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Clinical and Imaging Response to Tumor Necrosis Factor Alpha Inhibitors in Treatment of Cardiac Sarcoidosis: A Multicenter Experience.

MedStar author(s):

Ahmed, Sara

Constantinescu, Florina

1071-9164

Name of journal: Journal of cardiac failureAbstract: BACKGROUND: Cardiac sarcoidosis (CS) is an increasingly recognized cause of cardiomyopathy, however data on immunosuppressive strategies are limited. Treatment with tumor necrosis factor (TNF) alpha inhibitors is not well described; moreover, there may be heart failure (HF)-related safety concerns.CONCLUSIONS: TNF alpha inhibitor treatment guided by FDG-PET may minimize corticosteroid use and effectively reduce cardiac inflammation without significant adverse effect on cardiac function. However infections were common, some of which were serious, and therefore patients require close monitoring for both infection and cardiac symptoms. Copyright (c) 2020. Published by Elsevier Inc.METHODS: Retrospective multicenter study of TNF alpha inhibitor treated CS patients. Baseline characteristics, treatments, and outcomes were adjudicated.RESULTS: Thirty-eight patients with CS (mean 49.9 years old, 42% women, 53% African American) were treated with TNF alpha inhibitor (30 infliximab, 8 adalimumab). Prednisone dose decreased from time of TNF alpha inhibitor initiation (21.7+/-17.5 mg) to 6-months (10.4+/-6.1 mg, p=0.001) and 12-months post (7.3+/-7.3 mg, p=0.002). On pre-TNF alpha inhibitor treatment 18-flourodoxyglucose position emission tomography (FDG-PET), 84% of patients had cardiac FDG uptake. Post-treatment, there was a significant decrease in number of segments involved (3.5+/-3.8 to 1+/-2.5, p=0.008) and maximum standardized uptake value (3.59+/-3.7 to 0.57+/-1.6, p=0.0005), with 73% of patients demonstrating complete resolution or improvement of cardiac FDG uptake. Left ventricular ejection fraction remained stable (45+/-16.5 to 47+/-15.0%, p=0.10). Four patients required inpatient HF treatment, and 8 had infections; 2 required treatment cessation.All authors: Ahmed S, Chen ES, Constantinescu F, Devraj M, Garcia C, Gilotra NA, Griffin JM, Kasper EK, Mohammed SF, Okada DR, Pavlovic N, Pillarisetty A, Saad E, Sheikh FH, Solnes L, Wand ALOriginally published: Journal of Cardiac Failure. 2020 Sep 01Fiscal year: FY2021Digital Object Identifier:

https://dx.doi.org/10.1016/j.cardfail.2020.08.013

Date added to catalog: 2020-10-06

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Title notes ( 6 )

Holdings
Item type	Current library	Collection	Call number	Status	Date due	Barcode
Journal Article	MedStar Authors Catalog	Article	32889044	Available		32889044

Available online from MWHC library: 1995 - present

BACKGROUND: Cardiac sarcoidosis (CS) is an increasingly recognized cause of cardiomyopathy, however data on immunosuppressive strategies are limited. Treatment with tumor necrosis factor (TNF) alpha inhibitors is not well described; moreover, there may be heart failure (HF)-related safety concerns.

CONCLUSIONS: TNF alpha inhibitor treatment guided by FDG-PET may minimize corticosteroid use and effectively reduce cardiac inflammation without significant adverse effect on cardiac function. However infections were common, some of which were serious, and therefore patients require close monitoring for both infection and cardiac symptoms. Copyright (c) 2020. Published by Elsevier Inc.

METHODS: Retrospective multicenter study of TNF alpha inhibitor treated CS patients. Baseline characteristics, treatments, and outcomes were adjudicated.

RESULTS: Thirty-eight patients with CS (mean 49.9 years old, 42% women, 53% African American) were treated with TNF alpha inhibitor (30 infliximab, 8 adalimumab). Prednisone dose decreased from time of TNF alpha inhibitor initiation (21.7+/-17.5 mg) to 6-months (10.4+/-6.1 mg, p=0.001) and 12-months post (7.3+/-7.3 mg, p=0.002). On pre-TNF alpha inhibitor treatment 18-flourodoxyglucose position emission tomography (FDG-PET), 84% of patients had cardiac FDG uptake. Post-treatment, there was a significant decrease in number of segments involved (3.5+/-3.8 to 1+/-2.5, p=0.008) and maximum standardized uptake value (3.59+/-3.7 to 0.57+/-1.6, p=0.0005), with 73% of patients demonstrating complete resolution or improvement of cardiac FDG uptake. Left ventricular ejection fraction remained stable (45+/-16.5 to 47+/-15.0%, p=0.10). Four patients required inpatient HF treatment, and 8 had infections; 2 required treatment cessation.

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