Published online before print July 21, 2008, doi: 10.1161/CIRCULATIONAHA.108.769489
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(Circulation. 2008;118:639-648.)
© 2008 American Heart Association, Inc.
Heart Failure |
Predictors of Outcome in Patients With Suspected Myocarditis
From the Universitätsklinikum des Saarlandes, Klinik für Innere Medizin III (Kardiologie, Angiologie, Internistische Intensivmedizin) (I.K., M.K., T.M., M.B.) and Klinik für Pädiatrische Kardiologie (A.L.), Homburg/Saar, Germany; and Universitätsklinikum Tübingen, Abteilung Molekulare Pathologie, Institut für Pathologie (R.K., K.K.) and Abteilung Allgemeine Pathologie (B.B.), Tübingen, Germany.
Correspondence to Ingrid Kindermann, MD, or Michael Böhm, MD, Universitätsklinikum des Saarlandes, Klinik für Innere Medizin III (Kardiologie, Angiologie, Internistische Intensivmedizin), Kirrberger Straβe, 66421 Homburg/Saar, Germany. E-mail i.kindermann{at}med-in.uni-saarland.de
Received February 6, 2008; accepted June 2, 2008.
Background— The objective of this study was to identify the prognostic indicators in patients with suspected myocarditis who underwent endomyocardial biopsy.
Methods and Results— Between 1994 and 2007, 181 consecutive patients (age, 42±15 years) with clinically suspected viral myocarditis were enrolled and followed up for a mean of 59±42 months. Endomyocardial biopsies were studied for inflammation with histological (Dallas) and immunohistological criteria. Virus genome was detected by polymerase chain reaction. The primary end point was time to cardiac death or heart transplantation. In 38% of the patients (n=69), the Dallas criteria were positive. Immunohistological signs of inflammation were shown in 50% (n=91). Genomes of cardiotropic virus species were detected in 79 patients (44%). During follow-up, 22% of the patients (n=40) reached the primary end point. Three independent predictors were identified for the primary end point, namely New York Heart Association class III or IV at entry (hazard ratio, 3.20; 95% confidence interval, 1.36 to 7.57; P=0.008), immunohistological evidence of inflammatory infiltrates in the myocardium (hazard ratio, 3.46; 95% confidence interval, 1.39 to 8.62; P=0.008), and β-blocker therapy (hazard ratio, 0.43; 95% confidence interval, 0.21 to 0.91; P=0.027). Ejection fraction, left ventricular end-diastolic pressure, and left ventricular end-diastolic dimension index were predictive only in univariate, not in multivariate, analysis. Neither the Dallas criteria nor the detection of viral genome was a predictor of outcome.
Conclusions— For patients with suspected myocarditis, advanced New York Heart Association functional class, immunohistological signs of inflammation, and lack of β-blocker therapy, but not histology (positive Dallas criteria) or viral genome detection, are related to poor outcome.
CLINICAL PERSPECTIVE
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Clinical Summaries
Circulation 2008 118: 607-608.[Extract] [Full Text]
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