Release of necrosis markers and cardiovascular magnetic resonance-derived microvascular perfusion in reperfused ST-elevation myocardial infarction

• Published in: Thrombosis research 2009-11, Vol.124 (5), p.592-600
• Main Authors: Husser, Oliver, Bodi, Vicente, Sanchis, Juan, Nunez, Julio, Mainar, Luis, Rumiz, Eva, Lopez-Lereu, Maria P, Monmeneu, Jose V, Forteza, Maria J, Oltra, Ricardo, Riegger, Günter A.J, Chorro, Francisco J, Llacer, Angel
• Format: Article
• Language: English
• Subjects: Adult; Aged; Angioplasty, Balloon, Coronary; Biological and medical sciences; Biomarkers - blood; Blood and lymphatic vessels; Cardiac necrosis markers; Cardiology. Vascular system; Cardiovascular magnetic resonance; Coronary Angiography - methods; Creatine Kinase MB; Creatine Kinase, MB Form - blood; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous; Female; Hematology, Oncology and Palliative Medicine; Humans; Magnetic Resonance Imaging - methods; Male; Medical sciences; Microvascular perfusion; Middle Aged; Myocardial Infarction - blood; Myocardial Infarction - metabolism; Myocardial Infarction - pathology; Myocardial Infarction - therapy; Myocardial Reperfusion Injury - blood; Myocardial Reperfusion Injury - metabolism; Myocardial Reperfusion Injury - pathology; Myocardial Reperfusion Injury - therapy; Myocardium - pathology; Myoglobin; Myoglobin - blood; Necrosis; Neurology; Prognosis; Prospective Studies; ST-elevation myocardial infarction; Treatment Outcome; Troponin; Troponin - blood; Vascular diseases and vascular malformations of the nervous system
• ISSN: 0049-3848; 1879-2472
• DOI: 10.1016/j.thromres.2009.05.015

Abstract Introduction The association of the temporal evolution of cardiac necrosis marker release with cardiovascular magnetic resonance-derived microvascular perfusion after ST-elevation myocardial infarction is unknown. Methods We 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. Results Abnormal 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). Conclusions In 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.