title: Effects of cardiovascular risk factors on coronary artery remodeling in patients with mild atherosclerosis.
abstract: BACKGROUND
  Vascular remodeling counteracts luminal encroachment during the progression of coronary artery disease (CAD) and modulates the manifestation of hemodynamically significant lesions. However, the role of cardiovascular risk factors for coronary remodeling has not been fully clarified.
  
  
  METHODS
  Therefore, we investigated the role of local plaque burden and systemic risk factors on coronary vascular remodeling in 25 patients (49 segments) with angiographically normal or minimally diseased coronary arteries by intravascular ultrasound. In an additional 12 patients without coronary atherosclerosis, physiological vessel tapering was determined and used to calculate the extent of remodeling in diseased segments.
  
  
  RESULTS
  An increase in local plaque burden was directly correlated with positive vascular remodeling (r = 0.54, P<0.001). However, cardiovascular risk factors like hypertension (P<0.001) and hypercholesterolemia (P = 0.03) were associated with reduced positive or even negative remodeling. Moreover, the total number of classical cardiovascular risk factors was a strong predictor for reduced positive remodeling (P for trend <0.001). In contrast, coronary flow reserve, a measure of shear stress imposed on the vessel wall, positively correlated with compensatory enlargement (r = 0.44, P = 0.002). By multivariate analysis, plaque burden (P = 0.001), hypertension (P = 0.001) and coronary flow reserve (P = 0.018) proved to be independent determinants of vascular remodeling of epicardial coronary arteries.
  
  
  CONCLUSIONS
  Cardiovascular risk factors impair compensatory arterial enlargement and even predispose to shrinkage of epicardial arteries during the initial stage of atherosclerosis. Reduced positive vascular remodeling might contribute to the clinical manifestation of CAD by facilitating the development of flow-limiting stenoses in patients at risk.
authors.affiliation: Department of Internal Medicine IV, Division of Cardiology, J.W. Goethe-University, Theodor-Stern-Kai 7, D-60590 Frankfurt, Germany.
authors.forename: Martina B
authors.initials: MB
authors.lastname: Britten
authors.forename: Andreas M
authors.initials: AM
authors.lastname: Zeiher
authors.forename: Volker
authors.initials: V
authors.lastname: Schächinger
mesh_terms: D000368:Aged; D001158:Arteries / Q000378:metabolism / Q000503:physiopathology*; D015415:Biomarkers / Q000097:blood; D002318:Cardiovascular Diseases / Q000453:epidemiology* / Q000378:metabolism / Q000503:physiopathology*; D003324:Coronary Artery Disease / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology; D003326:Coronary Circulation / Q000502:physiology; D003331:Coronary Vessels / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology; D008075:Lipoproteins, HDL / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D010496:Pericardium / Q000378:metabolism / Q000503:physiopathology; D011237:Predictive Value of Tests; D012307:Risk Factors; D012720:Severity of Illness Index; D013223:Statistics as Topic; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D015415:Biomarkers; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL