title: Detection of silent cerebrovascular disease refines risk stratification of hypertensive patients.
abstract: OBJECTIVE
  Detection of preclinical hypertension-related cardiorenal damage has been recommended in the identification of patients most at risk of cardiovascular complications. The inclusion of silent cerebrovascular disease (SCD) as an additional marker of hypertensive organ involvement might improve risk stratification.
  
  
  METHODS
  In 192 hypertensive patients (98 men) without a history of cardiovascular and cerebrovascular disease, a mean age of 51.6 +/- 12.3 years and untreated office blood pressure levels of 170 +/- 23/104 +/- 12 mmHg, we obtained detailed information on preclinical cardiac (left ventricular hypertrophy), renal (microalbuminuria, impaired kidney function or both) and cerebrovascular damage (white matter hyperintensities, infarcts, microbleeds or all), and estimated the associated cardiovascular risk on the basis of the presence of common cardiovascular risk factors.
  
  
  RESULTS
  Hypertensive target-organ damage involved the heart in 41 (21%), the kidneys in 50 (26%) and the brain in 84 (44%) participants. When considering only patients with demonstrable cardiac, renal damage or both (n = 72), 42 participants (58%) had also SCD. Of the remaining 120 participants without cardiorenal damage, 42 (35%) had brain damage. In other words, half of all patients with SCD were classified as having no target-organ (i.e., cardiorenal) involvement. The cardiovascular risk score of patients without cardiorenal but with brain damage was significantly higher than that of participants without any organ involvement (37 +/- 11 versus 27 +/- 11, P < 0.001), and similar to the risk score of those with cardiorenal damage (38 +/- 14, P > 0.05).
  
  
  CONCLUSIONS
  These data suggest that SCD should be recognized as an additional, independent and prognostically relevant marker of preclinical hypertensive target-organ damage.
authors.affiliation: Department of Internal Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands.
authors.forename: Léon H
authors.initials: LH
authors.lastname: Henskens
authors.forename: Robert J
authors.initials: RJ
authors.lastname: van Oostenbrugge
authors.forename: Abraham A
authors.initials: AA
authors.lastname: Kroon
authors.forename: Paul A
authors.initials: PA
authors.lastname: Hofman
authors.forename: Jan
authors.initials: J
authors.lastname: Lodder
authors.forename: Peter W
authors.initials: PW
authors.lastname: de Leeuw
mesh_terms: D000328:Adult; D000368:Aged; D002543:Cerebral Hemorrhage / Q000209:etiology; D002544:Cerebral Infarction / Q000209:etiology; D002561:Cerebrovascular Disorders / Q000209:etiology*; D003430:Cross-Sectional Studies; D005260:Female; D006331:Heart Diseases / Q000209:etiology; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000188:drug therapy; D007674:Kidney Diseases / Q000209:etiology; D008297:Male; D008875:Middle Aged; D012307:Risk Factors