TY - JOUR
T1 - Coronary high-signal-intensity plaques on T 1 -weighted magnetic resonance imaging reflect intraplaque hemorrhage
AU - Kuroiwa, Yasuyoshi
AU - Uchida, Akiko
AU - Yamashita, Atsushi
AU - Miyati, Tosiaki
AU - Maekawa, Kazunari
AU - Gi, Toshihiro
AU - Noguchi, Teruo
AU - Yasuda, Satoshi
AU - Imamura, Takuroh
AU - Asada, Yujiro
N1 - Funding Information:
This work was supported in part by Grants-in-Aid for Scientific Research in Japan ( 16K08670 , 16H05163 , 16K09019 ) from the Ministry of Education, Culture, Sports, Science and Technology of Japan ; the Intramural Research Fund ( 25-4-3 ) for Cardiovascular Diseases from the National Cerebral and Cardiovascular Center ; and the Clinical Research Fund from Miyazaki University Hospital .
Publisher Copyright:
© 2019 Elsevier Inc.
PY - 2019/5/1
Y1 - 2019/5/1
N2 - Coronary high-signal-intensity plaques (HIPs) detected by T 1 -weighted magnetic resonance imaging are associated with future cardiovascular events. This study aimed to identify pathological findings reflecting HIPs in coronary arteries obtained from autopsy cases. Formalin-fixed hearts were imaged with noncontrast T 1 -weighted imaging with a 1.5-T magnetic resonance system. We defined HIPs or non-HIPs as a coronary plaque to myocardial signal intensity ratio (PMR) of ≥1.4 or <1.4, respectively. We found HIPs in 4 of 37 (10.8%) hearts and analyzed 7 hearts in detail. The corresponding sections to HIPs (n=11) or non-HIPs (n=25) were histologically and immunohistochemically analyzed. We calculated the T 1 relaxation time of human venous blood in vitro. Plaque and necrotic core areas, and the frequency of intraplaque hemorrhage in HIPs were significantly larger/higher than those in non-HIPs. HIPs were immunopositive for CD68 (11/11), glycophorin A (10/11), and fibrin (11/11). Glycophorin-A-, matrix metalloprotease 9 (MMP9)-, and tissue factor-immunopositive areas were larger in HIPs than in non-HIPs. The PMR was positively correlated with glycophorin-A-, fibrin-, MMP9-, and tissue factor-immunopositive areas. Blood coagulation shortened the T 1 relaxation time of the blood and plasma, and the T 1 relaxation times in coagulated whole blood and erythrocyte-rich blood were significantly shorter than those in plasma. Coronary HIPs may reflect intraplaque hemorrhage and may be a novel marker for plaque instability and thrombogenic potential.
AB - Coronary high-signal-intensity plaques (HIPs) detected by T 1 -weighted magnetic resonance imaging are associated with future cardiovascular events. This study aimed to identify pathological findings reflecting HIPs in coronary arteries obtained from autopsy cases. Formalin-fixed hearts were imaged with noncontrast T 1 -weighted imaging with a 1.5-T magnetic resonance system. We defined HIPs or non-HIPs as a coronary plaque to myocardial signal intensity ratio (PMR) of ≥1.4 or <1.4, respectively. We found HIPs in 4 of 37 (10.8%) hearts and analyzed 7 hearts in detail. The corresponding sections to HIPs (n=11) or non-HIPs (n=25) were histologically and immunohistochemically analyzed. We calculated the T 1 relaxation time of human venous blood in vitro. Plaque and necrotic core areas, and the frequency of intraplaque hemorrhage in HIPs were significantly larger/higher than those in non-HIPs. HIPs were immunopositive for CD68 (11/11), glycophorin A (10/11), and fibrin (11/11). Glycophorin-A-, matrix metalloprotease 9 (MMP9)-, and tissue factor-immunopositive areas were larger in HIPs than in non-HIPs. The PMR was positively correlated with glycophorin-A-, fibrin-, MMP9-, and tissue factor-immunopositive areas. Blood coagulation shortened the T 1 relaxation time of the blood and plasma, and the T 1 relaxation times in coagulated whole blood and erythrocyte-rich blood were significantly shorter than those in plasma. Coronary HIPs may reflect intraplaque hemorrhage and may be a novel marker for plaque instability and thrombogenic potential.
KW - Coronary artery
KW - Erythrocyte
KW - Intraplaque hemorrhage
KW - Magnetic resonance imaging
KW - T -weighted image
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U2 - 10.1016/j.carpath.2019.01.002
DO - 10.1016/j.carpath.2019.01.002
M3 - Article
C2 - 30797186
AN - SCOPUS:85061641880
VL - 40
SP - 24
EP - 31
JO - Cardiovascular Pathology
JF - Cardiovascular Pathology
SN - 1054-8807
ER -