Endothelial Dysfuntion of Coronary Microvasculature in Patients with Chest Pain and Normal Coronary Angiograms.
10.4070/kcj.1994.24.6.777
- Author:
Young Hoon KIM
;
Chang Gyu PARK
;
Do Sun LIM
;
Hong Seog SUH
;
Wan Joo SHIM
;
Dong Joo OH
;
Young Moo RO
- Publication Type:Original Article
- Keywords:
Acetylcholine;
Vasodilatory reserve;
Coronary microvasculature;
Chest
- MeSH:
Acetylcholine;
Arteries;
Catheters;
Chest Pain*;
Coronary Vessels;
Depression;
Electrocardiography;
Endothelium;
Humans;
Microvessels*;
Myocardial Ischemia;
Nitroglycerin;
Spasm;
Thorax*;
Vasodilation;
Veins
- From:Korean Circulation Journal
1994;24(6):777-787
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: A group of patients with chest pain and normal coronary angiograms without spasm of epicardial artery is known to have decreased coronary flow reserve in response to vasodilatory stimuli, but the mechanisms responsible for the impairment of vasodilatory reserve are undefined. The purpose of this study was to determine whether dysfunction of coronary microvascular endothelium contributes to the reduced vasodilatory responses in patients with chest pain and normal coronary angiograms. METHODS: Twenty patients, 12(group A) with and 8(group B) without ST depression on exercise ECG or 24 hours ambulatory ECG. with chest pain and normal coronary angiograms and no spasm of epicardial coronary artery. were studied. As the endothelium-independent vasodilator, acetylcholine at doses of 20microg, 50microg and 100microg, and as the endothelium-independent vasodilator, nitroglycerin 200microg were infused into left coronary artery. The functional response of coronary vasomotion was studied with atrial pacing. By themodilution pacing catheter. great cardiac vein flow(GCVF) was measured. The changes in the diameter of proximal and distal of left anterior descending artery were analyzed. RESULTS: Intracoronary acetylcholine increased GCVF by 12.3% with 20microg(NS),by 38.9% with 50microg(p<0.05) and by 14.8% with 100microg(NS). The changes in GCVF with 20microg and 50microg dose of acetylcholine were positively related with those with atrial pacing(r=0.59 and r=0.62, respectively), but not at dose of 100microg(r=0.12). Thus, patients with diminished flow response with atrial pacing had reduced endothelium-dependent dilation with low dose acetylcholine. Also changes in GCVF with atrial pacing and acetylcholine were smaller in the patients of group A than group B. However, the changes in GCVF to nitroglycerin was not related with the changes with acetylcholine and did not differ between A and B group, indicating this vasodilatory response was not associated with the endothelium-independent vasodilation. Acetylcholine caused similar degree of change in diameter at proximal and distal epicardial artery in two groups and their changes were not related with changed in GCVF with acetylcholine, suggesting the changes in GCVF with acetylcholine were mainly influenced by the changes at the level of microvasculature. CONCLUSION: In patients with chest pain and normal coronary angiograms without spasm of epicardial artery, reduced vasodilatory response with atrial pacing was associated with the impairment of endothelium-dependent dilation at the level of coronary microvasculature, suggesting the endothelial dysfunction of coronary microvessels is one of the causes of inducible myocardial ischemia.
