Blood oxygen level-dependent magnetic resonance imaging in patients with stress-induced angina

Abstract

Background-Blood oxygen level-dependent (BOLD) MRI reflects tissue oxygenation and may be useful for the detection of myocardial ischemia in patients with suspected coronary artery disease. Methods and Results-We studied 25 patients with stress-induced angina using a T 2 *-sensitive echo planar imaging sequence before and during adenosine in a single-slice approach. BOLD-MRI results were compared with quantitative angiography and adenosine thallium single-photon emission computed tomography (SPECT). Although image quality was variable because of artifacts, no data were excluded from the analysis. During adenosine, a mean signal intensity decrease was observed for myocardial segments related to coronary stenoses Ͼ75%. On average, a nonsignificant increase was observed in the other segments. The angiographically determined stenosis was correlated with BOLD-MRI results. Including all segments and using BOLD-MRI signal intensity increase cutoff value of 1.2%, BOLD-MRI had a sensitivity of 88% and a specificity of 47% to correctly classify severe stenoses. Adenosine thallium SPECT data from distal segments of the same coronary territory were also correlated with BOLD-MRI. However, variability was substantial. Conclusions-In patients with stress-induced angina, adenosine BOLD-MRI detects myocardial ischemia in myocardial segments related to severe coronary stenoses. Its potential will increase with additional improvement of spatial coverage and image quality.

Three-dimensional contrast-enhanced and non-contrast-enhanced cardiac magnetic resonance imaging for the assessment of myocardial ischemic reactions

“…These results confirmed previous study data reporting a close correlation between BOLD signal intensity changes and the degree of coronary stenosis ( Figure 8). 44 Overall, an improved diagnostic value for the detection of significant coronary stenosis was seen (Table 1). In addition, myocardial segments consisting predominantly of scar tissue as defined by LGE imaging exhibited constant BOLD signal intensities at rest and during vasodilator stress as a result from the scarcely capillarized scarred myocardium without any vasodilatory capacity.…”

“…Consequently, in patients with chest pain syndromes BOLD CMR imaging offered a good sensitivity in comparison to quantitative coronary angiography but resulted in a low specificity. 44 Considering only patients with angiographically diagnosed triple-vessel disease a stress-induced decrease of the BOLD signal was observed in 81% of segments though a global change affecting all myocardial segments was expected. 47 It was speculated that the stress-induced increase in myocardial oxygenation in the remaining myocardial segments may be attributed to a still existing residual vasodilator capacity and, thus, the morphological stenoses did not result in an overall functional relevance.…”

“…21,43,44 These studies were performed using clinically available 1.5 Tesla scanners and predominantly utilized vasodilator stress protocols to provoke myocardial ischemic reactions. Vasodilator stress leads to a BOLD signal enhancement due to luxuriant perfusion with increased myocardial oxygenation as verified by an increase of myocardial T2* values over baseline values.…”

Myocardial T2* Mapping with Ultrahigh Field Magnetic Resonance: Physics and Frontier Applications

“…A T 2 increase would also result in increased T 2 * as seen from Equation (1). Further to this, reduced myocardial perfusion and ischemia are common in HCM [109], effectively reducing the tissue blood volume fraction resulting in a T 2 * increase as suggested by Equation (5). These conditions are also associated with a higher risk for a poor outcome in HCM patients [110].…”

“…By exploiting the blood oxygenation level-dependent (BOLD) effect [3], T 2 * sensitized CMR has been proposed as a means of assessing myocardial tissue oxygenation and perfusion. T 2 * mapping has been shown to be capable of detecting myocardial ischemia caused by coronary artery stenosis [4], to reveal myocardial perfusion deficits under pharmacological stress [5][6][7][8][9][10], to study endothelial function [11] or to assess breathing maneuver-dependent oxygenation changes in the myocardium [12][13][14][15]. Preclinical studies have also demonstrated the potential of T 2 * mapping to detect structural changes in the infarcted heart muscle and even to distinguish between focal and diffuse fibrosis [16][17][18].…”