TY - JOUR
T1 - Platelet Activation in Essential Hypertension: Implications for Antiplatelet Treatment
AU - Gkaliagkousi, Eugenia
AU - Passacquale, Gabriella
AU - Douma, Stella
AU - Zamboulis, Chrysanthos
AU - Ferro, Albert
PY - 2010/3
Y1 - 2010/3
N2 - Essential hypertension is associated with increased risk of arterial thrombotic disease. Among other factors, enhanced platelet activity contributes significantly to this phenomenon An increased level of circulating monocyte-platelet aggregates (MPAs) represents one of the most robust markers of platelet activation, furthermore, these aggregates are also believed to contribute to the pathophysiology of atherothrombotic disease Putative mechanisms that contribute to platelet activation in essential hypertension include endothelial dysfunction, neurohumoral (sympathetic and renin-angiotensin systems) overactivity, decreased platelet nitric oxide (NO) biosynthesis, and platelet degranulation secondary to increased shear Current recommendations are that hypertensive patients receive aspirin therapy only if their calculated cardiovascular risk is high and their blood pressure (BP) is adequately controlled By contrast, the use of antiplatelet treatment in low-risk hypertensive patients is not established and merits further investigation Moreover, the place of alternative antiplatelet agents other than aspirin, such as clopidogrel, is unclear at present Some experimental evidence suggests that clopidogrel may confer an additive protective effect over and above aspirin in hypertensive patients, by virtue of effects on the evolution of the atherosclerotic process This now needs to be investigated in long-term clinical outcome studies.
AB - Essential hypertension is associated with increased risk of arterial thrombotic disease. Among other factors, enhanced platelet activity contributes significantly to this phenomenon An increased level of circulating monocyte-platelet aggregates (MPAs) represents one of the most robust markers of platelet activation, furthermore, these aggregates are also believed to contribute to the pathophysiology of atherothrombotic disease Putative mechanisms that contribute to platelet activation in essential hypertension include endothelial dysfunction, neurohumoral (sympathetic and renin-angiotensin systems) overactivity, decreased platelet nitric oxide (NO) biosynthesis, and platelet degranulation secondary to increased shear Current recommendations are that hypertensive patients receive aspirin therapy only if their calculated cardiovascular risk is high and their blood pressure (BP) is adequately controlled By contrast, the use of antiplatelet treatment in low-risk hypertensive patients is not established and merits further investigation Moreover, the place of alternative antiplatelet agents other than aspirin, such as clopidogrel, is unclear at present Some experimental evidence suggests that clopidogrel may confer an additive protective effect over and above aspirin in hypertensive patients, by virtue of effects on the evolution of the atherosclerotic process This now needs to be investigated in long-term clinical outcome studies.
U2 - 10.1038/ajh.2009.247
DO - 10.1038/ajh.2009.247
M3 - Article
VL - 23
SP - 229
EP - 236
JO - American Journal of Hypertension
JF - American Journal of Hypertension
IS - 3
ER -
