title: Enhanced coronary vasoconstriction after PTCA in patients with acute ischemia.
abstract: Coronary vasoconstriction of the distal vessel segment has been reported after percutaneous transluminal coronary angiography (PTCA), which was explained by increased vasoconstrictor influences. In patients with acute ischemia these changes may be even enhanced. Thus, vasomotion of the epicardial coronary arteries was studied before and after PTCA in patients with acute ischemia due to unstable angina or acute infarction.
  
  
  METHODS
  52 patients were divided into 2 groups: Group 1 (controls) consisted of 31 patients who underwent elective (PTCA) and group 2 of 21 patients who underwent emergency PTCA for unstable angina or acute infarction. Coronary artery dimensions proximal and distal to the culprit lesion were determined by quantitative coronary angiography before and after PTCA as well as after 0.2 mg nitroglycerin i.c. at the end of the procedure.
  
  
  RESULTS
  Stenosis severity was similar before and after PTCA in both groups (before, 91 +/- 8% in group 1 vs 90 +/- 9% in group 2; after, 28 +/- 9% vs 23 +/- 10%, resp.). Heart rate and mean blood pressure remained unchanged. In the group with acute ischemia no vasodilation of the proximal (2 +/- 3%) and distal vessel (-1 +/- 4%) occurred after PTCA, whereas in the control group significant vasodilation of both vessel segments (11 +/- 2% resp. 13 +/- 3%) was found. The response to nitroglycerin was maintained in both groups. In the control group there was a significant correlation between stenosis severity and percent diameter change of the distal vessel segment. However, in the acute ischemic group this relationship was shifted downwards suggesting an enhanced vasoconstrictor response in these patients.
  
  
  CONCLUSIONS
  Epicardial coronary arteries in patients with acute ischemia show an enhanced vasoconstriction after PTCA. Nevertheless, the response to nitroglycerin is maintained suggesting that functional (endothelial dysfunction) rather than structural factors are responsible for this phenomenon.
authors.forename: L
authors.initials: L
authors.lastname: Mandinov
authors.forename: P
authors.initials: P
authors.lastname: Kaufmann
authors.forename: F
authors.initials: F
authors.lastname: Eberli
authors.forename: O M
authors.initials: OM
authors.lastname: Hess
mesh_terms: D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D003331:Coronary Vessels / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000503:physiopathology*; D009569:Nitric Oxide / Q000502:physiology; D014661:Vasoconstriction
chemical_list: D009569:Nitric Oxide