Blood Oxygenation Level–Dependent Magnetic Resonance Imaging of the Skeletal Muscle in Patients With Peripheral Arterial Occlusive Disease

Abstract

Background-Blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) has been used to measure T2* changes in skeletal muscle tissue of healthy volunteers. The BOLD effect is assumed to primarily reflect changes in blood oxygenation at the tissue level. We compared the calf muscle BOLD response of patients with peripheral arterial occlusive disease (PAOD) to that of an age-matched non-PAOD group during postischemic reactive hyperemia. Methods and Results-PAOD patients (nϭ17) with symptoms of intermittent calf claudication and an age-matched non-PAOD group (nϭ11) underwent T2*-weighted single-shot multiecho planar imaging on a whole-body magnetic resonance scanner at 1.5 T. Muscle BOLD MRI of the calf was performed during reactive hyperemia provoked by a cuff-compression paradigm. T2* maps were generated with an automated fitting procedure. Maximal T2* change (⌬T2* max ) and time to peak to reach ⌬T2* max for gastrocnemius, soleus, tibial anterior, and peroneal muscle were evaluated. Compared with the non-PAOD group, patients revealed significantly lower ⌬T2* max -values, with a mean of 7.3Ϯ5.3% versus 13.1Ϯ5.6% (PϽ0.001), and significantly delayed time-to-peak values, with a mean of 109.3Ϯ79.3 versus 32.2Ϯ13.3 seconds (PϽ0.001). Conclusions-T2* time courses of the muscle BOLD MRI signal during postocclusive reactive hyperemia revealed statistically significant differences in the key parameters (⌬T2* max ; time to peak) in PAOD patients compared with age-matched non-PAOD controls.

Blood oxygenation level‐dependent (BOLD) MRI of human skeletal muscle at 1.5 and 3 T

“…It was more pronounced in slowtwitch soleus muscle when compared with fast-twitch gastrocnemius muscle, a finding that is well known and may be explained by the larger capillary density and thus higher degree of oxygen diffusion into muscle tissue of that muscle (19). After cuff deflation the larger T2* increase in the soleus muscle compared with the gastrocnemius muscle has also been previously described and may be explained by the better vascularity or perfusion reserve of the mostly oxidative fiber containing soleus muscle (3,4,6,14). As the muscle BOLD effect has a complex origin that is still not completely understood, other mechanisms may also contribute to the observed intermuscular differences.…”

“…All volunteers showed a common overall time dependence of the muscle BOLD time course that can be compared with previous studies (6,7,16,19). The ischemic decrease of BOLD signal is the result of oxygen consumption after interruption of blood flow at the mid-thigh level.…”

“…This paradigm has been extensively applied and is well established in skeletal muscle BOLD studies due to its easy feasibility and almost complete independence on patient compliance. For muscle BOLD MRI, we used a previously described multiecho gradient-echo EPI sequence that only had to be minimally adapted between the two MRI systems of 1.5 T and 3.0 T (4,6,7,16). This sequence allows the differentiation of tissue oxygen related contrast (''true'' BOLD signal) from changes in T1, baseline drifts, and inflow effects which frequently interfere in conventional single-echo EPI imaging (17,18).…”

“…We used a cuff-compression paradigm previously applied in other muscle BOLD imaging studies to provoke reactive hyperemia (2,3,(5)(6)(7)16). Our study protocol consisted of a 60-second resting period to obtain a preocclusive baseline, followed by 240 seconds of ischemia, and finally 600 seconds of reactive hyperemia.…”

“…T2* changes in gradient-echo (GE) echo-planar-imaging (EPI) sequences can mainly be attributed to changes in the intravascular ratio of oxy-to deoxyhemoglobin of the muscle microvasculature (1)(2)(3)(4)(5). Muscle BOLD imaging has been shown to be capable of detecting disturbances of muscle microperfusion in diseases such as peripheral arterial occlusive disease, chronic compartment syndrome, and ischemic heart disease (6)(7)(8)(9).…”