05/22/2002 By David Loshak
The enhanced potential to release endothelin-1 in patients with unstable angina might
account, at least in part, for greater vasoreactivity of the unstable plaque.
Moreover, because production of endothelin-1, the most potent endogenous asoconstrictor, stimulated by inflammatory mechanisms, this extra potential further supports the part played by inflammatory mechanisms in destabilising the atherosclerotic plaque.
Cardiologists and other specialists in L’Aquila, Italy, and Rome, Italy, say their findings suggest that more selective vasodilators, such as endothelin antagonists, might be much more
effective than currently available vasodilators for treating acute coronary syndromes.
The specialists pointed out that increased tissue endothelin-1 immunoreactivity had been shown at the site of the culprit lesion in patients with unstable angina. It was this which suggested that endothelin-1 might be involved in the abnormal vasoreactivity of the culprit lesion in unstable angina. A study was conducted to investigate if an enhanced local release of endothelin-1 was involved in the pathogenesis of the enhanced vasoreactivity of the unstable plaque in
unstable angina.
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