Effect of Immunosuppressive Therapy and Biopsy Status in Monitoring Therapy Response in Suspected Cardiac Sarcoidosis.


Journal

JACC. Cardiovascular imaging
ISSN: 1876-7591
Titre abrégé: JACC Cardiovasc Imaging
Pays: United States
ID NLM: 101467978

Informations de publication

Date de publication:
11 2022
Historique:
received: 08 02 2022
revised: 20 05 2022
accepted: 23 05 2022
entrez: 10 11 2022
pubmed: 11 11 2022
medline: 15 11 2022
Statut: ppublish

Résumé

Patients with suspected cardiac sarcoidosis frequently undergo fluorodeoxyglucose (FDG)-positron emission tomography (PET)/computed tomography (CT) imaging to assess disease activity at baseline and after treatment initiation. This study investigated the effect of immunosuppressive therapy and biopsy status to achieve complete treatment response (CTR), partial treatment response (PTR), or no response (NR) on myocardial FDG-PET/CT. This study analyzed 83 patients with suspected cardiac sarcoidosis (aged 53 ± 1.8 years, 71% were male, 69% were White, 61% had a history of biopsy-confirmed sarcoidosis) who were treatment naive, had evidence of myocardial FDG at baseline, and underwent repeat PET imaging after treatment initiation. CTR was graded visually, and PTR/NR were measured both visually and quantitatively using the total glycolytic activity. Patients were also evaluated for the occurrence of death, sustained ventricular arrhythmias, and heart failure admissions. Overall, 59 patients (71%) achieved CTR/PTR (30%/41%) at follow-up scan (P = 0.04). Total glycolytic activity and visual estimate of PTR/NR had excellent agreement (κ = 0.86 [95% CI: 0.72-0.99]; P < 0.0001). In patients receiving prednisone only, the highest rates of CTR/PTR were observed in patients initiated on moderate or high dose (P < 0.01). In a regression model, moderate prednisone start dose (P = 0.03) was more strongly associated with achieving CTR/PTR than was high prednisone start dose. However, the latter patients were tapered faster between start dose and follow-up scan (P < 0.01). After a median follow-up of 4.7 (IQR: 3.1-7.8) years, patients who were biopsy-proven (vs non-biopsy-proven; P = 0.029) and with preserved left ventricular function (P = 002) were less likely to experience major adverse cardiac events. Outcomes based on treatment response status (CTR vs PTR vs NR; P = 0.23) were not significantly different. Among patients with suspected sarcoidosis and evidence of myocardial inflammation, treatment response by serial FDG-PET was variable, but a favorable response was more common when using moderate-to-high intensity prednisone dose. Biopsy-proven individuals and those with preserved systolic function were less likely to experience adverse outcomes during follow-up.

Sections du résumé

BACKGROUND
Patients with suspected cardiac sarcoidosis frequently undergo fluorodeoxyglucose (FDG)-positron emission tomography (PET)/computed tomography (CT) imaging to assess disease activity at baseline and after treatment initiation.
OBJECTIVES
This study investigated the effect of immunosuppressive therapy and biopsy status to achieve complete treatment response (CTR), partial treatment response (PTR), or no response (NR) on myocardial FDG-PET/CT.
METHODS
This study analyzed 83 patients with suspected cardiac sarcoidosis (aged 53 ± 1.8 years, 71% were male, 69% were White, 61% had a history of biopsy-confirmed sarcoidosis) who were treatment naive, had evidence of myocardial FDG at baseline, and underwent repeat PET imaging after treatment initiation. CTR was graded visually, and PTR/NR were measured both visually and quantitatively using the total glycolytic activity. Patients were also evaluated for the occurrence of death, sustained ventricular arrhythmias, and heart failure admissions.
RESULTS
Overall, 59 patients (71%) achieved CTR/PTR (30%/41%) at follow-up scan (P = 0.04). Total glycolytic activity and visual estimate of PTR/NR had excellent agreement (κ = 0.86 [95% CI: 0.72-0.99]; P < 0.0001). In patients receiving prednisone only, the highest rates of CTR/PTR were observed in patients initiated on moderate or high dose (P < 0.01). In a regression model, moderate prednisone start dose (P = 0.03) was more strongly associated with achieving CTR/PTR than was high prednisone start dose. However, the latter patients were tapered faster between start dose and follow-up scan (P < 0.01). After a median follow-up of 4.7 (IQR: 3.1-7.8) years, patients who were biopsy-proven (vs non-biopsy-proven; P = 0.029) and with preserved left ventricular function (P = 002) were less likely to experience major adverse cardiac events. Outcomes based on treatment response status (CTR vs PTR vs NR; P = 0.23) were not significantly different.
CONCLUSIONS
Among patients with suspected sarcoidosis and evidence of myocardial inflammation, treatment response by serial FDG-PET was variable, but a favorable response was more common when using moderate-to-high intensity prednisone dose. Biopsy-proven individuals and those with preserved systolic function were less likely to experience adverse outcomes during follow-up.

Identifiants

pubmed: 36357136
pii: S1936-878X(22)00380-1
doi: 10.1016/j.jcmg.2022.05.015
pii:
doi:

Substances chimiques

Fluorodeoxyglucose F18 0Z5B2CJX4D
Radiopharmaceuticals 0
Prednisone VB0R961HZT

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1944-1955

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Chaitanya Rojulpote (C)

Division of Nuclear Medicine, Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA; Department of Medicine, The Wright Center for Graduate Medical Education, Scranton, Pennsylvania, USA.

Abhijit Bhattaru (A)

Division of Nuclear Medicine, Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Christopher Jean (C)

Division of Nuclear Medicine, Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Sarah L Adams (SL)

Division of Nuclear Medicine, Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Vandan Patel (V)

Division of Nuclear Medicine, Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Mahesh K Vidula (MK)

Division of Cardiology, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Senthil Selvaraj (S)

Division of Cardiology, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Jacob Dubroff (J)

Division of Nuclear Medicine, Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Eliot Peyster (E)

Division of Cardiology, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Caitlin B Clancy (CB)

Division of Pulmonology, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Karen Patterson (K)

Division of Pulmonology, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Francis E Marchlinski (FE)

Division of Cardiology, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Milton Rossman (M)

Division of Pulmonology, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Lee Goldberg (L)

Division of Cardiology, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Paco E Bravo (PE)

Division of Nuclear Medicine, Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA; Division of Cardiology, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA. Electronic address: paco.bravo@pennmedicine.upenn.edu.

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