Quantitative blood oxygenation level‐dependent (BOLD) response of the left ventricular myocardium to hyperoxic respiratory challenge at 1.5 and 3.0 T

The aim of this study was to quantify the response of the myocardial transverse relaxation times (Δ T 2 *) to hyperoxic respiratory challenge (HRC) at different field strengths in an intra‐individual comparison of healthy volunteers and in a patient with coronary artery disease. Blood oxygenation level‐dependent (BOLD) cardiovascular MR (CMR) data were acquired in 10 healthy volunteers (five women, five men; mean age, 29 ± 3 years; range, 22–35 years) at 1.5 and 3.0 T. Medical air (21% O 2 ), pure oxygen and carbogen (95% O 2 , 5% CO 2 ) were administered in a block‐design temporal pattern to induce normoxia, hyperoxia and hyperoxic hypercapnia, respectively. Average T 2 * times were derived from measurements by two independent and blind readers in 16 standard myocardial segments on three short‐axis slices per patient. Inter‐ and intra‐reader correlations of T 2 * measurements were good [intra‐class correlation coefficient (ICC) = 0.75 and ICC = 0.79, both p  < 0.001]. During normoxia, the mean T 2 * times were 29.9 ± 6.1 ms at 1.5 T and 27.1 ± 6.6 ms at 3.0 T. Both hyperoxic gases induced significant (all p  < 0.01) T 2 * increases (∆ T 2 * hyperoxia: 1.5 T, 12.7%; 3.0 T, 11.2%; hyperoxic hypercapnia: 1.5 T, 13.1%; 3.0 T, 17.7%). Analysis of variance (ANOVA) results indicated a significant (both p  < 0.001) effect of the inhaled gases on the T 2 * times at both 1.5 T ( F  = 17.74) and 3.0 T ( F  = 39.99). With regard to the patient imaged at 1.5 T, HRC induced significant T 2 * increases during hyperoxia and hyperoxic hypercapnia in normal myocardial segments, whereas the T 2 * response was not significant in ischemic segments ( p  > 0.23). The myocardial ∆ T 2 * response to HRC can reliably be imaged and quantified with BOLD CMR at both 1.5 and 3.0 T. During HRC, hyperoxia and hyperoxic hypercapnia induce a significant increase in T 2 *, with ∆ T 2 * being largest at 3.0 T and during hyperoxic hypercapnia in normal myocardial segments. Copyright © 2014 John Wiley & Sons, Ltd.