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Coronary vasoconstriction in response to acetylcholine after balloon angioplasty: possible role of endothelial
C Vassanelli1, G Menegatti, L Zanolla
1Division of Cardiology, University of Verona, Italy.
Insights
Coronary angioplasty impairs endothelium-dependent vasomotion 3-6 months post-procedure, affecting even uninjured segments. Endothelium-independent vasodilation remains intact, suggesting persistent endothelial dysfunction after balloon dilation.
Area of Science:
- Cardiovascular Research
- Interventional Cardiology
- Endothelial Function
Background:
- Abnormal endothelium-dependent vasomotion is common after coronary angioplasty.
- Endothelial function is crucial for regulating vascular tone.
Purpose of the Study:
- To investigate endothelium-mediated coronary vasomotion post-angioplasty.
- To assess vasomotion in epicardial coronary arteries 3-6 months after successful angioplasty without restenosis.
Main Methods:
- Intracoronary acetylcholine infusions were used to assess vasomotion.
- Coronary artery dimensions were measured using automated edge-detection during angiography.
- Nitroglycerin was administered to evaluate endothelium-independent vasodilation.
Main Results:
- Acetylcholine caused abnormal dose-related vasoconstriction in angioplasty-treated segments.
- Impaired vasoreactivity was observed at the site of previous stenosis and in balloon-injured segments.
- Nitroglycerin-induced vasodilation was preserved but reduced in lesion-related segments.
Conclusions:
- Endothelium-dependent vasodilation is impaired 3-6 months after coronary angioplasty.
- Endothelial dysfunction persists in balloon-dilated segments.
- Endothelium-independent vasodilation remains functional, highlighting specific endothelial damage.
Background:
Abnormal endothelium-dependent vasomotion has frequently been observed early after coronary angioplasty. The aim of this study was to investigate endothelium-mediated coronary vasomotion caused by increasing intracoronary infusions of acetylcholine into epicardial coronary arteries 3-6 months after coronary angioplasty in patients without restenosis (50% luminal diameter reduction).
Methods:
Intracoronary acetylcholine was infused during follow-up coronary angiography followed by an intracoronary bolus of 250 g nitroglycerin in 18 patients who had undergone successful angioplasty of 21 isolated coronary artery lesions. Using an automated edge-detection program, coronary artery measurements were performed in the proximal reference segment, in the proximal part of the angioplasty site, at the site of previous maximal stenosis, in the distal part of the angioplasty site, and in the distal reference segment.
Results:
In the segments of the coronary artery not manipulated by balloon catheter, acetylcholine did not produce significant luminal diameter changes (+2 +/- 23% in the proximal segment and -3 +/- 27% in the distal segment at 10(-4) mol/l). All the angioplasty vessel segments, excluding the proximal reference segments, showed an abnormal dose-related reactivity to the acetylcholine. Maximal vasoconstriction was observed at 10(-4) mol/l and was 4.9 +/- 11.1% in the proximal reference segment, 9.3 +/- 19.1% in the proximal angioplasty site (P = 0.0314), 20.3 +/- 24.1% at the site of previous maximal stenosis (P = 0.0005), 10.7 +/- 16.8% at the distal angioplasty site (P = 0.0098), and 9.3 +/- 14.1% in the distal reference segment (P = 0.0032). The maximal response of the angioplasty site to acetylcholine and to nitroglycerin did not correlate either with the time to follow-up or with the follow-up stenosis. Nitroglycerin-induced vasodilation was significant in all segments, but was lower in the lesion-related segments. Acetylcholine evoked the same effect on both the vessels that were manipulated and those that were not.
Conclusions:
Three to 6 months after coronary angioplasty, endothelium-dependent vasodilation was impaired not only at the site of previous maximal stenosis, but also in segments directly injured by balloon inflation. In contrast, endothelium-independent vasodilation by nitroglycerin is maintained in all segments. These observations suggest that the endothelium is still functionally impaired in the area of balloon dilation.