Quantification of coronary artery stenosis in vivo.
Author(s) -
K. Lance Gould
Publication year - 1985
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/01.res.57.3.341
Subject(s) - in vivo , cardiology , stenosis , artery , medicine , biology , microbiology and biotechnology
VISUAL interpretations of coronary arteriograms are marked by such great interobserver and intraobserver variability (Bjork et al., 1975; Detre et al., 1975; Zir et al., 1976; DeRouen et al., 1977; Meyers et al., 1978) that comparison of arteriograms from different subjects, or at different times in the same subject, are of limited value for assessing severity, changes in severity, or functional significance of coronary artery stenoses. The universal use of relative percent diameter narrowing as a clinical measure of severity ignores other geometric characteristics of stenoses such as length, absolute diameter, multiple lesions in series, or eccentric narrowings which may be worse in one view, compared with another view. In vivo quantification of coronary stenosis is necessary for studying the pathogenesis, pathophysiology, and progression/regression of coronary artery disease. For example, what severity of coronary artery stenosis is necessary for altering ventricular function or metabolism? What degree of coronary artery narrowing can be detected by noninvasive methods? What are the quantitative effects of a variety of pharmacological agents on stenosis severity? Why do patients develop resting angina pectoris at one time but not at other times during equal supply-demand conditions? Is percent narrowing or absolute stenosis dimension the more important measurement? How do we quantify the shear forces on the endothelial wall at sites of arterial bending, branching, and/or narrowing which are important in the pathogenesis of cholesterol deposition, atheroma formation, and abnormal endothelial behavior, including platelet activation or release of substances causing arterial vasospasm?
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