Abstract
Background
Uncontrolled severe hypertension is associated with alarming rates of cardiovascular
events but the mechanisms of vascular injury are not well understood. Recent investigative
interest has focused on platelet activation and platelet P-selectin (CD62P) as direct
mediators of vascular inflammation and injury. We investigated the association of
extreme blood pressure (BP) elevation with platelet P-selectin and fibrinolytic markers
in high risk patients with severe hypertension.
Methods
Cross-sectional comparison of platelet CD62, tissue plasminogen activator antigen
(tPA), and plasminogen activator inhibitor-1 activity (PAI-1) among 3 BP groups: untreated
severely hypertensive patients (SHT; n = 18), untreated mildly hypertensive patients (MHT; n = 19), and normotensive controls (NT; n = 16).
Results
Platelet CD62 was greatest in SHT (p = 0.00008) and showed a strong correlation with both systolic (p = 0.0002, r = 0.52) and diastolic (p = 0.0003, r = 0.52) BP. tPA was greater in SHT than MHT or NT (ANOVA; p = 0.02) and correlated with diastolic BP but not SBP. PAI-1 did not correlate with either
SBP or DBP but was related to body mass index, diabetes, and dyslipidemia.
Conclusions
Platelet CD62 demonstrated a strong and graded association with both systolic and
diastolic BP that persisted in the presence of multiple concomitant risk factors.
The association of BP with CD62P was stronger than with either PAI-1 or tPA-Ag. Platelet
activation and platelet CD62 increase in a BP-dependent manner and this relationship
persists at extreme levels of BP. Platelet activation and platelet CD62 may participate
in the accelerated target organ injury observed in high risk patients with severe
hypertension.
Keywords
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Article info
Publication history
Published online: June 08, 2006
Accepted:
April 20,
2006
Received in revised form:
March 30,
2006
Received:
December 26,
2005
Footnotes
☆This work has not been published elsewhere except as an abstract.
Identification
Copyright
© 2006 Elsevier Ireland Ltd. Published by Elsevier Inc. All rights reserved.
