1321756 - Just Breathe! The Ins and Outs of Oxygenation-Sensitive Cardiovascular Magnetic Resonance (OS-CMR)

Current standard tests for coronary artery disease (coronary angiography, SPECT, stress echocardiography,  first-pass perfusion cardiac magnetic resonance imaging, CMR) require the application of pharmacological or physical stress and/or the administration of a contrast agent or radioactive tracer. None of these methods measure coronary vascular function on a microvascular level or can assess tissue oxygenation changes as the relevant biomarker. Recently, oxygenation-sensitive CMR (OS-CMR) has been established as a non-invasive technique to track changes in myocardial oxygenation and assess coronary vascular function during vasoactive breathing maneuvers. This presentation will explain the protocol for breathing-enhanced OS-CMR and the acquisition of the breathing-induced myocardial oxygenation reserve in healthy volunteers and patients.



Methods:

OS-CMR uses the so-called BOLD (blood oxygen level dependent) effect on myocardial T2* associated with an increased presence of iron or de-oxygenated hemoglobin to visualize changes in tissue oxygenation¹. BOLD- or T2*-“sensitive” sequences are used to assess myocardial iron overload in patients with hemochromatosis but can also be used to track changes in myocardial oxygenation. Hyperventilation and breath-holds lead to endothelium-dependent coronary vasoconstriction and vasodilation, respectively, thus can be used as physiological vasoactive maneuvers that do not require the administration of a pharmacological stress agent. Current protocols typically start with an OS-CMR image acquisition during a short breath-hold. These baseline images are used to verify that both short axis slices have a good quality, are void of artifacts, and are well-positioned (Fig.1). The second series is a continuous acquisition with 2 minutes of relaxed breathing followed by 1 minute of paced hyperventilation using a pre-recorded metronome (set at 30 beats per minute) and ending with a voluntary, end-expiratory breath hold of at least 40 seconds to ensure that images of 3 full cardiac cycles for each planned slice are obtained (Fig.2).



Results:

The global myocardial signal intensity at end-systole acquired at 30 seconds of the post-hyperventilation breath-hold is compared to the end-systolic image acquired at the beginning of the post-hyperventilation breath-hold. The Breathing-induced Myocardial Oxygenation REserve (B-MORE) is then calculated as a percentage change in signal intensity over the breath-hold (Fig.3). It reflects the change of myocardial oxygenation from vasoconstriction (immediately post hyperventilation) to vasodilation (voluntary apnea), and directly reflects the entire endothelium-dependent vasoactive capacity of the coronary vascular system.



Conclusion:

This novel acquisition method has the potential to eliminate the use of pharmacological stress and contrast agents. The results can be presented as a vascular function map and thereby provide important information for clinical decision-making.