title: Risk prediction is improved by adding markers of subclinical organ damage to SCORE.
abstract: OBJECTIVE
  It is unclear whether subclinical vascular damage adds significantly to Systemic Coronary Risk Evaluation (SCORE) risk stratification in healthy subjects.
  
  
  RESULTS
  In a population-based sample of 1968 subjects without cardiovascular disease or diabetes not receiving any cardiovascular, anti-diabetic, or lipid-lowering treatment, aged 41, 51, 61, or 71 years, we measured traditional cardiovascular risk factors, left ventricular (LV) mass index, atherosclerotic plaques in the carotid arteries, carotid/femoral pulse wave velocity (PWV), and urine albumin/creatinine ratio (UACR) and followed them for a median of 12.8 years. Eighty-one subjects died because of cardiovascular causes. Risk of cardiovascular death was independently of SCORE associated with LV hypertrophy [hazard ratio (HR) 2.2 (95% CI 1.2-4.0)], plaques [HR 2.5 (1.6-4.0)], UACR > or = 90th percentile [HR 3.3 (1.8-5.9)], PWV > 12 m/s [HR 1.9 (1.1-3.3) for SCORE > or = 5% and 7.3 (3.2-16.1) for SCORE < 5%]. Restricting primary prevention to subjects with SCORE > or = 5% as well as subclinical organ damage, increased specificity of risk prediction from 75 to 81% (P < 0.002), but reduced sensitivity from 72 to 65% (P = 0.4). Broaden primary prevention from subjects with SCORE > or = 5% to include subjects with 1% < or = SCORE < 5% together with subclinical organ damage increased sensitivity from 72 to 89% (P = 0.006), but reduced specificity from 75 to 57% (P < 0.002) and positive predictive value from 11 to 8% (P = 0.07).
  
  
  CONCLUSIONS
  Subclinical organ damage predicted cardiovascular death independently of SCORE and the combination may improve risk prediction.
authors.affiliation: Department of Internal Medicine, The Cardiovascular Research Unit, Glostrup University Hospital, Nordre Ringvej, Glostrup, Denmark. ts@heart.dk
authors.forename: Thomas
authors.initials: T
authors.lastname: Sehestedt
authors.forename: Jørgen
authors.initials: J
authors.lastname: Jeppesen
authors.forename: Tine W
authors.initials: TW
authors.lastname: Hansen
authors.forename: Kristian
authors.initials: K
authors.lastname: Wachtell
authors.forename: Hans
authors.initials: H
authors.lastname: Ibsen
authors.forename: Christian
authors.initials: C
authors.lastname: Torp-Pedersen
authors.forename: Christian
authors.initials: C
authors.lastname: Torp-Petersen
authors.forename: Per
authors.initials: P
authors.lastname: Hildebrandt
authors.forename: Michael H
authors.initials: MH
authors.lastname: Olsen
mesh_terms: D000328:Adult; D000368:Aged; D000419:Albuminuria / Q000175:diagnosis / Q000401:mortality; D050197:Atherosclerosis / Q000401:mortality / Q000473:pathology; D015415:Biomarkers / Q000032:analysis; D001783:Blood Flow Velocity / Q000502:physiology; D002318:Cardiovascular Diseases / Q000401:mortality / Q000473:pathology / Q000517:prevention & control*; D003404:Creatinine / Q000652:urine; D004452:Echocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D011673:Pulsatile Flow; D018570:Risk Assessment; D012307:Risk Factors; D012720:Severity of Illness Index
chemical_list: D015415:Biomarkers; D003404:Creatinine