Novel dietary protocol prior to 18F-fluorodeoxyglucose positron emission tomography to evaluate for cardiac sarcoidosis
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Cardiovascular Medicine Department, Cleveland Clinic Foundation, Cleveland, OH
Received Sep 9, 2020; accepted Sep 10, 2020 doi:10.1007/s12350-020-02392-x
The diagnosis of cardiac sarcoidosis (CS) is challenging. Recently, guidelines incorporated cardiac positron emission tomography (PET) with 18F-Fluorodeoxyglucose (F18-FDG) as a non-invasive diagnostic modality for the detection and follow-up of CS. However, this technique is dependent of patient dietary preparation to suppress physiological myocardial F18-FDG uptake. We present a case of possible CS which highlights a novel preparation protocol that facilitated appropriate myocardial suppression. Key Words: Inflammation Æ diseases/processes Æ PET Æ modalities Æ metabolism Æ imaging agents Æ tracers Æ Image guided application Æ outcomes Æ sarcoid heart disease
INTRODUCTION The diagnosis of cardiac sarcoidosis (CS) is challenging, and histological confirmation with endomyocardial biopsy is limited due to patchy myocardial involvement and consequent poor sensitivity. More recently, guidelines have incorporated imaging criteria to aid in establishing a clinical diagnosis of CS.1-3 Cardiac positron emission tomography (PET) with rubidium-82 (Rb82) or N13-Ammonia for perfusion and 18F-Fluorodeoxyglucose (F18-FDG) for metabolism has become an important non-invasive diagnostic modality for the detection and follow-up of CS.4 Unlike cardiac magnetic resonance imaging (CMR), PET is more rapidly acquired, less dependent on patient cooperation during the exam, and not subject to interference by intracardiac devices. However, this technique is dependent on patient dietary preparation to suppress physiological myocardial F18-FDG uptake in the
Funding No funding received. Reprint requests: Erika Hutt, MD, Cardiovascular Medicine Department, Cleveland Clinic Foundation, 9500 Euclid Ave, NA3-129, Cleveland, OH ; [email protected] J Nucl Cardiol 1071-3581/$34.00 Copyright Ó 2020 American Society of Nuclear Cardiology.
myocardium. Several protocols have been utilized to suppress myocardial F18-FDG uptake including prolonged fasting, dietary modification (low carbohydrate and/or high fat diet) and intravenous administration of unfractionated heparin.5 We present a case of possible cardiac sarcoidosis which highlights a novel preparation protocol that facilitated appropriate suppression of physiological myocardial glucose utilization. A 36-year-old woman presented for evaluation of shortness of breath and recent diagnosis of heart failure with reduced ejection fraction of 31% by echocardiogram and 25% by CMR. CMR revealed diffuse multifocal delayed hyperenhancement in a nonischemic patchy mid-myocardial to subepicardial distribution (Figure 1). Given the above findings, a cardiac monitor was ordered to evaluate presence of arrhythmias, and a cardiac PET was ordered to evaluate for active inflammation possibly related to CS. Sarcoid PET with 15.5 h of fasting (resting glucose of 83 mg/dl) was nondiagnostic for inflammation due to failure to suppress myocardial glucose utilization (
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