Key result
Chronic coronary occlusion in a canine model induced upregulation of MMPs and significantly decreased TIMP-1 levels (p<0.001) in collateral vessels compared with normal LAD vessels.
Why the study?
Does chronic coronary occlusion alter the expression of extracellular matrix metalloproteinases and tissue plasminogen activator in collateral vessels in a canine model?
Population
Canine model of coronary occlusion (n=4)
Comparison
Surgical placement of an ameroid occluder around… vs Comparable-sized unoccluded arterial segments of…
Design
Preclinical
Follow-up
2-4 months
Authors
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Suggests MMP/TIMP imbalance as a collateral remodeling target; leaves open translation to human CAD.
Does chronic coronary occlusion alter the expression of extracellular matrix metalloproteinases and tissue plasminogen activator in collateral vessels in a canine model?
p-value: p=<0.001
Chronic coronary occlusion induces upregulation of vascular remodeling mechanisms, including increased MMP activity and decreased TIMP-1, subserving collateral development.
Tyagi et al. (1996) studied Coronary occlusion and collateral vessel development (n=4). Surgical placement of an ameroid occluder around the proximal left circumflex artery vs. Unoccluded arterial segments of the left anterior descending (LAD) artery was evaluated on Extracellular matrix metalloproteinase (MMP) expression and activity in coronary collateral arteries (p=<0.001). Chronic coronary occlusion in a canine model induced upregulation of MMPs and significantly decreased TIMP-1 levels (p<0.001) in collateral vessels compared with normal LAD vessels.
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