Contribution of dynamic vascular wall thickening to luminal narrowing during coronary arterial vasomotion

The hypothesis has been developed that increased coronary artery vasomotor tone superimposed on a preexisting obstruction is a possible mechanism responsible for resting and exertional angina. In 18 patients (22 stenotic lesions), the maximal changes in coronary artery diameter (mm) induced by an ergometrine test followed by an injection of isosorbide dinitrate were assessed by a quantitative computer-based angiographic system. If we assume that there is no change in the length of the artery as the result of changes in its diameter, then at any point of the artery the area of the arterial wall on a transverse cross section of the vessel will be constant regardless of its state of its contraction or dilatation. As vasoconstriction occurs, the luminal diameter decreases proportionally more than the outer diameter of the vessel and the wall thickness increases. Using elementary geometric principles, we calculated and reconstructed the changes that might occur at the stenotic sites as the result of vasomotion acting on the entire coronary segment. From the reference diameter in the control state (Ri: 3.7 ± 1.1 mm) and after vasoconstriction (Ric: 3.3 ± 1.0 mm) and the obstruction diameter in the control state (ri: 2.2 ± 0.9 mm), the minimal obstruction diameter after vasoconstriction (ric: 1.0 ± 0.8 mm) was derived using the following equation: ric² = ri² - Ri² + Ric². In four of 22 lesions, the decrease in diameter of the lumen of the normal vessel was fully translated to the stenotic point and the decrease in diameter at the stenosis was correctly predicted. In six lesions the vessel wall constricted less at the site of the lesion than predicted. Finally, 12 lesions exhibited clear arterial hypercontractility at the site of the stenosis (true spasm). These results demonstrate how unpredictable the effects of changes in vasomotor tone can be on large coronary arteries in individual patients. Understanding of these changes is essential before a rational definition of a critical stenosis can be made.