Author + information
- Received June 1, 2016
- Revision received September 12, 2016
- Accepted September 14, 2016
- Published online February 6, 2017.
- Matthew J. Kruse, MDa,
- Lara Kovell, MDb,
- Edward K. Kasper, MDb,
- Martin G. Pomper, MDa,
- David R. Moller, MDc,
- Lilja Solnes, MDa,
- Edward S. Chen, MDc and
- Thomas H. Schindler, MDa,b,∗ ()
- aDivision of Nuclear Medicine–Cardiovascular Section, Department of Radiology and Radiological Science, School of Medicine, Johns Hopkins University, Baltimore, Maryland
- bDivision of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland
- cDivision of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University, Baltimore, Maryland
- ↵∗Address for correspondence:
Dr. Thomas H. Schindler, Johns Hopkins University, School of Medicine, Division of Nuclear Medicine, Cardiovascular Nuclear Medicine, Department of Radiology and Radiological Science SOM, JHOC 3225, 601 North Caroline Street, Baltimore, Maryland 21287.
Objectives This study sought to evaluate the effects of inflammatory sarcoid disease on coronary circulatory function and the response to immune-suppressive treatment.
Background 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.
Methods Thirty-two individuals, who were referred for positron emission tomography/computed tomography, were evaluated for known or suspected cardiac sarcoidosis applying 18F-fluorodeoxyglucose to determine inflammation and 13N-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).
Results 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).
Conclusions 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.
- blood flow
- microvascular function
- myocardial flow reserve
- myocardial perfusion
- positron emission tomography
- sarcoid disease
Supported by Departmental Fund (175470) from Johns Hopkins University. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received June 1, 2016.
- Revision received September 12, 2016.
- Accepted September 14, 2016.
- American College of Cardiology Foundation