title: Myocardial Blood Flow and Inflammatory Cardiac Sarcoidosis.
abstract: This study sought to evaluate the effects of inflammatory sarcoid disease on coronary circulatory function and the response to immune-suppressive treatment.
  
  
  
  Although positron emission tomography assessment of myocardial inflammation is increasingly applied to identify active cardiac sarcoidosis, its effect on coronary flow and immune-suppressive treatment remains to be characterized.
  
  
  
  Thirty-two individuals, who were referred for positron emission tomography/computed tomography, were evaluated for known or suspected cardiac sarcoidosis applying18F-fluorodeoxyglucose to determine inflammation and13N-ammonia to assess for perfusion deficits following a high-fat/low-carbohydrate diet and fasting state >12 h to suppress myocardial glucose uptake. Inflammation was quantified with standardized uptake value and regional myocardial blood flow at rest and during regadenoson-stimulated hyperemia was determined in ml/g/min. Positron emission tomography studies were repeated in 18 cases with a median follow-up of 2.5 years (interquartile range [IQR]:1.3 to 3.4 years).
  
  
  
  Twenty-five exams had normal perfusion but evidence of regional inflammation (group 1), and 21 exams presented a regional perfusion deficit associated with inflammation (group 2). Median myocardial blood flow did not differ between inflamed and noninflamed myocardium in both groups (0.86 ml/g/min [IQR: 0.66 to 1.11 ml/g/min] vs. 0.83 ml/g/min [IQR: 0.64 to 1.12 ml/g/min] and 0.74 ml/g/min [IQR: 0.60 to 0.93 ml/g/min] vs. 0.77 ml/g/min [IQR: 0.59 to 0.95 ml/g/min], respectively). As regards median hyperemic myocardial blood flows, they were significantly lower in the inflamed than in the remote regions in group 1 and 2 (2.31 ml/g/min [IQR: 1.81 to 2.95 ml/g/min] vs. 2.70 ml/g/min [IQR: 2.07 to 3.30 ml/g/min] and 1.61 ml/g/min [IQR: 1.17 to 2.18 ml/g/min] vs. 1.94 ml/g/min [IQR: 1.49 to 2.39 ml/g/min]; p < 0.001, respectively). Immune-suppression-mediated decrease in inflammation was associated with preserved myocardial flow reserve (MFR) at follow-up, whereas MFR significantly worsened in regions without changes or even increases in inflammation (median ΔMFR: 0.07 [IQR: -0.29 to 0.45] vs. -0.24 [IQR: -0.84 to 0.21]; p < 0.001). There was an inverse correlation between pronounced alterations in myocardial inflammation (Δ regional myocardial volume with standardized uptake value >4.1) and ΔMFR (r = -0.47; p = 0.048).
  
  
  
  Sarcoid-mediated myocardial inflammation is associated with a regional impairment of coronary circulatory function. The association between immune-suppressive treatment-related alterations in myocardial inflammation and changes in coronary vasodilator capacity suggests direct adverse effect of inflammation on coronary circulatory function in cardiac sarcoidosis.
authors.affiliation: Division of Nuclear Medicine-Cardiovascular Section, Department of Radiology and Radiological Science, School of Medicine, Johns Hopkins University, Baltimore, Maryland.
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Kruse
authors.affiliation: Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland.
authors.forename: Lara
authors.initials: L
authors.lastname: Kovell
authors.affiliation: Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland.
authors.forename: Edward K
authors.initials: EK
authors.lastname: Kasper
authors.affiliation: Division of Nuclear Medicine-Cardiovascular Section, Department of Radiology and Radiological Science, School of Medicine, Johns Hopkins University, Baltimore, Maryland.
authors.forename: Martin G
authors.initials: MG
authors.lastname: Pomper
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University, Baltimore, Maryland.
authors.forename: David R
authors.initials: DR
authors.lastname: Moller
authors.affiliation: Division of Nuclear Medicine-Cardiovascular Section, Department of Radiology and Radiological Science, School of Medicine, Johns Hopkins University, Baltimore, Maryland.
authors.forename: Lilja
authors.initials: L
authors.lastname: Solnes
authors.affiliation: Division of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University, Baltimore, Maryland.
authors.forename: Edward S
authors.initials: ES
authors.lastname: Chen
authors.affiliation: Division of Nuclear Medicine-Cardiovascular Section, Department of Radiology and Radiological Science, School of Medicine, Johns Hopkins University, Baltimore, Maryland; Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland. Electronic address: tschind3@jhmi.edu.
authors.forename: Thomas H
authors.initials: TH
authors.lastname: Schindler
mesh_terms: D000641:Ammonia / Q000008:administration & dosage; D001783:Blood Flow Velocity; D009202:Cardiomyopathies / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology*; D003326:Coronary Circulation / Q000187:drug effects; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000008:administration & dosage; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D055414:Myocardial Perfusion Imaging / Q000379:methods; D009205:Myocarditis / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology*; D009590:Nitrogen Radioisotopes / Q000008:administration & dosage; D000072078:Positron Emission Tomography Computed Tomography; D011237:Predictive Value of Tests; D019275:Radiopharmaceuticals / Q000008:administration & dosage; D012189:Retrospective Studies; D012507:Sarcoidosis / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology*; D013997:Time Factors; D016896:Treatment Outcome; D014664:Vasodilation
chemical_list: D007166:Immunosuppressive Agents; D009590:Nitrogen Radioisotopes; D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18; D000641:Ammonia
keywords: blood flow; circulation; inflammation; microvascular function; myocardial flow reserve; myocardial perfusion; positron emission tomography; sarcoid disease