Phenotyping Individuals with Suspected Cardiac Sarcoidosis with CMR and PET: Focus on Outcomes (RF_TH_197)

Thursday, January 30, 2025

2:10 PM – 2:20 PM East Coast USA Time

Location: Blue Room PreFunction - Kiosk 1

Presenting Author(s)

MG

Mohamed Ghonim, MD

Postdoctoral Reasearch Fellow
Hospital of the University of Pennsylvania

Primary Author(s)

MG

Mohamed Ghonim, MD

Postdoctoral Reasearch Fellow
Hospital of the University of Pennsylvania

Co-Author(s)

MG

Mohanad Ghonim, MD

Postdoctoral Research Fellow
Hospital of the University of Pennsylvania
WO

William Ohley, MD, MA

Resident
Hospital of the University of Pennsylvania
AS

Ahmad S Alhamshari, MD

Post-doctoral Research Fellow
University of Pennsylvania
MV

Mahesh K. Vidula, MD

Assistant Professor of Cardiovascular Medicine
Hospital of the University of Pennsylvania
JH

Jui Hu, MD

Assistant Professor
Hospital of the University of Pennsylvania
Harold I. Litt, MD, PhD

Division Chief, Cardiothoracic Imaging
Hospital of the University of Pennsylvania
WW

Walter R. Witschey, PhD

Associate Professor of Radiology
Perelman School of Medicine, University of Pennsylvania
Paco E. Bravo, MD

Director of Nuclear Cardiology and Cardiovascular Molecular Imaging
Hospital of the University of Pennsylvania

Background: Cardiovascular magnetic resonance (CMR) imaging can phenotype based on late gadolinium enhancement (LGE) features for major adverse cardiovascular events (MACE) in patients with suspected cardiac sarcoidosis (CS). However, it remains to be determined if the combination with fluorodeoxyglucose (FDG) metabolic positron emission tomography (PET) imaging has added value for risk stratification. We hypothesize that FDG-PET findings are augmentative to LGE-CMR features and will positively correlate with future incidence of MACE in patients with suspected CS.

Methods: We included 230 patients who underwent sequential CMR and PET imaging for evaluation of CS. Subjects without LGE on CMR and/or FDG findings suggestive of incomplete metabolic suppression were excluded. LGE, FDG, and combined CMR-PET phenotypes were all graded as imaging findings typical, or not typical, of CS. MACE was defined as sustained ventricular arrhythmias (VA), heart transplantation and/or all-cause death during follow-up.

Results: We identified 69 subjects (30%) with combined CMR-PET features typical of CS. This cohort was younger (53 ± 8 vs. 59 ± 12; P< 0.001), had lower LVEF (40±15 vs. 45±14;P=0.045), and higher prevalence of biopsy-proven sarcoidosis (68% vs. 36%; P< 0.001), history of sustained VA (35% vs. 17%; P=0.005), and heart block (29% vs. 14%; P=0.008), compared to patients with CMR-PET features not typical of CS. Gender, race, and other baseline characteristics were not significantly different between groups. Patients with LGE (HR 3.6 [1.6-8.1];P=0.002), FDG [HR 5.6 [2.1-15];P=0.001), and combined CMR-PET (HR 3.7 [1.7-8.4]:P=0.001) features typical of CS had a higher incidence of MACE compared to their counterpart. Adjusting for LGE pattern did not change the strong association with future MACE for the CMR-PET phenotype (HR 5.2 [1.3-21]; P=0.023).

Conclusion:

Combination of CMR and PET imaging features not only can improve the diagnostic yield as has already been established, but also provide enhanced prognostication to individuals with suspected CS.