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Final Program


Program-At-A-Glance

Oral Abstracts Session

Session: Oral Abstracts Translation Session 1

In Vivo Assessment of Coronary Sinus Oxygen Saturation During Post-Exercise Cuff Occlusion and Hypercapnia Using Cardiovascular Magnetic Resonance

Thursday, February 5, 2026
3:30 PM - 3:40 PM  
Location: Oceania IV and V (2nd Floor)
Background: Coronary sinus (CS) oxygen saturation reflects myocardial oxygen extraction and serves as a potential biomarker of cardiac metabolic demand. However, measuring CS oxygen saturation is challenging due to the vessel’s small size, location, and confounding motion from both the heart and lung. Our group has previously reported on a motion-insensitive cardiac magnetic resonance (CMR) technique capable of reliably quantifying CS oxygen saturation, and validated in a large animal model by direct CS catheterization.1 The purpose of this study was to evaluate changes in coronary sinus oxygen saturation in vivo in human participants during two distinct physiologic provocations: post exercise cuff occlusion (PECO; to elevate myocardial oxygen demand) and hypercapnia (2% CO₂, 21% O₂, balance N₂; to elevate myocardial oxygen delivery).

Methods: Healthy adults underwent CMR imaging at 3T (MAGNETOM Vida, Siemens Healthineers, Forchheim, Germany). CS oxygen saturation was measured at baseline and during PECO and hypercapnia. PECO was induced via sustained isometric handgrip followed by upper arm cuff inflation to maintain post-exercise circulatory occlusion. Hypercapnia was delivered via a Douglas bag connected to a two-way valve and mouthpiece apparatus (Figure 1). CS oxygen saturation was quantified using a recently developed fast, motion-resolved T2-based MR oximetry sequence.1 Myocardial Oxygen Extraction Fraction (OEF) was measured by deriving the gradient between arterial oxygen saturation (SaO2) and coronary sinus oxygen saturation (SCSO2). The ScsO2 and OEF were compared between baseline and each provocation state.

Results: Preliminary data (Figure 2) demonstrate a significant decrease in CS oxygen saturation and increased OEF during PECO (N = 6, rest ScsO2 = 44.1±1.4%, PECO ScsO2 = 39.6±1.8%, ΔScsO₂ = -4.5%, p < 0.05; Rest OEF = 54.6±1.5%, PECO OEF = 59.6±2.4%, ΔOEF = 5.0%, p < 0.05), consistent with increased myocardial oxygen extraction. In contrast, hypercapnia elicited a modest increase in CS oxygen saturation (N = 4, Rest ScsO2 = 42.1±2.1%, hypercapnia ScsO2 = 47.6±1.9%, ΔScsO₂ = 5.5%, p < 0.05; Rest OEF = 56.9±2.3%, hypercapnia OEF = 52.2±2.0%, ΔOEF = -4.7%, p < 0.05), consistent with coronary vasodilation and increased oxygen delivery without changing metabolic demand.

Conclusion: To our knowledge, these data represent the first instance in which CS oxygen saturation has been measured by CMR-based methods during physiological provocation in humans. The data show that CMR-based assessment of CS oxygen saturation is both feasible and responsive to physiological stress. Together, these findings underscore the potential of CS MR oximetry as a valuable tool for investigating myocardial oxygen extraction and may provide a foundation for future research examining myocardial oxygen extraction reserve across the spectrum of age and cardiovascular disease.

Figure 1. Experimental setup and depiction of the physiologic provocations. After localization, coronary sinus oxygen saturation was measured at rest, during post-exercise cuff occlusion (PECO), and hypercapnia (2% CO2). Coronary sinus oxygen saturation and myocardial oxygen extraction fraction were derived under each provocation.
Figure 2. Representative coronary sinus oxygen saturation (SCSO2) from a subject during post-exercise cuff occlusion (PECO) and hypercapnia (2% CO2). The SCSO2 is significantly reduced during PECO and elevated during hypercapnia. The same trend is presented in OEF derived from the arterial-venous SO2 gradient. The OEF response reflects the potential changes of oxygen demand under cardiac provocation.