Background-Contrast MRI enhancement patterns in several pathophysiologies resulting from ischemic myocardial injury are controversial or have not been investigated. We compared contrast enhancement in acute infarction (AI), after severe but reversible ischemic injury (RII), and in chronic infarction. Methods and Results-In dogs, a large coronary artery was occluded to study AI and/or chronic infarction (nϭ18), and a second coronary artery was chronically instrumented with a reversible hydraulic occluder and Doppler flowmeter to study RII (nϭ8). At 3 days after surgery, cine MRI revealed reduced wall thickening in AI (5Ϯ6% versus 33Ϯ6% in normal, PϽ0.001). In RII, wall thickening before, during, and after inflation of the occluder for 15 minutes was 35Ϯ5%, 1Ϯ8%, and 21Ϯ10% and Doppler flow was 19.8Ϯ5.3, 0.2Ϯ0.5, and 56.3Ϯ17.7 (peak hyperemia) cm/s, respectively, confirming occlusion, transient ischemia, and reperfusion. Gd-DTPA-enhanced MR images acquired 30 minutes after contrast revealed hyperenhancement of AI (294Ϯ96% of normal, PϽ0.001) but not of RII (98Ϯ6% of normal, PϭNS). Eight weeks later, the chronically infarcted region again hyperenhanced (253Ϯ54% of normal, nϭ8, PϽ0.001).High-resolution (0.5ϫ0.5ϫ0.5 mm) ex vivo MRI demonstrated that the spatial extent of hyperenhancement was the same as the spatial extent of myocyte necrosis with and without reperfusion at 1 day (Rϭ0.99, PϽ0.001) and 3 days (Rϭ0.99, PϽ0.001) and collagenous scar at 8 weeks (Rϭ0.97, PϽ0.001). Conclusions-In the pathophysiologies investigated, contrast MRI distinguishes between reversible and irreversible ischemic injury independent of wall motion and infarct age.

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Background-Contractile dysfunction develops in the chronically instrumented canine myocardium after bouts of low-flow ischemia and persists after reperfusion. The objective of this study is to identify whether changes in the phosphorylation state of myosin-binding protein C (MyBP-C) are a potential cause of dysfunction. Methods and Results-During low-flow ischemia, MyBP-C is dephosphorylated, and the number of actomyosin cross-bridges in the central core of the sarcomere decreases as thick filaments dissemble from the periphery of the myofibril. During reperfusion, MyBP-C remains dephosphorylated, and its degradation is accelerated. Conclusions-Dephosphorylation of MyBP-C may initiate changes in myofibril thick filament structure that decrease the interaction of myosin heads with actin thin filaments. Limiting the formation of actomyosin cross-bridges may contribute to the contractile dysfunction that is apparent after low-flow ischemia.

Concurrent directionally opposite changes in infarcted and noninfarcted myocardium can be defined serially, noninvasively, and with high spatial resolution and full ventricular coverage following myocardial infarction.