Thomas Crawford1, Gisela Mueller2, Sinan Sarsam2, Hutsaya Prasitdumrong2, Naiyanet Chaiyen2, Xiaokui Gu2, Joseph Schuller2, Jordana Kron2, Khaled A Nour2, Alan Cheng2, Sang Yong Ji2, Shawn Feinstein2, Sanjaya Gupta2, Karl Ilg2, Mohamad Sinno2, Saddam Abu-Hashish2, Mouaz Al-Mallah2, William H Sauer2, Kenneth Ellenbogen2, Fred Morady2, Frank Bogun2. 1. From the Section of Cardiac Electrophysiology, Division of Cardiovascular Medicine, Department of Internal Medicine (T.C., X.G., S.G., K.I., M.S., S.A.-H., F.M., F.B.), and Department of Radiology (G.M., H.P., N.C.), University of Michigan, Ann Arbor; Department of Internal Medicine, Detroit Medical Center, MI (S.S.); Section of Cardiac Electrophysiology, Division of Cardiology, Department of Internal Medicine, University of Colorado, Aurora (J.S., W.H.S.); Department of Cardiac Electrophysiology, Virginia Commonwealth University, Richmond (J.K., S.F., K.E.); Division of Cardiology, Department of Internal Medicine, Henry Ford Hospital, Detroit, MI (K.A.N., M.A.-M.); and Section of Cardiac Electrophysiology, Division of Cardiology, Department of Internal Medicine, Johns Hopkins University, Baltimore, MD (A.C., S.Y.J.). thomcraw@umich.edu. 2. From the Section of Cardiac Electrophysiology, Division of Cardiovascular Medicine, Department of Internal Medicine (T.C., X.G., S.G., K.I., M.S., S.A.-H., F.M., F.B.), and Department of Radiology (G.M., H.P., N.C.), University of Michigan, Ann Arbor; Department of Internal Medicine, Detroit Medical Center, MI (S.S.); Section of Cardiac Electrophysiology, Division of Cardiology, Department of Internal Medicine, University of Colorado, Aurora (J.S., W.H.S.); Department of Cardiac Electrophysiology, Virginia Commonwealth University, Richmond (J.K., S.F., K.E.); Division of Cardiology, Department of Internal Medicine, Henry Ford Hospital, Detroit, MI (K.A.N., M.A.-M.); and Section of Cardiac Electrophysiology, Division of Cardiology, Department of Internal Medicine, Johns Hopkins University, Baltimore, MD (A.C., S.Y.J.).
Abstract
BACKGROUND: The purpose of this study was to assess whether delayed enhancement (DE) on MRI is associated with ventricular tachycardia (VT)/ventricular fibrillation or death in patients with cardiac sarcoidosis and left ventricular ejection fraction >35%. METHODS AND RESULTS: Fifty-one patients with cardiac sarcoidosis and left ventricular ejection fraction >35% underwent DE-MRI. DE was assessed by visual scoring and quantified with the full-width at half-maximum method. The patients were followed for 48.0 ± 20.2 months. Twenty-two of 51 patients (63%) had DE. Forty patients had no prior history of VT (primary prevention cohort). Among those, 3 patients developed VT and 2 patients died. DE was associated with risk of VT/ventricular fibrillation or death (P=0.0032 for any DE and P<0.0001 for right ventricular DE). The positive predictive values of the presence of any DE, multifocal DE, and right ventricular DE for death or VT/ventricular fibrillation at mean follow-up of 48 months were 22%, 48%, and 100%, respectively. Among the 11 patients with a history of VT before the MRI, 10 patients had subsequent VTs, 1 of whom died. CONCLUSIONS: RV DE in patients with cardiac sarcoidosis is associated with a risk of adverse events in patients with cardiac sarcoidosis and preserved ejection fraction in the absence of a prior history of VT. Patients with DE and a prior history of VT have a high VT recurrence rate. Patients without DE on MRI have a low risk of VT.
BACKGROUND: The purpose of this study was to assess whether delayed enhancement (DE) on MRI is associated with ventricular tachycardia (VT)/ventricular fibrillation or death in patients with cardiac sarcoidosis and left ventricular ejection fraction >35%. METHODS AND RESULTS: Fifty-one patients with cardiac sarcoidosis and left ventricular ejection fraction >35% underwent DE-MRI. DE was assessed by visual scoring and quantified with the full-width at half-maximum method. The patients were followed for 48.0 ± 20.2 months. Twenty-two of 51 patients (63%) had DE. Forty patients had no prior history of VT (primary prevention cohort). Among those, 3 patients developed VT and 2 patients died. DE was associated with risk of VT/ventricular fibrillation or death (P=0.0032 for any DE and P<0.0001 for right ventricular DE). The positive predictive values of the presence of any DE, multifocal DE, and right ventricular DE for death or VT/ventricular fibrillation at mean follow-up of 48 months were 22%, 48%, and 100%, respectively. Among the 11 patients with a history of VT before the MRI, 10 patients had subsequent VTs, 1 of whom died. CONCLUSIONS: RV DE in patients with cardiac sarcoidosis is associated with a risk of adverse events in patients with cardiac sarcoidosis and preserved ejection fraction in the absence of a prior history of VT. Patients with DE and a prior history of VT have a high VT recurrence rate. Patients without DE on MRI have a low risk of VT.
Authors: Felipe Kazmirczak; Ko-Hsuan Amy Chen; Selcuk Adabag; Lisa von Wald; Henri Roukoz; David G Benditt; Osama Okasha; Afshin Farzaneh-Far; Jeremy Markowitz; Prabhjot S Nijjar; Pratik S Velangi; Maneesh Bhargava; David Perlman; Sue Duval; Mehmet Akçakaya; Chetan Shenoy Journal: Circ Arrhythm Electrophysiol Date: 2019-08-21
Authors: G Cameron Coleman; Peter W Shaw; Pelbreton C Balfour; Jorge A Gonzalez; Christopher M Kramer; Amit R Patel; Michael Salerno Journal: JACC Cardiovasc Imaging Date: 2016-07-20
Authors: Yan Yatsynovich; Damian Valencia; Mikhail Petrov; Juan David Linares; Mufti M Rahman; Nathaniel Dittoe Journal: Curr Treat Options Cardiovasc Med Date: 2018-08-07
Authors: Tomas Vita; David R Okada; Mahdi Veillet-Chowdhury; Paco E Bravo; Erin Mullins; Edward Hulten; Mukta Agrawal; Rachna Madan; Viviany R Taqueti; Michael Steigner; Hicham Skali; Raymond Y Kwong; Garrick C Stewart; Sharmila Dorbala; Marcelo F Di Carli; Ron Blankstein Journal: Circ Cardiovasc Imaging Date: 2018-01 Impact factor: 7.792