LAUSR

Imaging Modalities: Coronary artery disease (CAD) is currently a worldwide epidemic, with an ever-increasing impact on the healthcare systems. Noninvasive myocardial perfusion assessment is clinically valuable for patients with known or suspected CAD, myocardial dysfunction, and who may benefit from coronary revascularization. Single photon emission computed tomography (SPECT), positron emission tomography (PET), and cardiac magnetic resonance imaging (MRI) have been used for assessing myocardial perfusion. Cardiac MR is considered the first-choice technique for the diagnostic work-up of patients having CAD because of the lack of radiation, its high spatial resolution, and it provides complementary information on myocardial viability, global/regional ventricular function, and myofiber orientation/fiber tracking. Adenosine: Adenosine receptors A1, A2A, A2B, and A3 are bunched on the P1 purinergic receptors family. Adenosine receptors are ubiquitous and, depending on their localization, may mediate opposite effects. This phenomenon is evident in the interaction of adenosine with different adenosine receptors in the heart and spleen, where it produces vasodilation mediated via A2B in the coronary arteries and vasoconstriction mediated via A2A receptors in the splenic arteries. 3 In healthy coronary arteries, adenosine causes vasodilation, thereby increasing coronary flow up to four times the basal blood flow through a mechanism commonly referred to as “coronary reserve.” In CAD, where the arteries are already dilated, adenosine has the opposite effect by reducing blood flow in the stenosed artery through a mechanism known as the “steal phenomenon.” Patients with known or suspected CAD are routinely examined by infusion of adenosine at the standard dose (140 μg/kg/min). During the first passage of gadolinium contrast media at the standard dose of adenosine, investigators observed sufficient contrast (≥25% difference in regional signal intensity) between the hypoperfused territory compared to the normally perfused remote territory (≥25% difference in regional signal intensity). De Bruyne et al confirmed that such a dose is sufficient to produce maximum vasodilation and a higher dose does not create further vasodilation. Others, however, found that a 140 μg/kg/min dose provides inconsistent findings. For instance, Karamitsos et al indicated that 18% of the patients did not respond to the 140 μg/kg/min dose. For the remaining patients (82%), the standard dose was insufficient to induce maximum coronary vasodilation. Therefore, they assert that an inadequate adenosine dose is a major cause for false-negative ischemic myocardial testing. Splenic Switch-Off: The recent work of Manisty et al used a special approach by adopting a splenic switch-off (SSO) technique to determine adequate adenosine stress to assess the myocardial perfusion reserve of CAD patients. The SSO technique measures whether there is a visible decrease in splenic signal intensity, as compared to a baseline, during adenosine infusion. It is a straightforward technique that does not rely on special hardware, software, or imaging sequences to cover the heart and spleen. On this basis, the article by Giusca et al in this issue of JMRI sought to determine the optimal dose of adenosine, in terms of effectiveness and safety, by using the SSO technique in a study of 100 randomly selected patients with known or suspected CAD. The study was carefully performed and included a moderate number of patients for analysis. Single-shot saturation recovery gradient echo (GRE) images were acquired to cover the heart and spleen at rest and adenosine stress. Patients received either the standard dose (140 μg/kg/min) or higher doses (175 μg/kg/min or 210 μg/kg/min). The presence and absence of SSO was based on the regional signal intensity ratio (adenosine stress/rest signal intensity) and the difference in the upslope of signal intensity at rest and stress. The authors found that the presence of SSO is significantly higher in patients receiving 175 μg/kg/min (94%) and 210 μg/kg/min (93%) than patients receiving 140 μg/kg/min (58%). Quantitatively, the decrease of splenic signal intensity during adenosine stress was