The relation between extent of coronary artery disease measured by quantitative coronary angiography and changes in lipid profile: insights from trials of atherosclerosis regression

• Published in: The Journal of invasive cardiology 2008-06, Vol.20 (6), p.261-265
• Main Authors: Brener, Sorin J, Ivanc, Thomas B, Hu, Tingfei
• Format: Article
• Language: English
• Subjects: Anticholesteremic Agents - therapeutic use; Atorvastatin Calcium; Cholesterol, HDL - blood; Cholesterol, LDL - blood; Coronary Angiography - methods; Coronary Artery Disease - blood; Coronary Artery Disease - drug therapy; Coronary Artery Disease - pathology; Coronary Stenosis - blood; Coronary Stenosis - drug therapy; Coronary Stenosis - pathology; Coronary Vessels - diagnostic imaging; Coronary Vessels - pathology; Disease Progression; Female; Fluorobenzenes - therapeutic use; Follow-Up Studies; Heptanoic Acids - therapeutic use; Humans; Male; Middle Aged; Pravastatin - therapeutic use; Pyrimidines - therapeutic use; Pyrroles - therapeutic use; Randomized Controlled Trials as Topic; Risk Factors; Rosuvastatin Calcium; Sulfonamides - therapeutic use; Treatment Outcome; Ultrasonography, Interventional
• ISSN: 1557-2501

While favorable changes in atherogenic lipids are indisputably associated with improved clinical outcomes, a similar correlation with quantitative coronary angiography (QCA) parameters is more difficult to document. To assess the relation between changes in lipid profile and parameters of coronary artery disease (CAD) extent measured by QCA. We evaluated 1,315 patients enrolled in trials of atherosclerosis regression and correlated their lipid profile with annualized changes in CAD score (average minimal lumen diameter for all segments evaluated), cumulative stenosis score (sum of stenoses for all segments evaluated) and average plaque area for all segments evaluated. During the study, average low-density lipoprotein (LDL) decreased by 28% (p < 0.001), and average high-density lipoprotein (HDL) increased by 8% (p < 0.001). There was no statistical correlation between annualized changes in CAD score and change in LDL (p = 0.31) or % change in LDL (p = 0.53). There was also no statistically significant correlation between change in cumulative stenosis score and change in LDL (p = 0.20) or % change in LDL (p = 0.10). Neither of these parameters of CAD extent correlated with the summation of % changes in LDL and HDL (p = 0.80 and p = 0.34, respectively). Patients with CAD regression (i.e., greater average MLD at follow up, n = 756) had similar LDL, HDL and C-reactive protein levels while on therapy as patients with CAD progression (n = 555). Detailed analysis of CAD extent by QCA did not reveal a significant association with changes in lipid profile. These findings challenge the use of QCA as a surrogate endpoint for the effect of antiatherosclerotic therapy.