Inversion-recovery-prepared SSFP for cardiac-phase-resolved delayed-enhancement MRI.

Delayed-enhancement magnetic resonance imaging (DE-MRI) can be used to visualize myocardial infarction (MI). DE-MRI is conventionally acquired with an inversion-recovery gradient-echo (IR-GRE) pulse sequence that yields a single bright-blood image. IR-GRE imaging requires an accurate estimate of the inversion time (TI) to null the signal from the myocardium, and a separate cine acquisition is required to visualize myocardial wall motion. Simulations were performed to examine the effects of a steady-state free precession (SSFP) readout after an inversion pulse in the setting of DE-MRI. Using these simulations, a segmented IR-SSFP sequence was optimized for infarct visualization. This sequence yields both viability and wall motion images over the cardiac cycle in a single breath-hold. Viability images at multiple effective TIs are produced, providing a range of image contrasts. In a study of 11 patients, IR-SSFP yielded infarct sizes and left ventricular ejection fractions (LVEFs) similar to those obtained by IR-GRE and standard SSFP, respectively. IR-SSFP images yielded improved visualization of the infarct-blood border because of the simultaneous nulling of healthy myocardium and blood. T(1) (*) recovery curves were extracted from IR-SSFP images and showed excellent qualitative agreement with theoretical simulations.

MRI relaxation fluctuations in acute reperfused hemorrhagic infarction.

MRI evaluations of intramyocardial hemorrhage in acute infarction have relied on T(2) and T(2)(*) shortening only. We propose a more comprehensive evaluation of hemorrhagic infarction based on the concept that fluctuations in T(2) and T(1) relaxation in acute reperfused infarction will reflect transient edema and hemoglobin oxidative denaturation to uncompartmentalized methemoglobin. Anteroapical infarction was created via percutaneous balloon in young swine (22-25 kg, N = 12). T(2), T(1), diastolic wall thickness (DWT), and the Gd-DTPA partition coefficient (lambda) were measured on days 0, 2, and 7. DWT was elevated at 1 hr postreperfusion (128% +/- 53%, P = 0.0001), and alleviated on days 2 and 7 (48% +/- 10%, P = 0.008; 53% +/- 24%, P = 0.003). T(2) and T(1) elevations were coincident with early edema (DeltaT(2) = 55% +/- 24%, P < 0.0001; DeltaT(1) = 27% +/- 18%, P < 0.04). T(2) and T(1) were nearly normal on day 2 (DeltaT(2) = 8% +/- 8%, P = 0.27; DeltaT(1) = 0% +/- 1%, P = 0.65). On day 7, T(2) increased while T(1) decreased (DeltaT(2) = 27% +/- 16%, P = 0.005; DeltaT(1) = -14% +/- 10%, P = 0.02). Lambda was elevated by >150% at all time points (P < or = 0.002). Histology verified hemorrhagic injury. T(1) and T(2) fluctuations are consistent with transient edema, as well as hemoglobin oxidative denaturation to decompartmentalized methemoglobin. This methodological development may broaden our understanding of hemorrhagic microvascular injury and improve its detection in clinical populations.

T2 fluctuations in ischemic and post-ischemic viable porcine myocardium in vivo.

T2 relaxation can augment delayed-enhancement viability imaging because it is sensitive to tissue edema and microcirculatory oxygen state. We demonstrate the T2 'signatures' of sub-lethal ischemia and stunning in porcine myocardium perfused by the distal left anterior descending artery, by imaging during percutaneous balloon occlusion for 25 minutes and subsequent reperfusion (n = 9). Muscle displayed ischemic dysfunction and partial post-ischemic functional recovery (p < or = 0.0004), concommitant with an elevated post-ischemic T2 (deltaT2 = 27 +/- 18%, p = 0.005). TTC staining verified muscle viability. The T2 fluctuations may reflect hyperemia and tissue cellular edema in accord with the known pathophysiology of ischemic and post-ischemic yet viable muscle.