Key result
Atherosclerotic coronary arteries show ~3-fold greater sensitivity to big ET-1 than non-diseased arteries.
Why the study?
Does exposure to big ET-1 elicit an enhanced vasoconstrictor response in atherosclerotic human coronary arteries compared to non-diseased arteries?
Population
Endothelium-denuded human coronary arteries from patients with coronary artery disease and non-diseased…
Comparison
Exposure to big endothelin-1 (big ET-1) vs Non-diseased arteries (DCM)
Design
Preclinical
Authors
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Suggests ECE upregulation drives CAD vasoreactivity; hypothesis-generating for inhibition trials before clinical consideration.
Does exposure to big ET-1 elicit an enhanced vasoconstrictor response in atherosclerotic human coronary arteries compared to non-diseased arteries?
Absolute Event Rate: 96% vs 274%
p-value: p=<0.05
Atherosclerotic human coronary arteries show an enhanced response to big ET-1 due to up-regulation of endothelin-converting enzyme activity, suggesting it as a potential therapeutic target in CAD.
Maguire et al. (1998) studied Coronary artery disease (n=17). Atherosclerotic coronary artery disease vs. Non-diseased arteries (dilated cardiomyopathy) was evaluated on Response to big ET-1 (EC50 value in nM) (p=<0.05). Atherosclerotic human coronary arteries exhibited a significantly enhanced response to big endothelin-1 (EC50 96 nM) compared to non-diseased arteries (EC50 274 nM; P<0.05).
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