Abstract

Patterns of constriction and dilatation of angiographically normal coronary artery segments and coronary stenoses, in response to vasoactive stimuli, remain speculative. We compared the vasomotor response of angiographically normal and stenotic coronary segments and assessed the effects of stenosis location and morphology on coronary stenosis vasomotion in 52 patients with chronic stable angina (40 men and 12 women) who underwent intracoronary ergonovine or isosorbide dinitrate administration or both. Changes in coronary diameter in response to nitrate and ergonovine were assessed by computed arteriography. The "predicted" change in stenosis diameter was calculated according to the "geometric theory" (based on the vasomotor response of angiographically normal segments adjacent to the lesion and on stenosis severity). Coronary diameter was assessed at baseline and after nitrate administration in 58 stenoses (34 concentric and 24 eccentric), of which 40 were located proximally and 18 distally, and also after ergonovine administration (23 stenoses: 14 proximal and 9 distal, 14 concentric and 9 eccentric). Significant (> or = 10% lumen diameter change) vasoconstriction was observed after ergonovine administration in 14 of the 23 stenoses (61%), and significant vasodilation was noted after nitrate administration in 29 of 58 stenoses (50%). A larger proportion of distal (89%) and eccentric (89%) compared with proximal (43%) and concentric (43%) stenoses showed a greater than 10% vasoconstriction after ergonovine administration (P < 0.05). Vasodilatation after nitrate administration was also observed in a larger proportion of distal (78%) and eccentric (67%) than in proximal (38%) and concentric (38%) stenoses (P < 0.05). On average, the "observed" changes in coronary diameter in response to nitrate and ergonovine administration were of significantly less magnitude than those "predicted" by the geometric theory in both proximal and distal stenoses and in concentric and eccentric stenoses. In only 17% of stenoses were observed and predicted vasoconstriction similar. Our results suggest that in patients with chronic stable angina, calculations based on the "geometric theory" cannot predict the actual vasomotor response of a stenosis. Factors other than severity, such as baseline coronary tone, stenosis location, and stenosis morphology, appear to modulate stenosis vasomotion in vivo.

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