Julia Rockstroh1, B Greg Brown. 1. Department of Medicine, Cardiology Division, University of Washington School of Medicine, Seattle, WA 98195, USA.
Abstract
BACKGROUND: Stimulation of coronary collateral growth has potential clinical value, yet techniques to assess such growth in patients are limited. METHODS AND RESULTS: A cineangiographic approach to classify the dominant collaterals and to quantify their lumen caliber and flow capacity was developed and validated. For measurement of 0.4- to 1.5-mm-diameter phantoms, mean error ranged from -0.01 to +0.02 mm. To illustrate the utility of such a method, 52 collateral pathways were measured in 13 patients with 17 occluded arteries before and after 10 years of intensive lipid therapy. The mean variance, final sigma, of 9 separate measurements of each collateral was +/-0.101 mm. At pretreatment, collateral diameter averaged 0.50+/-0.11 mm (SD) (range, 0.3 to 1.4 mm) without tapering or central narrowing. Over 10 years, mean increase in diameter was +16% (P=0.028); in area, +64% (P=0.015); and in estimated flow capacity, +214% (P=0.009). Certain lipoprotein characteristics tended to predict collateral growth. Patients for whom angina disappeared during 10 years had a greater increase in flow capacity than those for whom it persisted (+331% versus 4%; P=0.05). CONCLUSIONS: Coronary collateral diameter can be estimated with a precision of 0.10 mm. Flow capacity of the network is well approximated by measurement of the 2 or 3 largest connections serving an occluded artery. Initial studies with this method show that disappearance of angina is significantly associated with growth in collateral flow capacity. Collateral growth tends to associate with lipid therapy and with certain in-treatment lipid measures.
BACKGROUND: Stimulation of coronary collateral growth has potential clinical value, yet techniques to assess such growth in patients are limited. METHODS AND RESULTS: A cineangiographic approach to classify the dominant collaterals and to quantify their lumen caliber and flow capacity was developed and validated. For measurement of 0.4- to 1.5-mm-diameter phantoms, mean error ranged from -0.01 to +0.02 mm. To illustrate the utility of such a method, 52 collateral pathways were measured in 13 patients with 17 occluded arteries before and after 10 years of intensive lipid therapy. The mean variance, final sigma, of 9 separate measurements of each collateral was +/-0.101 mm. At pretreatment, collateral diameter averaged 0.50+/-0.11 mm (SD) (range, 0.3 to 1.4 mm) without tapering or central narrowing. Over 10 years, mean increase in diameter was +16% (P=0.028); in area, +64% (P=0.015); and in estimated flow capacity, +214% (P=0.009). Certain lipoprotein characteristics tended to predict collateral growth. Patients for whom angina disappeared during 10 years had a greater increase in flow capacity than those for whom it persisted (+331% versus 4%; P=0.05). CONCLUSIONS: Coronary collateral diameter can be estimated with a precision of 0.10 mm. Flow capacity of the network is well approximated by measurement of the 2 or 3 largest connections serving an occluded artery. Initial studies with this method show that disappearance of angina is significantly associated with growth in collateral flow capacity. Collateral growth tends to associate with lipid therapy and with certain in-treatment lipid measures.
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