Double-Contrast Enhanced Mr Imaging of Myocardial Infarction in the Pig

1993 ◽  
Vol 34 (1) ◽  
pp. 64-71 ◽  
Author(s):  
M. Wikström ◽  
H. J. Martinussen ◽  
A. Ericsson ◽  
G. Wikström ◽  
A. Waldenström ◽  
...  

Myocardial infarction was induced by ligating a diagonal branch of the left anterior descending artery in 18 pigs. All pigs were sacrificed 6 h after the occlusion. Dysprosium diethylenetriaminepentaacetic acid bismethylamide (Dy-DTPA-BMA, 1.0 mmol/kg) was administered i.v. to 6 pigs, starting 3 min before sacrifice (injection time approximately 1 min). In a second group of 6 pigs, a double-contrast technique was used, consisting of an i.v. injection of gadolinium-DTPA-BMA (0.4 mmol/kg) 2 h before sacrifice, followed by an i.v. injection of Dy-DTPA-BMA (1.0 mmol/kg) 3 min before sacrifice. Six additional pigs, subjected to 6 h of coronary artery occlusion without administration of contrast medium, served as controls. The hearts were excised and imaged with MR. In the control animals, the infarctions demonstrated an increased signal intensity in the proton density- and T2-weighted images. Administration of Dy-DTPA-BMA primarily improved infarct visualization in the proton density- and T2-weighted images, due to reduction of signal intensity in nonischemic myocardium. The double-contrast technique further improved infarct visualization in all sequences.

Circulation ◽  
1969 ◽  
Vol 40 (5s4) ◽  
Author(s):  
DONALD B. HACKEL ◽  
E. HARVEY ESTES ◽  
ABE WALSTON ◽  
STEPHEN KOFF ◽  
EUGENE DAY

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Irene Cuadrado ◽  
Maria Jose Garcia Miguel ◽  
Irene Herruzo ◽  
Mari Carmen Turpin ◽  
Ana Martin ◽  
...  

Extracellular matrix metalloproteinase inducer EMMPRIN, is highly expressed in patients with acute myocardial infarction (AMI), and induces activation of several matrix metalloproteinases (MMPs), including MMP-9 and MMP-13. To prevent Extracellular matrix degradation and cardiac cell death we targeted EMMPRIN with paramagnetic/fluorescent micellar nanoparticles with an EMMPRIN binding peptide AP9 conjugated (NAP9), or an AP9 scramble peptide as a negative control (NAPSC). NAP9 binds to endogenous EMMPRIN as detected by confocal microscopy of cardiac myocytes and macrophages incubated with NAP and NAPSC in vitro, and in vivo in mouse hearts subjected to left anterior descending coronary artery occlusion (IV injection 50mγ/Kg NAP9 or NAP9SC). Administration of NAP9 at the same time or 1 hour after AMI reduced infarct size over a 20% respect to untreated and NAPSC injected mice, recovered left ventricle ejection fraction (LVEF) similar to healthy controls, and reduced EMMPRIN downstream MMP9 expression. In magnetic resonance scans of mouse hearts 2 days after AMI and injected with NAP9, we detected a significant gadolinium enhancement in the left ventricle respect to non-injected mice and to mice injected with NAPSC. Late gadolinium enhancement assays exhibited NAP9-mediated left ventricle signal enhancement as early as 30 minutes after nanoprobe injection, in which a close correlation between the MRI signal enhancement and left ventricle infarct size was detected. Taken together, these results point EMMPRIN targeted nanoprobes as a new tool for the treatment of AMI.


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