Cardiovascular magnetic resonance (CMR) is increasingly applied in clinical routine to determine myocardial perfusion [1–4] using contrast enhanced first-pass perfusion techniques [5–8]. Non-invasive characterization of myocardial microcirculation is thought to reflect myocardial tissue supply much better than mere luminographic detection and quantification of epicardial coronary stenosis, and has been shown to be useful for planning of revascularization procedures and cardiac risk stratification.

Blood Oxygen Level Dependent (BOLD) CMR is based on the paramagnetic properties of deoxyhemoglobin as an endogenous contrast agent with increased deoxyhemoglobin content leading to signal reduction on T2*- or T2-weighted images. Thus, BOLD CMR directly reflects myocardial oxygenation status [9, 10]. Coronary artery stenosis leads to poststenotic microvascular dilatation in a compensatory effort to maintain sufficient myocardial oxygen supply [11] and blood-oxygen level dependent imaging has been successfully introduced to determine capillary reserve [12, 13].

However, data on myocardial BOLD CMR during vasodilator stress in patients with coronary artery disease (CAD) is limited to experimental studies [13–15] and small patient populations [11, 12]. The main challenge was low signal intensity differences between normal and pathologic areas of myocardium at 1.5T, and therefore BOLD CMR at 3T may benefit from the inherently higher signal-to-noise ratio (SNR). Hence, in the present study we determined the ability of BOLD CMR to detect stress induced myocardial ischemia and to differentiate between ischemic, non-ischemic, and normal myocardial segments in a population of patients with suspected or known CAD.

In the present study, BOLD CMR at 3T was shown to be feasible at 3T resulting in an overall good image quality at rest and during vasodilator stress. BOLD CMR at rest and under stress conditions distinguished between normal, ischemic and non-ischemic myocardial segments. In addition, adenosine stress BOLD CMR gave a good diagnostic performance with regard to the detection of angiographically defined coronary stenosis.

The non-invasive detection of ischemic myocardium is one of the major strengths of CMR. BOLD imaging represents a promising alternative to first-pass CMR perfusion techniques, which rely on the application of exogenous contrast agents. BOLD imaging allows to directly assess the myocardial oxygenation status taking advantage of the paramagnetic properties of intravascular deoxyhemoglobin [11]. During adenosine stress, myocardial segments being supplied by normal coronary arteries show an increased oxygen content while deoxyhemoglobin concentration is low resulting in a higher signal on T2*- or T2-weighted images. On the contrary, myocardial segments being supplied by a stenosed coronary artery exhibit a dilated capillary bed already under resting conditions in order to maintain sufficient blood supply. Hence, additional vasodilatation under stress is minimal and the hyperaemic response is abolished.

In the present study, ischemic myocardial segments showed significantly reduced T2* values under resting conditions, while during adenosine stress T2* values increased in normal myocardial segments only. Our findings were consistent with previous reports by Wacker et al. and Niemi et al. [11, 18], but somewhat contrasted the results by Friedrich et al. [12] even demonstrating a signal decrease during vasodilator stress in myocardial territories supplied by coronary arteries with >75% luminal narrowing.

Interestingly, in the present study non-ischemic myocardial segments did not show a significant increase of T2* values during stress. These findings may be explained by microvascular disease [19], which is present in myocardial segments of patients with CAD despite the absence of significant epicardial coronary artery narrowing. The T2* measurements of the current study showed a relation between the degree of coronary stenosis and the T2* value at rest and under adenosine stress.

The T2* CMR values at rest in patients without CAD were within the range of previously published data by Story et al. (33.3 ± 8.3 ms, outliers were excluded) [20] and O'Regan et al. (27.3 ± 6.4 ms) [21] using a single-slice image acquisition. However, in our study, the standard deviation of T2* values was substantially larger, which can be explained by the imaging strategy employing a 3-slice acquisition per patient in order to achieve coverage of all 16-standard myocardial segments. Susceptibility artifacts appeared predominantly in the inferolateral segments of the myocardium on images with the longest echo times and resulted mainly from interference with cardiac veins [22] and the heart-lung interface [23]. In order to reduce these artifacts an end-expiratory breath hold was used as proposed by Wacker et al.[9] in conjunction with a black blood prepulse to reduce possible sources of artifacts arising from the blood pool. Furthermore, the use of only six echo times and a relatively short echo spacing and repletion time of 13 ms in our study prevents susceptibility artefacts caused by longer echo times [9]. Recently, O'Regan et al. [21] reported that black blood breath-hold multiecho T2* imaging can be adequately performed at 3T and resulted in only minor susceptibility artifacts in the inferolateral region of the heart.

Importantly, the current study population consisted of consecutive patients with a high proportion of known CAD and prior myocardial infarctions but such patients were usually not considered in previous studies [11, 12, 21]. However, a direct comparison to first pass CMR perfusion or SPECT imaging would have been desirable and may be considered a limitation of the present study.

Rest and stress BOLD CMR at 3T proved feasible and may be used to differentiate between ischemic, non-ischemic, and normal myocardial segments in a clinical patient population. BOLD CMR during vasodilator stress identified patients with significant CAD.