What question did this study set out to answer?

The study aims to assess the hemodynamic effects and myocardial T1 responses to ferumoxytol during stress cardiac MRI, particularly in ischemic heart disease.

March 21, 2026Open Access

Safety and T1 Reactivity for Vasodilator Stress Ferumoxytol-Enhanced Cardiac Magnetic Resonance Imaging

Key Points

The study aims to assess the hemodynamic effects and myocardial T1 responses to ferumoxytol during stress cardiac MRI, particularly in ischemic heart disease.
Seventy-two participants underwent ferumoxytol-enhanced cardiac MRI with regadenoson.
Cumulative doses of ferumoxytol (3.0 or 4.0 mg/kg) were administered.
Continuous hemodynamic monitoring was performed during the imaging.
T1 maps were analyzed to quantify vasoreactivity across different myocardial tissue types.
Responses were compared against gadobutrol and regadenoson alone.
No severe adverse events occurred, with only minor symptoms reported in five participants.
Mean arterial pressure (MAP) increased slightly post-ferumoxytol but was not statistically significant.
MAP decreased modestly post-regadenoson, with significant results.
A blunted FE-T1 vasoreactivity was observed across all tissue types compared to healthy myocardium.
Receiver operating characteristic analysis indicated good discrimination between tissue types.

Abstract

Ferumoxytol, an intravenous iron supplement that can be used off-label as a contrast agent in cardiovascular magnetic resonance (CMR), has been proposed to enhance the amplitude and dynamic range of myocardial T 1 vasoreactivity. Its combined use with vasodilators during stress testing may pose additional risks for hypotension. We aim to evaluate the hemodynamic profile and myocardial T 1 response of ferumoxytol and regadenoson for ferumoxytol-enhanced stress CMR (FE-CMR). Seventy-two participants (ischemic heart disease IHD: N=44, healthy: N=28) underwent FE-CMR under continuous hemodynamic monitoring. All IHD patients underwent clinically-indicated regadenoson stress cardiac positron emission tomography (PET) between 6 days and 31 weeks before FE-CMR. Ferumoxytol was administered in cumulative doses of 3.0 or 4.0 mg/kg, followed by regadenoson. Hemodynamic responses were compared with gadobutrol alone and with regadenoson alone. Post-contrast T 1 maps were segmented to quantify FE-T 1 vasoreactivity in healthy, remote, ischemic, and infarcted tissues. Linear mixed-effects models evaluated the effects of ferumoxytol and regadenoson on mean arterial pressure (MAP) and heart rate (HR), and compared FE-T 1 vasoreactivity across tissue types. No severe or life-threatening adverse events occurred. Five patients had mild symptoms. One study was terminated early due to moderate hypotension. Post-ferumoxytol MAP increased slightly (0.1−3.4%) at rest, without statistical significance. MAP decreased modestly post-regadenoson (−5.3 to −2.8%; all P<0.05). HR remained stable after ferumoxytol administration at rest and increased transiently after regadenoson, consistent with its pharmacologic effect. Unlike the modest MAP increase with ferumoxytol at rest, gadobutrol produced minor MAP decreases (−2.1 to −0.8%), with no significant between-agent differences. FE-T 1 vasoreactivity demonstrated a consistently blunted response across tissue types (ΔFE-T 1 in remote: −7.6±0.2%, ischemic: −4.6±0.3%, scar: −1.6±0.4%, healthy: −9.5±0.3%; all P<0.05). Receiver operating characteristic analysis showed strong remote versus scar discrimination (AUC 0.86) and modest remote vs. ischemia discrimination (0.69). Regadenoson stress FE-CMR is well-tolerated. Hemodynamic changes from combined ferumoxytol and regadenoson were small in magnitude and generally not clinically significant. Relative to healthy myocardium, blunted responses were observed in remote, ischemic, and infarcted tissues. Despite early promise, FE-T 1 vasoreactivity requires further dedicated study to fully evaluate its diagnostic performance as a gadolinium-free imaging biomarker in IHD.

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