Background—This research describes an early preclinical study of the biophysical mechanisms governing changes in myocardial T₂ during vasodilation in normal myocardium.

Methods and Results—Theoretical modeling and experimental studies in an instrumented pig model (n=7) provided measures of changes in myocardial T₂, relative blood volume (BV), and microcirculation oxygen levels (%O₂) during intracoronary adenosine infusion. Intracoronary adenosine increases perfusion without increasing blood volume or cardiac metabolic rate; thus, T₂ elevations should reflect elevated microcirculation oxygen levels. Robust strategies were used for magnetic resonance imaging (MRI) data collection. Measures of myocardial and vascular T₁ before and after Clariscan (Amersham Health) injection provided blood volume assessment. Changes in microcirculation oxygen levels were estimated via direct blood sampling from the left anterior descending (LAD) coronary vein. Perfusion changes were monitored using a Doppler flow wire within the left main coronary artery. Myocardial T₂ elevations (T₂=17±8%) within the LAD arterial perfusion bed were related to elevations in perfusion (coronary velocity reserve=3.2±0.4) and coronary venous %O₂ [(LAD CV%O₂) =56±11%], whereas blood volume (BV=0 ±2%) and cardiac metabolic rate [(heart rate x blood pressure) = -4±11%] remained constant.

Conclusions—Myocardial T₂ elevation during intracoronary adenosine infusion was significant and repeatable, caused by increases in microcirculation oxygen levels. Changes in microcirculation oxygen levels of approximately 40%O₂ should be detectable by this technique. This sensitivity should suffice for differentiating normal from abnormal myocardium via measurement of myocardial perfusion reserve.