Key result
Chronic pressure-overload left ventricular hypertrophy in a swine model significantly decreased plasma NOx levels (1.2% vs 1.8%, P<0.05) and impaired endothelium-dependent relaxations.
Why the study?
Does pressure-overload LVH alter endothelial signal transduction pathways in porcine epicardial coronary arteries?
Population
Swine model of left ventricular hypertrophy (LVH)
Comparison
Aortic banding 3 cm above the coronary ostia to… vs Control swine
Design
Preclinical
Follow-up
60 days
Authors
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Should not change human LVH practice; hypothesis-generating for coronary endothelial dysfunction in pressure-overload models.
Does pressure-overload LVH alter endothelial signal transduction pathways in porcine epicardial coronary arteries?
Absolute Event Rate: 1.2% vs 1.8%
p-value: p=<0.05
Chronic pressure-overload LVH in a swine model induces coronary endothelial dysfunction involving Gi and Gq protein-mediated relaxations and the EDHF pathway.
Malo et al. (2003) studied Left ventricular hypertrophy. Aortic banding (pressure-overload) vs. Control was evaluated on Plasma NOx levels (p=<0.05). Chronic pressure-overload left ventricular hypertrophy in a swine model significantly decreased plasma NOx levels (1.2% vs 1.8%, P<0.05) and impaired endothelium-dependent relaxations.
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