Coronary vasomotion after percutaneous transluminal coronary angioplasty depends on the severity of the culprit lesion

Department of Cardiology, University Hospital, Zurich, Switzerland.

OBJECTIVES: This study sought to evaluate coronary vasomotor response to percutaneous transluminal coronary angioplasty (PTCA) and its influence on proximal and distal vessel diameters with regard to stenosis severity and coronary blood flow. BACKGROUND: Coronary vasoconstriction of the distal vessel segment has been reported after PTCA. This vasoconstrictive effect was thought to be due to balloon-induced injury of the vessel wall, with release of local vasoconstrictors or stimulation of the sympathetic system with release of catecholamines, or both. METHODS: Thirty-nine patients were prospectively studied before and after PTCA. Patients were classified into two groups according to the severity of the culprit lesion: group 1 = > or = 70% to < or = 85% diameter stenosis (n = 23); and group 2 = > 85% to < or = 95% diameter stenosis (n = 16). The coronary vessel diameter of the proximal and distal vessel segments as well as the minimal lumen diameter were determined by quantitative coronary angiography. In a subgroup of 16 patients, basal and maximal coronary flow velocity was measured before and after PTCA with the Doppler FloWire system. RESULTS: The groups were comparable with regard to age, gender, serum cholesterol levels and medical therapy. The proximal vessel segment remained unchanged after PTCA in group 1 ([mean +/- SD] 0.9 +/- 3.5%, p = 0.8) but showed vasodilation in group 2 (+13.7 +/- 3.6%, p < 0.05). However, the distal segment showed vasoconstriction in group 1 (-6.7 +/- 2.0%, p < 0.01) and vasodilation in group 2 (+31 +/- 8.0%, p < 0.01). A significant correlation was found between the change in distal vessel diameter after PTCA and stenosis severity (r = 0.61, p < 0.0001). Changes in blood flow were directly correlated to stenosis severity (r = 0.85, p < 0.002); that is, rest flow increased after PTCA in narrow lesions but remained unchanged in moderate lesions. The diameter changes in the distal vessel segment after PTCA were significantly related to flow changes (r = 0.90, p < 0.0001). Coronary distending pressure of the distal vessel segment increased significantly in both groups; however, this increase was significantly greater in group 2 than in group 1 (55 +/- 4 vs. 14 +/- 3 mm Hg, p < 0.0001). CONCLUSIONS: Coronary vasomotion of the proximal and distal vessel segments after PTCA depends on the severity of the culprit lesion; that is, vasoconstriction of the distal segment is found in patients with moderate lesions and vasodilation in those with severe lesions. Thus, vasomotion of the post-stenotic vessel segment depends on the severity of the culprit lesion and is influenced by changes in coronary flow or distending pressure, or both.

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