardiac magnetic resonance imaging, we were more inclined to treat this patient as giant cell myocarditis with cyclosporine. This resulted in excellent improvement of patient's cardiac function as shown by delayed hyperenhancement images, early perfusion images, and SSFP videos.

No MeSH data available.


Related in: MedlinePlus

Delayed gadolinium hyperenhancement images. DHE-CMR pattern of patchy delayed hyperenhancement secondary to giant cell myocarditis or a severe form of cardiac sarcoidosis. Patchy hyperenhancement in left ventricular wall and diffuse enhancement in right ventricular wall in the initial exam (a1, a2, and a3) has improved to coalescence of hyperenhancement in seven weeks on cyclosporine and prednisone (b1, b2, and b3). The nine-month exam (c1, c2, and c3) shows a stabilization of change in hyperenhancement as compared to the seven-week exam.
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fig2: Delayed gadolinium hyperenhancement images. DHE-CMR pattern of patchy delayed hyperenhancement secondary to giant cell myocarditis or a severe form of cardiac sarcoidosis. Patchy hyperenhancement in left ventricular wall and diffuse enhancement in right ventricular wall in the initial exam (a1, a2, and a3) has improved to coalescence of hyperenhancement in seven weeks on cyclosporine and prednisone (b1, b2, and b3). The nine-month exam (c1, c2, and c3) shows a stabilization of change in hyperenhancement as compared to the seven-week exam.

Mentions: Cardiovascular magnetic resonance imaging (CMR) was done for further evaluation of fulminant myocarditis. CMR showed top normal left ventricular size, mildly dilated by 3D, LVEF of 27%, with severe regional wall dysfunction, worse at base and sparing the apex (see Video 1 in Supplementary Material available on line at doi:10.1155/2011/647041). First-pass perfusion demonstrated nonspecific subtle subendocardial hypoperfusion defect, not following any coronary distribution (Figure 1). Delayed hyperenhancement imaging (DHE) showed an extremely heterogeneous, dense, and patchy, near complete enhancement of the myocardium, with increased T1 signal by gadolinium imaging. Late imaging after the postedema washout period reveals a marked patchy signal consistent with a severe inflammatory or infiltrative process (Figure 2). Right ventricular segmental dysfunction exactly colocalized with the transmural RV signal. Right paratracheal and perihilar lymphadenopathy was also noted. The official CMR report suggested that this pattern was most consistent with GCM.


Cardiac sarcoidosis or giant cell myocarditis? On treatment improvement of fulminant myocarditis as demonstrated by cardiovascular magnetic resonance imaging.

Bogabathina H, Olson P, Rathi VK, Biederman RW - Case Rep Cardiol (2011)

Delayed gadolinium hyperenhancement images. DHE-CMR pattern of patchy delayed hyperenhancement secondary to giant cell myocarditis or a severe form of cardiac sarcoidosis. Patchy hyperenhancement in left ventricular wall and diffuse enhancement in right ventricular wall in the initial exam (a1, a2, and a3) has improved to coalescence of hyperenhancement in seven weeks on cyclosporine and prednisone (b1, b2, and b3). The nine-month exam (c1, c2, and c3) shows a stabilization of change in hyperenhancement as compared to the seven-week exam.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4008442&req=5

fig2: Delayed gadolinium hyperenhancement images. DHE-CMR pattern of patchy delayed hyperenhancement secondary to giant cell myocarditis or a severe form of cardiac sarcoidosis. Patchy hyperenhancement in left ventricular wall and diffuse enhancement in right ventricular wall in the initial exam (a1, a2, and a3) has improved to coalescence of hyperenhancement in seven weeks on cyclosporine and prednisone (b1, b2, and b3). The nine-month exam (c1, c2, and c3) shows a stabilization of change in hyperenhancement as compared to the seven-week exam.
Mentions: Cardiovascular magnetic resonance imaging (CMR) was done for further evaluation of fulminant myocarditis. CMR showed top normal left ventricular size, mildly dilated by 3D, LVEF of 27%, with severe regional wall dysfunction, worse at base and sparing the apex (see Video 1 in Supplementary Material available on line at doi:10.1155/2011/647041). First-pass perfusion demonstrated nonspecific subtle subendocardial hypoperfusion defect, not following any coronary distribution (Figure 1). Delayed hyperenhancement imaging (DHE) showed an extremely heterogeneous, dense, and patchy, near complete enhancement of the myocardium, with increased T1 signal by gadolinium imaging. Late imaging after the postedema washout period reveals a marked patchy signal consistent with a severe inflammatory or infiltrative process (Figure 2). Right ventricular segmental dysfunction exactly colocalized with the transmural RV signal. Right paratracheal and perihilar lymphadenopathy was also noted. The official CMR report suggested that this pattern was most consistent with GCM.

Bottom Line: Giant cell myocarditis, but not cardiac sarcoidosis, is known to cause fulminant myocarditis resulting in severe heart failure.This patient was treated with cyclosporine and prednisone and recovered well.This case we believe challenges our current understanding of these intertwined conditions.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiovascular Magnetic Resonance Imaging, Gerald McGinnis Cardiovascular Institute, Allegheny General Hospital, 320 East North Avenue, Pittsburgh, PA 15212, USA.

ABSTRACT
Giant cell myocarditis, but not cardiac sarcoidosis, is known to cause fulminant myocarditis resulting in severe heart failure. However, giant cell myocarditis and cardiac sarcoidosis are pathologically similar, and attempts at pathological differentiation between the two remain difficult. We are presenting a case of fulminant myocarditis that has pathological features suggestive of cardiac sarcoidosis, but clinically mimicking giant cell myocarditis. This patient was treated with cyclosporine and prednisone and recovered well. This case we believe challenges our current understanding of these intertwined conditions. By obtaining a sense of severity of cardiac involvement via delayed hyperenhancement of cardiac magnetic resonance imaging, we were more inclined to treat this patient as giant cell myocarditis with cyclosporine. This resulted in excellent improvement of patient's cardiac function as shown by delayed hyperenhancement images, early perfusion images, and SSFP videos.

No MeSH data available.


Related in: MedlinePlus