Simulation Study of Susceptibility Gradients Leading to Focal Myocardial Signal Loss

MODERN CARDIAC MR imaging has shown the ability to reveal information beyond simple anatomy. Current techniques include evaluations of cardiac mass (1–4), measures of ejection fraction and contractility (5,6), as well as susceptibility-based contrast methods to assess myocardial perfusion and viability using exogenous contrast agents including gadolinium chelates (3,7–9) or by taking advantage of the BOLD effect using stress-inducing compounds such as dobutamine (10) or dipyridamole (10–12). Several cardiac imaging groups have reported large static field inhomogeneities in and near the heart (11–18) giving rise to a characteristic “bite”-shaped artifact. The artifact is seen as a highly focal, “bite”-shaped signal void along the infero-apical margin of the heart (Fig. 1). Pulse sequences that are highly sensitive to susceptibility differences such as many gradient echo methods, scans with echo planar readouts, and several other fast imaging techniques are most affected (14). The presence of this artifact can affect the interpretation of cardiac MR images. Figure 1 Human cardiac MR image at 3T. TFE black blood technique. θ = 25°, TR = 25 ms, TE = 11.53 ms, FOV = 290 mm, BW = 543 Hz. This is the third image of a four image set used to map T2* decay. Note the loss of signal in the inferoapical region ... Previous studies into the cause of this artifact have agreed that it is caused by magnetic susceptibility gradients but the relative influence of the various gradients around the heart has not been agreed upon. One study noted that the artifacts appeared near large epicardial veins, specifically the posterior vein of the left ventricle (PVLV) and, in some subjects, the great cardiac vein (17). The authors suggested that areas of high field inhomogeneity in measured field maps were generated by the difference in susceptibility between the deoxygenated blood flowing in large epicardial veins and the susceptibility of surrounding myocardium. In another study, experiments with a porcine model were conducted to examine several possible causes for the artifact (14). The study showed that there was very little dependence of the artifact on lung volume. The authors did note there was a slight improvement in the end-inspiratory images and attributed this to a shift in the artifact to a more apical position. The authors found that the artifact was not dependent on the oxygenation of the blood in the coronary sinus (14), apparently contradicting the conclusions of the human study (17). The porcine study also showed that surgical resection of the lungs away from the myocardium removed the artifact. When the chest was opened, the lungs partially collapsed. Significant artifacts were still seen near the “points” of the now collapsed, triangular lungs. When the lungs were resected out of the chest, and the cavity was filled with copper sulfate solution, the artifacts were removed. Furthermore, the artifact was removed independent of the position of the diaphragm, reducing the likelihood that sub-diaphragmatic structures are responsible. The authors of this study concluded lung tissue is the most likely source of the susceptibility artifacts although they noted that structural differences in heart and lung anatomy between pigs and humans prevent making this conclusion unequivocally for humans (14). An earlier report by the same group showed that free air in the chest after lung resection also did not produce the artifact, leading to the conclusion that the packaging of air into alveoli and small bronchioles rather than the extreme susceptibility difference between air and soft tissue is the source of the artifact (13). The results and conclusions of the previous studies (13,14,17) lead to some interesting questions. If the large epicardial veins are the primary cause of the artifact, as suggested in the human study, why did increasing the oxygen saturation of the vessels and thus reducing the susceptibility difference between the blood and the myocardium not lead to a reduction in the artifact in the porcine study? Second, if the heart–lung interface is the primary source of the susceptibility gradient, why does the artifact appear so focally rather than along the entirety of the heart–lung interface? It is the purpose of this study to assess by means of rigorous simulations the specific contributions of the PVLV and coronary sinus (CS) versus the heart–lung interface to the formation of static field inhomogeneities in the heart and thus imaging artifacts, with particular emphasis on the focal “bite”-shaped artifact. Simulating experiments allows control over the experiment such as setting blood oxygenation levels, changing the susceptibility of an entire organ, and eliminating motion, things not possible in real life. The simulations also provide the ability to completely remove or change internal structures without disrupting the rest of the body as would be required with surgical preparation of an in vivo study.