PT - JOURNAL ARTICLE AU - V Bodí AU - J Sanchis AU - M P López-Lereu AU - J Núñez AU - R Sanz AU - P Palau AU - C Gómez AU - D Moratal AU - F J Chorro AU - À Llácer TI - Microvascular perfusion 1 week and 6 months after myocardial infarction by first-pass perfusion cardiovascular magnetic resonance imaging AID - 10.1136/hrt.2005.077305 DP - 2006 Dec 01 TA - Heart PG - 1801--1807 VI - 92 IP - 12 4099 - http://heart.bmj.com/content/92/12/1801.short 4100 - http://heart.bmj.com/content/92/12/1801.full SO - Heart2006 Dec 01; 92 AB - Objective: To characterise the evolution of myocardial perfusion during the first 6 months after myocardial infarction by first-pass perfusion cardiovascular magnetic resonance imaging (CMR) and determine its significance. Design: Prospective cohort design. Setting: Single-centre study in a teaching hospital in Spain. Patients: 40 patients with a first ST-elevation myocardial infarction, single-vessel disease and thrombolysis in myocardial infarction (TIMI) grade 3 flow (stent in 33 patients) underwent rest and low-dose dobutamine CMR 7 (SD 1) and 184 (SD 11) days after infarction. Microvascular perfusion was assessed at rest by visual assessment and quantitative analysis of first-pass perfusion CMR. Of the 640 segments, 290 segments subtended by the infarct-related artery (IRA) were focused on. Results: Both 1 week and 6 months after infarction, segments with normal perfusion showed more wall thickening, contractile reserve and wall thickness, and less transmural necrosis, p <0.05 in all cases. Of 76 hypoperfused segments at the first week, 47 (62%) normalised perfusion at the sixth month. However, 42 segments (14% of the whole group) showed chronic abnormal perfusion; these segments showed worse CMR indices in the late phase (p<0.05 in all cases). Conclusions: In patients with an open IRA, more than half of the segments with abnormal perfusion at the first week are normally perfused after six months. First-pass perfusion CMR shows that in a small percentage of segments, abnormal perfusion may become a chronic phenomenon—these areas have a more severe deterioration of systolic function, wall thickness, contractile reserve and the transmural extent of necrosis.