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

Abstract

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.

Effect of Microvascular Obstruction and Intramyocardial Hemorrhage by CMR on LV Remodeling and Outcomes After Myocardial Infarction

“…MVO is thought to be caused by an abrupt release of cytotoxic factors (7) that promote vasoconstriction, myocardial cellular edema (2,8), capillary endothelial cells swelling, and distal microembolization of atherosclerotic debris leading to plugging of vascular lumen with neutrophils, red blood cells, and platelets. MVO begins in the infarcted core and can increase in size for up to 48 h (9).…”

Intramyocardial haemorrhage after acute myocardial infarction

“…Instead, erythrocyte compounds, such as haemoglobin, or iron deposits can be stained with a haemoglobin antibody or Perl's Prussian blue staining, which stains ferritin deposits. 18,20,109 Erythrocytes can also be labelled with radioisotopes or erythrocyte extravasation can be mimicked by injection of radioactive or gold-labelled microspheres, and can be visualized using spectroscopy. 47,51,[110][111][112][113] Predicting the risk of haemorrhage…”

Labeling monocytes with gold nanoparticles to track their recruitment in atherosclerosis with computed tomography

“…15–16 Of the few studies regarding monocyte tracking, SPECT and MRI modalities were used. 17–18 SPECT and MRI face challenges due to chest and heart motion when imaging the coronary arteries. 19 Therefore, we sought to develop a technique to monitor the monocyte accumulation in atherosclerotic plaques non-invasively through computed tomography.…”