AIM: To determine whether extracellular or intravascular contrast agents could detect chronic scarred myocardium in magnetic resonance imaging (MRI). METHODS: Eighteen pigs underwent a 4 week ligation of 1 or 2 diagonal coronary arteries to induce chronic myocardial infarction. The hearts were then removed and perfused in a Langendorff apparatus. Eighteen hearts were divided into 2 groups. The hearts in groups I (n=9) and II (n=9) received the bolus injection of Gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA, 0.05 mmol/kg) and gadolinium- based macromolecular agent (P792, 15 micromol/kg), respectively. First pass T2* MRI was acquired using a FLASH sequence. Delayed enhancement T1 MRI was acquired with an inversion recovery prepared TurboFLASH sequence. RESULTS: Wash-in of both agents resulted in a sharp and dramatic T2* signal loss of scarred myocardium similar to that of normal myocardium. The magnitude and velocity of T2* signal recovery caused by wash-out of extracellular agents in normal myocardium was significantly less than that in scarred myocardium. Conversely, the T2* signal of scarred and normal myocardium recovered to plateau rapidly and simultaneously due to wash-out of intravascular agents. At the following equilibrium, extracellular agent-enhanced T1 signal intensity was significantly greater in scarred myocardium than in normal myocardium, whereas there was no significantly statistical difference in intravascular agent-enhanced T1 signal intensity between scarred and normal myocardium. CONCLUSION: After administration of extracellular agents, wash-out T2* first-pass and delayed enhanced T1 MRI could identify scarred myocardium as a hyperenhanced region. Conversely, scarred myocardium was indistinguishable from normal myocardium during first-pass and the steady state of intravascular agents.
AIM: To determine whether extracellular or intravascular contrast agents could detect chronic scarred myocardium in magnetic resonance imaging (MRI). METHODS: Eighteen pigs underwent a 4 week ligation of 1 or 2 diagonal coronary arteries to induce chronic myocardial infarction. The hearts were then removed and perfused in a Langendorff apparatus. Eighteen hearts were divided into 2 groups. The hearts in groups I (n=9) and II (n=9) received the bolus injection of Gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA, 0.05 mmol/kg) and gadolinium- based macromolecular agent (P792, 15 micromol/kg), respectively. First pass T2* MRI was acquired using a FLASH sequence. Delayed enhancement T1 MRI was acquired with an inversion recovery prepared TurboFLASH sequence. RESULTS: Wash-in of both agents resulted in a sharp and dramatic T2* signal loss of scarred myocardium similar to that of normal myocardium. The magnitude and velocity of T2* signal recovery caused by wash-out of extracellular agents in normal myocardium was significantly less than that in scarred myocardium. Conversely, the T2* signal of scarred and normal myocardium recovered to plateau rapidly and simultaneously due to wash-out of intravascular agents. At the following equilibrium, extracellular agent-enhanced T1 signal intensity was significantly greater in scarred myocardium than in normal myocardium, whereas there was no significantly statistical difference in intravascular agent-enhanced T1 signal intensity between scarred and normal myocardium. CONCLUSION: After administration of extracellular agents, wash-out T2* first-pass and delayed enhanced T1 MRI could identify scarred myocardium as a hyperenhanced region. Conversely, scarred myocardium was indistinguishable from normal myocardium during first-pass and the steady state of intravascular agents.