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Heterogeneity of vasomotor response to acetylcholine along the human coronary artery
Insights
Coronary arteries show varied responses to acetylcholine, with segments constricting and dilating within the same vessel. Optimal assessment requires analyzing the entire artery and using quantitative angiography limits.
Area of Science:
- Cardiovascular research
- Pharmacology
- Medical imaging
Background:
- Acetylcholine is known to constrict atherosclerotic arteries.
- Endothelium-dependent dilation dysfunction can occur even without visible disease.
Purpose of the Study:
- To investigate the heterogeneous vasomotion of coronary arteries in response to acetylcholine.
- To determine if acetylcholine causes varied responses based on vessel segment, drug dose, and analysis criteria.
Main Methods:
- Developed algorithms to quantify coronary artery dimensions along their entire length.
- Utilized graded doses of intracoronary acetylcholine.
- Established a detection limit of 0.31 mm for diameter changes using triplicate angiograms.
Main Results:
- Heterogeneous responses to acetylcholine were observed in 27 of 31 patients at a 10(-4) mol/liter dose.
- Constriction and dilation in the same vessel occurred in 45% of patients when multiple doses were combined.
- Vasoconstriction (24.6%) and vasodilation (6.9%) were most frequent at the 10(-4) mol/liter dose, with effects seen up to 7.3 cm from infusion.
Conclusions:
- Coronary artery response to acetylcholine is heterogeneous, even in mild disease.
- Different segments of the same coronary artery can exhibit disparate dimensional changes.
- Analyzing all accessible regions and employing reproducibility limits in quantitative angiography are crucial for assessing segmental vasomotion.
Objectives:
In view of the segmental occurrence of coronary atherosclerosis, we postulated that acetylcholine may cause heterogeneous vasomotion, depending on the extent of vessel analyzed, criteria for change in vessel caliber and dose of drug administered.
Background:
Previous studies have reported that acetylcholine causes constriction of atherosclerotic arteries. This dysfunction of endothelium-dependent dilation may be seen without angiographically detectable disease.
Methods:
We developed algorithms to quantitate the dimensions of a single coronary artery over virtually its entire length during a control state and during graded doses of intracoronary acetylcholine. On the basis of triplicate control angiograms, the limit of detection of a change from control diameter was 0.31 mm (> or = 2 SD).
Results:
Analysis of multiple segments (each 5.6 +/- 1.1 [mean +/- SD] mm) along a single coronary artery revealed a heterogeneous response to acetylcholine in 27 of 31 patients at the 10(-4) mol/liter dose and in 29 of 31 patients when responses at 10(-6), 10(-5) and 10(-4) mol/liter doses were combined; in this latter analysis, constriction and dilation in the same vessel occurred in 45% of the patients. With acetylcholine, most of 349 segments demonstrated no change, but the greatest frequency of vasoconstriction (24.6%) and vasodilation (6.9%) was seen at the 10(-4) mol/liter dose. Inducible vasomotion was observed as far distally as 7.3 cm from the site of acetylcholine infusion.
Conclusions:
Response to intracoronary acetylcholine with mild coronary disease is heterogeneous; disparate dimensional responses may occur in different segments of the same vessel. Inclusion of all analyzable regions of a coronary artery and the use of a reproducibility limit for quantitative angiography are optimal for assessment of segmental coronary vasomotion.