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      MRSA-Associated Bacterial Myocarditis Causing Ruptured Ventricle and Tamponade

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          We report a case of an 81-year-old man with bacterial myocarditis presenting with elevated troponins and sepsis, who succumbed due to a ruptured ventricle. The infecting organism was found to be methicillin-resistant Staphylococcus aureus. Bacterial myocarditis is a rare occurrence when independent of infective endocarditis. Generally, this is a complication of bacteremia that is discovered post-mortem. Rarely, as in our patient, it causes significant necrosis of the myocardium leading to rupture of a ventricle. As with viral myocarditis, this disease can present with signs and symptoms of acute myocardial infarction, complicating the diagnosis. Much of the available data on bacterial myocarditis was collected before the development of many modern diagnostic tests and before antibiotics. Accordingly, the appropriate workup, diagnosis and treatment remain unclear. Our patient represents the first reported case of ventricular rupture due to methicillin-resistant S. aureus-associated bacterial myocarditis.

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          Most cited references 6

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          MRI changes in myocarditis--evaluation with spin echo, cine MR angiography and contrast enhanced spin echo imaging.

          Myocarditis is probably under-diagnosed with clinical criteria generally used for diagnosis. Magnetic resonance imaging (MRI) has shown promise in detecting heart muscle disorders and we set out to assess the role of cine magnetic resonance angiography (MRA) and contrast enhancement in myocarditis, as there is a need for a non-invasive tool that can aid prognosis and follow-up. Twenty patients were evaluated with T1 SE pre- and post-gadolinium enhancement and cine MRA. Four patients were histologically proven to have myocarditis, eight others were diagnosed as having myocarditis by clinical criteria and eight did not have myocarditis. Images were evaluated in a blinded fashion for regional wall motion abnormality and contrast enhancement pattern. Analysis of contrast enhancement by signal intensity measurement was also performed. Focal myocardial enhancement with associated regional wall motion abnormality correlated with myocarditis in 10 out of 12 patients, two patients with abnormal focal enhancement alone also clinically had myocarditis. None of the non-myocarditis patients showed abnormal focal enhancement. Enhancement analysis suggests that focal corrected myocardial enhancement of > 40% is abnormal. In the correct clinical context, focal myocardial enhancement on spin echo MRI strongly supports a diagnosis of myocarditis, especially when associated with regional wall motion abnormality.Roditi, G. H. (2000). Clinical Radiology55, 752-758. Copyright 2000 The Royal College of Radiologists.
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            Primary bacterial infection of the myocardium.

            Primary bacterial infection of myocardial tissue without associated endocarditis occurs only rarely. It is generally seen in the setting of overwhelming bacteremia. The most common bacterial cause of myocarditis is Staphylococcus aureus, although infections with a broad range of bacterial pathogens have been described. Pathologically, the disease process is characterized by multifocal studding of the myocardium with tiny abscesses, and the left ventricle is most commonly involved. Complications include cardiac dysfunction, rhythm disturbances, and myocardial rupture with secondary purulent pericarditis. Since virtually all information regarding primary bacterial myocarditis originates from autopsy studies conducted in the pre-antibiotic era, little is known about the modern approach to diagnosis and management of this clinical entity.
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                Author and article information

                S. Karger AG
                September 2008
                25 April 2008
                : 111
                : 3
                : 188-190
                Departments of aMedicine, and bPathology, Emory University School of Medicine, Atlanta, Ga., cAtlanta Veterans Affairs Medical Center, Decatur, Ga., and dEmory University School of Medicine, Atlanta, Ga., USA
                121602 Cardiology 2008;111:188–190
                © 2008 S. Karger AG, Basel

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                Figures: 2, References: 12, Pages: 3
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