title: Platelet indexes in relation to target organ damage in high-risk hypertensive patients: a substudy of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT).
abstract: OBJECTIVE
  We sought to investigate the relationship between target organ damage (TOD) in hypertension and a prothrombotic/hypercoagulable state, using a new technique of "platelet lysis" to quantify the amount of P-selectin per platelet (pP-sel), and to correlate it with other platelet markers (e.g., mass, volume and granularity, soluble P-selectin [sP-sel], and beta-thromboglobulin [beta-TG]).
  
  
  BACKGROUND
  The increased risk of TOD in hypertension may be related to a prothrombotic/hypercoagulable state, with abnormalities in platelets, such as increased expression of P-selectin.
  
  
  METHODS
  We studied 199 patients (mean age 68 years, 75% men) with hypertension. Of these, 125 had TOD (e.g., stroke, previous myocardial infarction, angina, left ventricular hypertrophy). Values obtained were compared with those from 59 healthy normotensive control subjects (mean age 68 years, 58% men).
  
  
  RESULTS
  Hypertensive patients had a higher mean platelet volume, mass, pP-sel, sP-sel, and beta-TG and lower platelet granularity (all p < 0.01), but a similar platelet count, as compared with controls. Within the hypertensive group, those with evidence of TOD had significantly larger platelets with greater mass but had lower granularity, sP-sel, and pP-sel levels than those without TOD, possibly reflecting increased aspirin use. On multivariate analysis, aspirin use was a determinant of pP-sel (p = 0.03) and sP-sel (p = 0.01), but the use of other drugs or other co-morbidity (e.g., diabetes, smoking) did not influence either P-selectin value.
  
  
  CONCLUSIONS
  Patients with hypertension have evidence of changes in platelet physiology, as reflected by a higher level of pP-sel. Patients with TOD also had larger platelets, with greater mass, and the use of aspirin lowered pP-sel and sP-sel levels. These changes may have implications for the pathophysiology of cardiovascular and cerebrovascular disease in hypertension.
authors.affiliation: Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, United Kingdom.
authors.forename: Sunil K
authors.initials: SK
authors.lastname: Nadar
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Blann
authors.forename: Sridhar
authors.initials: S
authors.lastname: Kamath
authors.forename: D Gareth
authors.initials: DG
authors.lastname: Beevers
authors.forename: Gregory Y H
authors.initials: GY
authors.lastname: Lip
mesh_terms: D000368:Aged; D001792:Blood Platelets / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D002318:Cardiovascular Diseases / Q000097:blood / Q000209:etiology*; D048429:Cell Size; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood*; D010976:Platelet Count; D051437:Renal Insufficiency / Q000209:etiology; D012307:Risk Factors; D019851:Thrombophilia / Q000097:blood / Q000209:etiology; D001620:beta-Thromboglobulin / Q000032:analysis
chemical_list: D019007:P-Selectin; D001620:beta-Thromboglobulin