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Angina Pectoris/MI
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my personal edition > angina pectoris/mi > news
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DGReview
More Selective Vasodilators Might Improve Treatment Of Acute Coronary Syndromes
A DGReview of :"The Enhanced Vasoreactivity of the Culprit Lesion in Unstable Angina is Associated with an Increased Local Release of Endothelin-1"
Journal of Clinical and Basic Cardiology Online
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 vasoconstrictor, is 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.
They studied nine patients (six males, three females), around 58 years old, with unstable angina class IIIB and nine patients (six male, three female), approximately 64 years old, with chronic stable angina class II-III with a single proximal lesion of the left anterior descending coronary artery.
Using quantitative coronary angiography, the luminal diameter of the culprit lesion and of the proximal, middle and distal normal-appearing coronary segments were measured at baseline, during cold pressor testing and after intracoronary nitroglycerine.
Endothelin-1 levels were measured in blood samples obtained proximally and distally to the coronary culprit lesion before and after stents had been successfully implanted.
During cold pressor testing, the culprit lesion in patients with unstable angina constricted by 25 ± 8 percent compared with baseline. This was a significantly greater reduction than the 8±10 percent compared with baseline in the stable angina patients.
After nitroglycerine, the culprit lesion in patients with unstable angina dilated by 48 ± 21 percent compared with baseline. This too was significantly more than in those with stable angina (22 ± 7 percent compared with baseline).
The uninvolved proximal, middle and distal coronary artery segments had similar changes in the two patient groups during cold pressor test and after nitroglycerine.
Baseline proximal and distal endothelin-1 levels before stenting were also similar in the two groups. After stenting, proximal and distal endothelin-1 levels rose significantly in both groups, although the relative increase was greater in unstable than in stable angina patients.
Journal of Clinical and Basic Cardiology 2002;5(1):87-92.
"The Enhanced Vasoreactivity of the Culprit Lesion in Unstable Angina is Associated with an Increased Local Release of Endothelin-1"
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