Assesses microvascular function in diabetes patients with and without foot ulcers, suggesting effective monitoring strategies for healing.
Introduction and Objective: Predicting risk of DFU development and resolution is clinically important to inform treatments and prognosis early in the disease. DFUs develop in part due to microvascular damage, however there is a paucity of clinical tests that are sensitive to microvascular health. The objective of this study is to quantify microvascular structure and function using quantitative MRI (qMRI) techniques in patients with and without DFUs. Methods: This ongoing prospective observational study enrolled 7 patients with unhealed plantar forefoot ulcers for at least 30 days. We enrolled 7 age- and BMI- matched patients with T2DM and without history of DFUs. Microvascular perfusion and function were evaluated using non-contrast qMRI techniques, including a dynamic cuff-occlusion protocol. DFU healing was followed for 12 weeks of standard wound care after the MRI. Perfusion markers were compared in the medial plantar compartment between patients with and without DFUs. Results: Ulcers healed in 42% of patients with DFUs. Control patients showed a significantly lower resting microvascular volume fraction (MVF) than DFU patients (0.60% vs 1.40%, p>0.01). There were qualitative trends for increased microvascular reactivity in control patients (49s vs 112s to peak hyperemia, p=0.11). Bivariate analysis (e.g., MVF vs reactivity) reveals separate clusters between diabetic controls and non-healing DFU patients, with healing DFU patients appearing closer to controls. Conclusion: qMRI markers reveal differences in microvascular perfusion and function in the presence of DFUs. These markers appear to be sensitive to wound healing in DFU. Combining perfusion and functional markers could help identify microvascular factors leading to poor outcomes and monitor treatment strategies. Disclosure S. Edwards: None. N. Soleimanmanesh: None. N.Y. Chaudhry: None. J. Flores: None. E. Watson: None. G. Santamarina: None. M. Schechter: None. M. Fayfman: Research Support; Current; Dexcom, Inc., Abbott Diabetes. D.A. Reiter: None. Funding NIH DK136983
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