Purpose: To explore the relationship of myocardial T 2 and oxygenation for the quantification of myocardial oxygen extraction fraction (OEF). Materials and Methods:A proposed myocardial T 2 -OEF relationship was evaluated by computer simulation and in nine normal dogs in vivo. The relationship was based on a simplified two-compartment T 2 model. In the dogs, dipyridamole was infused intravenously to increase blood flow and change in myocardial oxygen content. The accuracy of the measurement in myocardial OEF in vivo by magnetic resonance imaging (MRI) was determined by arterial and coronary sinus blood sampling.Results: Global myocardial T 2 increased 16.1% from rest to the peak of dipyridamole-induced vasodilation (44.6 Ϯ 2.1 msec vs. 51.4 Ϯ 2.1 msec, P Ͻ 0.001). Corresponding OEF measured by arterial and venous (AV) sampling decreased from 0.64 Ϯ 0.15 at rest to 0.18 Ϯ 0.08 during the dipyridamole vasodilation, whereas OEF calculated by MRI at the peak effect of dipyridamole was 20 Ϯ 4%. Global myocardial OEF measured dynamically by MRI showed a strong correlation with OEF measured by blood sampling (correlation coefficient (CC) ϭ 0.83) during pharmacologic vasodilation. Conclusion:When combined with vasodilator stress, assessment of OEF may provide a putative measure of myocardial flow reserve, allowing consecutive monitoring of myocardial dose-responses to a variety of interventions and offering a new tool for the detection of coronary artery disease.

The risk of atherosclerotic plaque disruption is thought to be closely related to plaque composition and rupture triggers such as external mechanical forces. The purpose of this study was to integrate MR imaging and computational techniques for the quantification of plaque vulnerability with morphologic data and biomechanical stress/strain distributions that were all based on high-resolution MR images of coronary artery plaque specimens ex vivo. Twenty-two coronary artery plaque specimens were selectively collected from 10 cadavers. Multislice T 2 -weighted spin echo images were acquired with a resolution of 100 ؋ 100 m 2 . Histopathological images were used as the gold standard for the identification of plaque components and vulnerability. Plaque components were classified on MR images, and the stress/strain components were calculated with a twodimensional computational model with fluid-structure interactions. As expected, vulnerable plaques appeared to result from a large lipid pool, a thin fibrous cap, and some critical stress/ strain conditions. An empiric vulnerability marker was derived and was closely related to the vulnerability score that was determined through pathologic examination. Acute coronary syndrome accounts for over 1 million deaths in the United States (1). Plaque rupture/erosion and fissures are the primary causes of acute coronary syndrome and may occur without any warning. This acute process that culminates with plaque rupture is complicated and the precise mechanism remains hypothetical. Largely derived from the observations of autopsy tissues by Davis and Thomas (2), the widely held concept of the general characteristics of a ruptured plaque is the formation of a large, soft, lipid-rich necrotic core (LRNC). This core occupies approximately 40% of the plaque area and is covered by a thin fibrous cap (Ͻ65 m), which is densely infiltrated by inflammation cells such as macrophages (3). Rupture of this thin cap and then the subsequent thrombus formation are thought to be the most important mechanisms underlying acute syndromes. However, rupture of plaque depends not only on its cap thickness, but also on biomechanical factors such as hemodynamic shear stress, transient compression, external compression, and bent plaque edges due to the propagating pulse wave (4,5).Our hypothesis is that comprehensive characterization of plaque geometry, components, and critical stress/strain distribution would greatly enhance the capability to assess the vulnerability of atherosclerotic lesions. Many imaging modalities have been applied to determine the characterization of plaques, including ultrafast CT (6), positron emission tomography (7), and MRI (8,9). However, only elastographic intravascular ultrasound, an invasive imaging modality, can provide information simultaneously about both plaque components and strain distribution (10). Compared with other imaging methods, MRI has the greatest potential for noninvasive and comprehensive assessments of atherosclerotic plaques, not only on luminal stenosis and ...