The following are key points to remember from an Expert Panel Statement on positron emission tomography (PET) for assessment of coronary microvascular dysfunction:

1. Myocardial PET can identify coronary microvascular dysfunction (CMD) noninvasively by quantifying reductions in hyperemic myocardial blood flow (MBF) and myocardial flow reserve (MFR). This consensus document aims to establish standardized cardiac PET diagnostic and reporting criteria for CMD.
2. Functional, structural, and/or myocardial factors may contribute to coronary microvascular dysfunction. Functional factors include impaired coronary vasodilation due to endothelial cell and/or smooth muscle cell dysfunction, primarily at the arteriolar level, and microvascular spasm. Structural factors include arterial remodeling with intimal and medial wall thickening, perivascular fibrosis, and reduced microvascular density (capillary rarefaction). Myocardial factors include left ventricular hypertrophy, diastolic dysfunction associated with interstitial and perivascular fibrosis, and increased intramyocardial and intracavitary pressure.
3. Multiple factors, including camera system, tracer kinetics, and imaging software, affect MBF quantification by PET. Therefore, establishing a universal threshold for normal MBF is challenging, but at most centers, CMD is defined as hyperemic MBF <1.7-2.3 mL/g/min. MFR (hyperemic MBF attained with a vasodilator such as adenosine or regadenoson, divided by rest MBF) offers the advantage of canceling out methodological errors, and MFR <2.0 is the universally accepted cutoff for identifying CMD. MFR <1.7 or <1.5 is associated with a high risk of major adverse cardiovascular events (MACE).
4. In the absence of obstructive epicardial coronary artery disease (CAD), global reductions in MBF can signify both CAD-related early structural/functional abnormalities of the epicardial vessels and/or coronary microcirculation.
5. Resting MBF by PET in healthy individuals is 0.7-1.2 mL/g/min. Lower resting MBF may occur with lower arterial blood pressure, bradycardia, or myocardial conditioning as seen in athletes. Increased resting MBF can occur with systemic hypertension, increased myocardial contractility, increased left ventricular wall stress, sympathetic activation, tachycardia, and obesity. Hyperemic MBF can decrease in the setting of obstructive epicardial CAD, hypertension, obesity, metabolic syndrome, diabetes, or increased left ventricular filling pressures (as seen in heart failure). Since MFR is calculated as hyperemic MBF/resting MBF, a decrease in MFR can be related to a decrease in hyperemic MBF, an increase in resting MBF, or both.
6. The “classical type” of CMD refers to impairment of hyperemic MBF due to dysfunction of the coronary arterioles and upstream vessels. In this situation, resting MBF is typically normal. Conversely, the “endogen type” of CMD is related to increased resting MBF in the setting of increased metabolic demand, associated with reduced coronary vasodilator capacity. MFR is reduced in both types of CMD.

Clinical Topics: Diabetes and Cardiometabolic Disease, Heart Failure and Cardiomyopathies, Noninvasive Imaging, Prevention, Vascular Medicine, Atherosclerotic Disease (CAD/PAD), Acute Heart Failure, Computed Tomography, Nuclear Imaging

Keywords: Angina Pectoris, Coronary Artery Disease, Coronary Circulation, Diabetes Mellitus, Diagnostic Imaging, Endothelial Cells, Fibrosis, Heart Failure, Hyperemia, Hypertrophy, Kinetics, Metabolic Syndrome, Microcirculation, Myocardial Ischemia, Myocardial Perfusion Imaging, Myocytes, Smooth Muscle, Obesity, Positron-Emission Tomography, Secondary Prevention, Spasm, Vasodilation, Vasodilator Agents

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