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.

Reversible myocardial dysfunction can be identified by contrast-enhanced MRI before coronary revascularization.

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Myocardial scarring is common in asymptomatic or mildly symptomatic HCM patients who have not suffered sudden death. When present, scarring occurs in hypertrophied regions, is consistently localized to the junctions of the septum and RV free wall, and correlates positively with regional hypertrophy and inversely with regional contraction.

Infarct size, EF and ESVI can predict the development of future cardiac events. Acute infarct size, which is independent of LV stunning and loading, directly relates to LV remodelling and is a stronger predictor of future events than measures of LV systolic performance.

Background-Mild elevations in creatine kinase-MB (CK-MB) are common after successful percutaneous coronary interventions and are associated with future adverse cardiac events. The mechanism for CK-MB release remains unclear.A new contrast-enhanced MRI technique allows direct visualization of myonecrosis. Methods and Results-Fourteen patients without prior infarction underwent cine and contrast-enhanced MRI after successful coronary stenting; 9 patients had procedure-related CK-MB elevation, and 5 did not (negative controls). The mean age of all patients was 61 years, 36% had diabetes, 43% had multivessel coronary artery disease, and all had a normal ejection fraction. Twelve patients (86%) received an intravenous glycoprotein IIb/IIIa inhibitor; none underwent atherectomy, and all had final TIMI 3 flow. Of the 9 patients with CK-MB elevation, 5 had a minor side branch occlusion during stenting, 2 had transient ECG changes, and none developed Q-waves. The median CK-MB was 21 ng/mL (range, 12 to 93 ng/mL), which is 2.3ϫ the upper limit of normal. Contrast-enhanced MRI demonstrated discrete regions of hyperenhancement within the target vessel perfusion territory in all 9 patients. Only one developed a new wall motion abnormality. The median estimated mass of myonecrosis was 2.0 g (range, 0.7 to 12.2 g), or 1.5% of left ventricular mass (range, 0.4% to 6.0%). Hyperenhancement persisted in 5 of the 6 who underwent a repeat MRI at 3 to 12 months. No control patient had hyperenhancement. Conclusions-Contrast-enhanced MRI provides an anatomical correlate to biochemical evidence of procedure-related myocardial injury, despite the lack of ECG changes or wall motion abnormalities. Mild elevation of CK-MB after percutaneous coronary intervention is the result of discrete microinfarction.

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