title: Effects of "newer" and "older" antihypertensive drugs on hemorrheological, platelet, and endothelial factors. A substudy of the Anglo-Scandinavian Cardiac Outcomes Trial.
abstract: BACKGROUND
  Different antihypertensive therapies may exert benefits via not only a reduction in blood pressure but also in improving the risk of thrombosis.
  
  
  METHODS
  We tested the hypothesis that a more modern antihypertensive drug regimen (ie, amlodipine +/- perindopril) would have a more beneficial effect on hemorheological markers (white blood-cell count [WCC], plasma viscosity [PV], hematocrit [HCT], and fibrinogen)--and on plasma von Willebrand factor (vWf, an index of endothelial damage and dysfunction) and soluble P-selectin (sP-sel, an index of platelet activation), compared with an older antihypertensive drug regimen (ie, atenolol +/- bendroflumethiazide).
  
  
  RESULTS
  After 6 months, PV, sP-sel, and HCT fell in both groups (P < .01), while fibrinogen was unchanged. However, those 74 patients randomized to amlodipine +/- perindopril had significant reductions in WCC (P = .005), with no significant changes in vWF or platelet count. Conversely, in those 85 patients randomized to atenolol +/- bendroflumethiazide, there were significant reductions in vWF (P = .001) and platelet count (P = .011) but no significant reductions in WCC. There were no significant differences in the levels of any of the variables between the two arms of the trial, nor a significant difference in the magnitude of reduction between the two treatment arms.
  
  
  CONCLUSIONS
  Within the constraints of this substudy design, there was no differential effect apparent of the two antihypertensive treatment arms on hemorheological parameters or endothelial and platelet function (as assessed by vWF and sP-sel), suggesting that other pathophysiological mechanisms may be involved.
authors.affiliation: Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK.
authors.forename: Charles G C
authors.initials: CG
authors.lastname: Spencer
authors.forename: Dirk C
authors.initials: DC
authors.lastname: Felmeden
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Blann
authors.forename: Gregory Y H
authors.initials: GY
authors.lastname: Lip
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D000368:Aged; D017311:Amlodipine / Q000494:pharmacology / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001262:Atenolol / Q000494:pharmacology / Q000627:therapeutic use; D001539:Bendroflumethiazide / Q000494:pharmacology / Q000627:therapeutic use; D001783:Blood Flow Velocity / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use; D004232:Diuretics / Q000494:pharmacology / Q000627:therapeutic use; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood* / Q000187:drug effects; D020913:Perindopril / Q000494:pharmacology / Q000627:therapeutic use; D015539:Platelet Activation / Q000187:drug effects / Q000502:physiology; D006113:United Kingdom; D014655:Vascular Resistance / Q000187:drug effects*; D014841:von Willebrand Factor / Q000187:drug effects / Q000378:metabolism*
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D004232:Diuretics; D019007:P-Selectin; D014841:von Willebrand Factor; D017311:Amlodipine; D001262:Atenolol; D001539:Bendroflumethiazide; D020913:Perindopril