BACKGROUND: In patients with sarcoidosis, sudden death is a leading cause of mortality, which may represent unrecognized cardiac involvement. Delayed-enhancement cardiovascular magnetic resonance (DE-CMR) can detect minute amounts of myocardial damage. We sought to compare DE-CMR with standard clinical evaluation for the identification of cardiac involvement. METHODS AND RESULTS: Eighty-one consecutive patients with biopsy-proven extracardiac sarcoidosis were prospectively recruited for a parallel and masked comparison of cardiac involvement between (1) DE-CMR and (2) standard clinical evaluation with the use of consensus criteria (modified Japanese Ministry of Health [JMH] guidelines). Standard evaluation included 12-lead ECG and at least 1 dedicated non-CMR cardiac study (echocardiography, radionuclide scintigraphy, or cardiac catheterization). Patients were followed for 21+/-8 months for major adverse events (death, defibrillator shock, or pacemaker requirement). Patients were predominantly middle-aged (46+/-11 years), female (62%), and black (73%) and had chronic sarcoidosis (median, 7 years) and preserved left ventricular ejection fraction (median, 56%). DE-CMR identified cardiac involvement in 21 patients (26%) and JMH criteria in 10 (12%, 8 overlapping), a >2-fold higher rate for DE-CMR (P=0.005). All patients with myocardial damage on DE-CMR had coronary disease excluded by x-ray angiography. Pathology evaluation in 15 patients (19%) identified 4 with cardiac sarcoidosis; all 4 were positive by DE-CMR, whereas 2 were JMH positive. On follow-up, 8 had adverse events, including 5 cardiac deaths. Patients with myocardial damage on DE-CMR had a 9-fold higher rate of adverse events and an 11.5-fold higher rate of cardiac death than patients without damage. CONCLUSIONS: In patients with sarcoidosis, DE-CMR is more than twice as sensitive for cardiac involvement as current consensus criteria. Myocardial damage detected by DE-CMR appears to be associated with future adverse events including cardiac death, but events were few, and this needs confirmation in a larger cohort.
BACKGROUND: In patients with sarcoidosis, sudden death is a leading cause of mortality, which may represent unrecognized cardiac involvement. Delayed-enhancement cardiovascular magnetic resonance (DE-CMR) can detect minute amounts of myocardial damage. We sought to compare DE-CMR with standard clinical evaluation for the identification of cardiac involvement. METHODS AND RESULTS: Eighty-one consecutive patients with biopsy-proven extracardiac sarcoidosis were prospectively recruited for a parallel and masked comparison of cardiac involvement between (1) DE-CMR and (2) standard clinical evaluation with the use of consensus criteria (modified Japanese Ministry of Health [JMH] guidelines). Standard evaluation included 12-lead ECG and at least 1 dedicated non-CMR cardiac study (echocardiography, radionuclide scintigraphy, or cardiac catheterization). Patients were followed for 21+/-8 months for major adverse events (death, defibrillator shock, or pacemaker requirement). Patients were predominantly middle-aged (46+/-11 years), female (62%), and black (73%) and had chronic sarcoidosis (median, 7 years) and preserved left ventricular ejection fraction (median, 56%). DE-CMR identified cardiac involvement in 21 patients (26%) and JMH criteria in 10 (12%, 8 overlapping), a >2-fold higher rate for DE-CMR (P=0.005). All patients with myocardial damage on DE-CMR had coronary disease excluded by x-ray angiography. Pathology evaluation in 15 patients (19%) identified 4 with cardiac sarcoidosis; all 4 were positive by DE-CMR, whereas 2 were JMH positive. On follow-up, 8 had adverse events, including 5 cardiac deaths. Patients with myocardial damage on DE-CMR had a 9-fold higher rate of adverse events and an 11.5-fold higher rate of cardiac death than patients without damage. CONCLUSIONS: In patients with sarcoidosis, DE-CMR is more than twice as sensitive for cardiac involvement as current consensus criteria. Myocardial damage detected by DE-CMR appears to be associated with future adverse events including cardiac death, but events were few, and this needs confirmation in a larger cohort.
Authors: Francis J Klocke; Michael G Baird; Beverly H Lorell; Timothy M Bateman; Joseph V Messer; Daniel S Berman; Patrick T O'Gara; Blase A Carabello; Richard O Russell; Manuel D Cerqueira; Martin G St John Sutton; Anthony N DeMaria; James E Udelson; J Ward Kennedy; Mario S Verani; Kim Allan Williams; Elliott M Antman; Sidney C Smith; Joseph S Alpert; Gabriel Gregoratos; Jeffrey L Anderson; Loren F Hiratzka; David P Faxon; Sharon Ann Hunt; Valentin Fuster; Alice K Jacobs; Raymond J Gibbons; Richard O Russell Journal: J Am Coll Cardiol Date: 2003-10-01 Impact factor: 24.094
Authors: Jan-Peter Smedema; Gabriel Snoep; Marinus P G van Kroonenburgh; Robert-Jan van Geuns; Willem R M Dassen; Anton P Gorgels; Harry J G M Crijns Journal: Chest Date: 2005-07 Impact factor: 9.410
Authors: Jan-Peter Smedema; Gabriel Snoep; Marinus P G van Kroonenburgh; Robert-Jan van Geuns; Willem R M Dassen; Anton P M Gorgels; Harry J G M Crijns Journal: J Am Coll Cardiol Date: 2005-04-25 Impact factor: 24.094
Authors: Y Matsui; K Iwai; T Tachibana; T Fruie; N Shigematsu; T Izumi; A H Homma; R Mikami; O Hongo; Y Hiraga; M Yamamoto Journal: Ann N Y Acad Sci Date: 1976 Impact factor: 5.691
Authors: Katherine C Wu; Gary Gerstenblith; Eliseo Guallar; Joseph E Marine; Darshan Dalal; Alan Cheng; Eduardo Marbán; João A C Lima; Gordon F Tomaselli; Robert G Weiss Journal: Circ Cardiovasc Imaging Date: 2012-01-20 Impact factor: 7.792