Monitoring of Monocyte Recruitment in Reperfused Myocardial Infarction With Intramyocardial Hemorrhage and Microvascular Obstruction by Combined Fluorine 19 and Proton Cardiac Magnetic Resonance Imaging

• DOI: 10.1161/circulationaha.113.000731
• Publication Date: 2013-09-12T04:25:01Z
• Authors: Yu-Xiang Ye; Thomas C. Basse-L...; Paula-Anahi Arias...; Vladimir Kocoski; Thomas Kampf; Qiang Gan; Elisabeth Bauer; Stefanie Sparka; Xavier Helluy; Kai Hu; Karl-Heinz Hiller; Valerie Boivin-Jahns; Peter M. Jakob; Roland Jahns; Wolfgang R. Bauer
• Keywords: Fluorine Radioisotopes; Wound Healing; Macrophages; Microcirculation; Myocardial Infarction; Hemorrhage; Myocardial Reperfusion; Magnetic Resonance Imaging; Monocytes; 3. Good health; Rats; Disease Models, Animal; 03 medical and health sciences; 0302 clinical medicine; Cell Movement; Coronary Circulation; Animals; Female; Protons; Rats, Wistar; Radionuclide Imaging

Background— Monocytes and macrophages are indispensable in the healing process after myocardial infarction (MI); however, the spatiotemporal distribution of monocyte infiltration and its correlation to prognostic indicators of reperfused MI have not been well described.

Methods and Results—

With combined fluorine 19/proton ( 1 H) magnetic resonance imaging, we noninvasively visualized the spatiotemporal recruitment of monocytes in vivo in a rat model of reperfused MI. Blood monocytes were labeled by intravenous injection of 19 F-perfluorocarbon emulsion 1 day after MI. The distribution patterns of monocyte infiltration were correlated to the presence of microvascular obstruction (MVO) and intramyocardial hemorrhage. In vivo, 19 F/ 1 H magnetic resonance imaging performed in series revealed that monocyte infiltration was spatially inhomogeneous in reperfused MI areas. In the absence of MVO, monocyte infiltration was more intense in MI regions with serious ischemia-reperfusion injuries, indicated by severe intramyocardial hemorrhage; however, monocyte recruitment was significantly impaired in MVO areas accompanied by severe intramyocardial hemorrhage. Compared with MI with isolated intramyocardial hemorrhage, MI with MVO resulted in significantly worse pump function of the left ventricle 28 days after MI.

Conclusions—

Monocyte recruitment was inhomogeneous in reperfused MI tissue. It was highly reduced in MVO areas defined by magnetic resonance imaging. The impaired monocyte infiltration in MVO regions could be related to delayed healing and worse functional outcomes in the long term. Therefore, monocyte recruitment in MI with MVO could be a potential diagnostic and therapeutic target that could be monitored noninvasively and longitudinally by 19 F/ 1 H magnetic resonance imaging in vivo.