Atherosclerotic lesions in genetically modified mice quantified in vivo by non-invasive high-resolution magnetic resonance microscopy

被引:48
作者
Choudhury, RP [1 ]
Aguinaldo, JG [1 ]
Rong, JX [1 ]
Kulak, JL [1 ]
Kulak, AR [1 ]
Reis, ED [1 ]
Fallon, JT [1 ]
Fuster, V [1 ]
Fisher, EA [1 ]
Fayad, ZA [1 ]
机构
[1] CUNY Mt Sinai Sch Med, Cardiovasc Inst, New York, NY 10029 USA
关键词
aorta; atherosclerosis; magnetic resonance imaging; plaque;
D O I
10.1016/S0021-9150(01)00730-4
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We have previously shown that magnetic resonance microscopy (MRM) accurately quantifies atherosclerosis in Apolipoprotein E deficient (ApoE(-/-)) mice aged 36-84 cheeks. The present study tests MRM in the quantification of aortic atherosclerosis over a broader range of lesion severity. Younger mice with less advanced disease were imaged in order to evaluate sensitivity, specificity and maximum practical resolution of MRM. Nineteen mice underwent in vivo MRM. Wall area measurements by MRM and light microscopy (LM) (n =43) were highly correlated (r = 0.85, slope = 0.88. P < 0.0001), Wall areas by MRM ranged front 0,114 to 0.934 (median. 0,334) mm(2). A threshold of 0.35 mm(2), for the upper limit of normal. gave MRM positive predictive value (PPV) for detecting abnormally thickened arteries = 89.5% and negative predictive value (NPV) = 75%. referred to LM. Lesion shape assessed by LM and MRM ere also kell correlated (r = 0.72, P < 0.001). Increased wall area in atherosclerosis as found by MRM (P = 0.01) and LM (P < 0.0001) to be accommodated entirely by 'positive remodeling', confirming the importance of determining plaque size directly. MRM accurately quantifies mouse aortic atherosclerosis and will enhance studies in this important animal model. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:315 / 321
页数:7
相关论文
共 43 条
[1]   ANGIOGRAPHIC PROGRESSION OF CORONARY-ARTERY DISEASE AND THE DEVELOPMENT OF MYOCARDIAL-INFARCTION [J].
AMBROSE, JA ;
TANNENBAUM, MA ;
ALEXOPOULOS, D ;
HJEMDAHLMONSEN, CE ;
LEAVY, J ;
WEISS, M ;
BORRICO, S ;
GORLIN, R ;
FUSTER, V .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1988, 12 (01) :56-62
[2]   STATISTICAL METHODS FOR ASSESSING AGREEMENT BETWEEN TWO METHODS OF CLINICAL MEASUREMENT [J].
BLAND, JM ;
ALTMAN, DG .
LANCET, 1986, 1 (8476) :307-310
[3]   Decreased lesion formation in CCR2-/- mice reveals a role for chemokines in the initiation of atherosclerosis [J].
Boring, L ;
Gosling, J ;
Cleary, M ;
Charo, IF .
NATURE, 1998, 394 (6696) :894-897
[4]   Mouse models of atherosclerosis [J].
Breslow, JL .
SCIENCE, 1996, 272 (5262) :685-688
[5]  
BROWN BG, 1995, ANN NY ACAD SCI, V748, P407
[6]  
BROWN BG, 1993, BRIT HEART J, V69, pS48
[7]   Apo A-I inhibits foam cell formation in apo E-deficient mice after monocyte adherence to endothelium [J].
Dansky, HM ;
Charlton, SA ;
Barlow, CB ;
Tamminen, M ;
Smith, JD ;
Frank, JS ;
Breslow, JL .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (01) :31-39
[8]   Complete atherosclerosis regression after human ApoE gene transfer in ApoE-deficient/nude mice [J].
Desurmont, C ;
Caillaud, JM ;
Emmanuel, F ;
Benoit, P ;
Fruchart, JC ;
Castro, G ;
Branellec, D ;
Heard, JM ;
Duverger, N .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2000, 20 (02) :435-442
[9]   Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels - Results of AFCAPS/TexCAPS [J].
Downs, JR ;
Clearfield, M ;
Weis, S ;
Whitney, E ;
Shapiro, DR ;
Beere, PA ;
Langendorfer, A ;
Stein, EA ;
Kruyer, W ;
Gotto, AM .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1998, 279 (20) :1615-1622
[10]   REDUCTION OF PARTIAL-VOLUME ARTIFACTS WITH ZERO-FILLED INTERPOLATION IN 3-DIMENSIONAL MR-ANGIOGRAPHY [J].
DU, YPP ;
PARKER, DL ;
DAVIS, WL ;
CAO, G .
JMRI-JOURNAL OF MAGNETIC RESONANCE IMAGING, 1994, 4 (05) :733-741