e41 Correspondence We thank Jansen and van Royen for their interest in our publica- tion. 1 They questioned whether the widely used contrast-enhanced MRI method indeed detects microvascular obstruction (MVO), because the incidence of MRI-defined intramyocardial hemorrhage (IMH) without MVO (isolated IMH) in our rat model was higher than those reported in large animals and patients. Described for the first time by Kloner et al 2 in 1974, MVO is the underlying cause of the no-reflow phenomenon in reperfused myo- cardial infarction (MI). It is attributable to (1) regional swelling, intraluminal protrusions, and the cytoplasm blebs of endothelium; (2) activation of blood leucocytes adhesion and subsequent plugging of erythrocytes, platelets, and neutrophils; and (3) capillary compres- sion by surrounding edematous tissue in experimental MI. In the 1990s, the hypoenhancement of MI area on contrast-enhanced MRI was carefully examined and established for detecting MVO noninva- sively. 3–5 In cardiac MRI, both terms MVO and no-reflow are used to describe the MI region with obstruction of microvasculature. 5 MVO is also found highly associated with IMH. 5 In our article, 1 the higher incidence of MRI-defined isolated IMH in comparison with that in large animals and patients, has been dis- cussed in detail. In brief, it would be attributable to the dynamic fea- tures and severity of the MVO, especially given the small extent of MVOs in rats, and the extravasation of gadolinium contrast agent. In addition, conventional T2-weighted imaging is believed to be less sensitive than T2*-weighted imaging in detecting IMH. It could underestimate both the incidence and area of IMH owing to the con- founding T2 effects of edema and hemorrhage after MI. 5 Jansen and van Royen claimed that the hyperenhancement but not the hypoenhancement of MI tissue indicates true MVO on con- trast-enhanced MRI. 6 They defined that MVO regions must contain intraluminal microthrombi within intact vessels positively stained by anti-CD31 immunohistochemistry in pathohistology (7 days after MI). Apparently, this definition excludes MVO regions that are attributable to other causes (eg, lumen blockage by edematous endo- thelium or mechanical compression by surrounding swelling tissue absent of microthrombi). In addition, the intact vasculature is not necessarily a characteristic of subacute MI tissue of MVO. Within an MVO area, the nonviable microvasculature and cardiomyocytes become a confluent necrosis and ultimately lose their physiological morphology. Therefore, it is not surprising that intact vasculature was rarely found in the hypoenhanced MI region. Furthermore, it is questionable whether their method using anti-CD31 immunohis- tochemistry is able to specifically detect necrotic endothelium and delineate the morphology of necrotic microvasculature. Likely, the positive CD31-stained microvessel wall within the hyperenhance- ment rim is viable endothelium, which seems contradictory to the primary characteristic of microvasculature within MVO area (nonvi- able endothelium). 2 In our opinion, the great disparity in the contrast-enhanced MRI pattern of MVO between Jansen and van Royen’s claim and those in the classical literature originates from the substantially different pathohistological definition of MVO by Jansen and van Royen. Disclosures None. Yu-Xiang Ye, MD, PhD Department of Experimental Physics 5 University of Wuerzburg Comprehensive Heart Failure Center/Deutsches Zentrum für Herzinsuffizienz Wuerzburg, Germany Thomas C. Basse-Lüsebrink, PhD Research Center for Magnetic Resonance Bavaria Wuerzburg, Germany Paula-Anahi Arias-Loza, PhD Department of Internal Medicine Ӏ University Hospital Wuerzburg Wuerzburg, Germany Vladimir Kocoski, PhD Institute of Virology and Immunobiology University of Wuerzburg Wuerzburg, Germany Thomas Kampf, MSc Department of Experimental Physics 5 University of Wuerzburg Wuerzburg, Germany Qiang Gan, PhD Rudolf Virchow Center University of Wuerzburg Wuerzburg, Germany Elisabeth Bauer, MSc Department of Internal Medicine Ӏ University Hospital Wuerzburg Wuerzburg, Germany Stefanie Sparka, PhD Institute of Inorganic Chemistry Wuerzburg, Germany Xavier Helluy, PhD Department of Experimental Physics 5 University of Wuerzburg Wuerzburg, Germany Kai Hu, MD Department of Internal Medicine Ӏ University Hospital Wuerzburg Wuerzburg, Germany Karl-Heinz Hiller, PhD Research Center for Magnetic Resonance Bavaria Wuerzburg, Germany Valerie Boivin-Jahns, PhD Institute of Pharmacology and Toxicology University of Wuerzburg Wuerzburg, Germany Peter M. Jakob, PhD Department of Experimental Physics 5 University of Wuerzburg Research Center for Magnetic Resonance Bavaria Wuerzburg, Germany Roland Jahns, MD Department of Internal Medicine Ӏ University Hospital Wuerzburg Wuerzburg, Germany (Circulation. 2014;130:e41-e42.) © 2014 American Heart Association, Inc. Circulation is available at http://circ.ahajournals.org DOI: 10.1161/CIRCULATIONAHA.114.009359 Response to Letter Regarding Article, “Monitoring of Monocyte Recruitment in Reperfused Myocardial Infarction With Intramyocardial Hemorrhage and Microvascular Obstruction By Combined Fluorine 19 and Proton Cardiac Magnetic Resonance Imaging” Downloaded from http://ahajournals.org by on June 13, 2020