Article

Left ventricular remodeling after experimental myocardial cryoinjury in rats.

Istituto di Clinica Medica Generale e Terapia Medica, Ospedale Maggiore di Milano, IRCCS, Center of Clinical Physiology and Hypertension, University of Milan, Milan, Italy.
Journal of Surgical Research (impact factor: 2.25). 02/2004; 116(1):91-7. pp.91-7
Source: PubMed

ABSTRACT The standard coronary ligation, the most studied model of experimental myocardial infarction in rats, is limited by high mortality and produces unpredictable areas of necrosis. To standardize the location and size of the infarct and to elucidate the mechanisms of myocardial remodeling and its progression to heart failure, we studied the functional, structural, and ultrastructural changes of myocardial infarction produced by experimental myocardial cryoinjury. The cryoinjury was successful in 24 (80%) of 30 male adult CD rats. A subepicardial infarct was documented on echocardiograms, with an average size of about 21%. Macroscopic examination reflected closely the stamp of the instrument used, without transition zones to viable myocardium. Histological examination, during the acute setting, revealed an extensive area of coagulation necrosis and hemorrhage in the subepicardium. An inflammatory infiltrate was evident since the 7th hour, whereas the reparative phase started within the first week, with proliferation of fibroblasts, endothelial cells, and myocytes. From the 7th day, deposition of collagen fibers was reported with a reparative scar completed at the 30th day. Ultrastructural study revealed vascular capillary damage and irreversible alterations of the myocytes in the acute setting and confirmed the histological findings of the later phases. The damage was associated with a progressive left ventricular (LV) remodeling, including thinning of the infarcted area, hypertrophy of the noninfarcted myocardium, and significant LV dilation. This process started from the 60th day and progressed over the subsequent 120 days period; at 180 days, a significant increase in LV filling pressure, indicative of heart failure, was found. In conclusion, myocardial cryodamage, although different in respect to ischemic damage, causes a standardized injury reproducing the cellular patterns of coagulation necrosis, early microvascular reperfusion, hemorrhage, inflammation, reparation, and scarring observed in myocardial infarction with a late evolution toward heart failure. This model is therefore suitable to study myocardial repair after injury.

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    Journal of Translational Medicine 02/2008; 6:30. · 3.41 Impact Factor
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Keywords

7th day
 
cellular patterns
 
coagulation necrosis
 
collagen fibers
 
experimental myocardial cryoinjury
 
experimental myocardial infarction
 
extensive area
 
Histological examination
 
histological findings
 
infarcted area
 
ischemic damage
 
Macroscopic examination
 
reparative phase
 
significant LV dilation
 
standard coronary ligation
 
standardized injury reproducing
 
study myocardial
 
subepicardial infarct
 
transition zones
 
vascular capillary damage