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(Circulation. 1995;92:2411-2418.)
© 1995 American Heart Association, Inc.

Articles

Compensatory Vascular Changes of Remote Coronary Segments in Response to Lesion Progression as Observed by Sequential Angiography From a Controlled Clinical Trial

Anne M. Shircore, MS; Wendy J. Mack, PhD; Robert H. Selzer, MS; Paul L. Lee, PhD; Stanley P. Azen, PhD; Petar Alaupovic, PhD; Howard N. Hodis, MD

From the Atherosclerosis Research Unit, Division of Cardiology and the Statistical Consultation Research Center, Departments of Medicine (A.M.S., H.N.H.) and Preventive Medicine (W.J.M., S.P.A., H.N.H.), University of Southern California School of Medicine, Los Angeles; the Jet Propulsion Laboratory (A.M.S., R.H.S., P.L.L.), Pasadena, CA; and the Oklahoma Medical Research Foundation (P.A.).

Background Local coronary artery enlargement to compensate for atherosclerotic plaques preserves the vessel lumen. The extent to which coronary segments remote from progressing lesions enlarge is unknown. This is clinically relevant since compensatory enlargement may be important in determining whether clinical complications result from progression of coronary artery disease (CAD). Additionally, compensatory change has implications for quantitative coronary angiographic (QCA) trials, since the effect of progression on diameter means may be mitigated by compensatory changes in remote coronary segments when QCA change is averaged over all lesions.

Methods and Results Serial QCA data from 78 subjects in the Monitored Atherosclerosis Regression Study were used to demonstrate compensatory changes in coronary segments remote from progressing or regressing lesions. Coronary segments were first classified as progressing (regressing) if percent diameter stenosis (PS) increased or decreased by >10 with a concurrent decrease or increase in minimum lumen diameter (MLD) of either >0.32 mm or >10% of the normal baseline reference diameter (DNORM). Segments not meeting these criteria were labeled stenosis stable. Stenosis-stable segments opposite progressing lesions showed increases in MLD (P=.0006), DNORM (P=.001), and average diameter (P=.001). On-trial apolipoprotein (apo) B, apo C-III, and blood pressure levels inversely correlated with these compensatory changes.

Conclusions Lesion progression in one coronary segment is associated with significant increases in segmental diameter of remote parts of the coronary tree. We hypothesize these increases to be vascular compensatory changes in response to progression of CAD. Vascular compensatory change is enhanced by LDL cholesterol and triglyceride-rich lipoprotein reduction and appears to be part of the treatment effect itself.

Key Words: coronary disease • apolipoproteins • angiography • cholesterol • lipoproteins • remodeling

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