| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3029514 | Thrombosis Research | 2009 | 9 Pages |
IntroductionThe association of the temporal evolution of cardiac necrosis marker release with cardiovascular magnetic resonance-derived microvascular perfusion after ST-elevation myocardial infarction is unknown.MethodsWe analyzed 163 patients with a first ST-elevation myocardial infarction and a patent infarct-related artery treated with thrombolysis (67%) or primary angioplasty (33%). Using first-pass perfusion CMR, abnormal perfusion was defined as a lack of contrast arrival into the infarct area in > 1 segment. Troponin I, creatine kinase MB and myoglobin were measured upon arrival and at 6, 12, 24, 48 and 96 hours after reperfusion.ResultsAbnormal perfusion was detected in 75 patients (46%) and was associated with a larger release of all 3 necrosis markers after reperfusion and higher peak values. This association was observed in the whole group and separately in patients treated with thrombolysis and primary angioplasty. Out of the 3 markers, troponin levels at 6 hours after reperfusion yielded the largest area under the receiver operating characteristic curve for prediction of abnormal perfusion (troponin: 0.69, creatine kinase MB: 0.65 and myoglobin: 0.58). In a comprehensive multivariate analysis, adjusted for clinical, angiographic, cardiovascular magnetic resonance parameters and all necrosis markers, high troponin levels at 6 hours after reperfusion (>median) independently predicted abnormal microvascular perfusion (OR 2.6 95%CI [1.2 - 5.5], p = .012).ConclusionsIn ST-elevation myocardial infarction, a larger release of cardiac necrosis markers soon after reperfusion therapy relates to abnormal perfusion. Troponin appears as the most reliable necrosis marker for an early detection of cardiovascular magnetic resonance-derived abnormal microvascular reperfusion.
