Comparative evaluation of coronary stenoses using fluid dynamic equations and standard quantitative coronary arteriography.

Abstract

Traditional quantitative coronary arteriographic measurements have largely ignored geometric variables, which may be important in determining the obstructive nature of coronary stenoses. To illustrate the relation between standard quantitative coronary arteriography and calculated transstenotic fluid dynamics, 25 patients with 1-vessel disease referred for coronary angioplasty were analyzed. Minimal lumen diameter and percent stenosis were measured and the values compared with calculations of pressure loss that used standard hydraulic formulas encompassing both frictional and separation components within the stenotic segments. Baseline flow velocity was assumed to equal 4 cm/s and normal hyperemic flow response was presumed to equal 5 times that of baseline. Fluid dynamic estimates suggested that initial translesional pressure gradients would develop at a minimal diameter of 0.6 mm (80% diameter), with an exponentially severe pressure differential beyond a minimal coronary diameter of 0.3 mm (92% diameter). Maximal velocities were calculated based upon an assumed normal hyperemic flow response of 5 times that of baseline, with the demonstration of early impairment of hyperemic flow reserve at minimal diameters of 1.2 mm (46% diameter). Furthermore, hyperemic flow reserve was completely abolished at a minimal diameter of 0.3 to 0.5 mm (89 to 92% diameter). Beyond a minimal diameter of 0.2 mm (93% diameter), resting hypoperfusion was anticipated with flow velocities below the initially assumed value (4 cm/s). Thus, it is feasible to estimate transstenotic pressure losses and maximal coronary flow velocity by applying Newtonian fluid dynamic equations to actual angiographic stenoses in man. These calculations generally correlate with traditional quantitative arteriographic estimates of stenosis severity, although other geometric parameters such as lesion length, "exit angle" and blood viscosity may alter transstenotic hemodynamics.