title: Coronary artery calcification and changes in atheroma burden in response to established medical therapies.
abstract: OBJECTIVE
  This study sought to determine the relationship between coronary calcification and plaque progression in response to established medical therapies.
  
  
  BACKGROUND
  Coronary calcification correlates with the extent of atherosclerosis and predicts clinical outcome.
  
  
  METHODS
  Atheroma volume was determined in serial intravascular ultrasound pullbacks in matched arterial segments of 776 patients with angiographic coronary artery disease. A calcium grade at baseline was assigned for each image (total 28,876) (0 = no calcium, 1 = calcium with acoustic shadowing <90 degrees and 2 = calcium with shadowing >90 degrees). Patients with a calcium index (average of calcium scores in a pullback) below versus above the median were compared with regard to plaque burden and progression.
  
  
  RESULTS
  Patients with a high calcium index were older (59 vs. 54 years, p < 0.001), more likely to be male (80% vs. 68%, p < 0.001), and more likely to have a history of hypertension (71% vs. 64%, p = 0.03). These patients had a greater percentage atheroma volume (PAV) (45% vs. 34%, p < 0.001), total atheroma volume (TAV) (210 vs. 151 mm3, p < 0.001), and percentage of images with maximal plaque thickness >0.5 mm (93% vs. 72%, p < 0.001). The continuous rate of change in PAV (1.1 +/- 0.4% vs. 0.8 +/- 0.4%, p = 0.34) and TAV (1.7 +/- 2.1% vs. -0.1 +/- 2.2%, p = 0.37) was similar in patients with a lower and higher calcium index, respectively. A lower calcium index was associated with a higher rate of patients showing substantial change in atheroma burden (at least 5% change in PAV, 70% vs. 53%, p < 0.001).
  
  
  CONCLUSIONS
  Calcific plaques are more resistant to undergoing changes in size in response to systemic interventions targeting atherosclerotic risk factors.
authors.affiliation: Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio 44195, USA. nichols1@ccf.org
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Nicholls
authors.forename: E Murat
authors.initials: EM
authors.lastname: Tuzcu
authors.forename: Kathy
authors.initials: K
authors.lastname: Wolski
authors.forename: Ilke
authors.initials: I
authors.lastname: Sipahi
authors.forename: Paul
authors.initials: P
authors.lastname: Schoenhagen
authors.forename: Timothy
authors.initials: T
authors.lastname: Crowe
authors.forename: Samir R
authors.initials: SR
authors.lastname: Kapadia
authors.forename: Stanley L
authors.initials: SL
authors.lastname: Hazen
authors.forename: Steven E
authors.initials: SE
authors.lastname: Nissen
mesh_terms: D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use; D050197:Atherosclerosis / Q000150:complications / Q000188:drug therapy / Q000473:pathology; D002114:Calcinosis / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology; D002118:Calcium / Q000378:metabolism; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000150:complications / Q000000981:diagnostic imaging* / Q000188:drug therapy* / Q000473:pathology; D003326:Coronary Circulation / Q000187:drug effects; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011336:Probability; D011379:Prognosis; D012189:Retrospective Studies; D018570:Risk Assessment; D018709:Statistics, Nonparametric; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional; D014654:Vascular Patency / Q000187:drug effects
chemical_list: D000959:Antihypertensive Agents; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D002118:Calcium