Functional interplay between platelet activation and endothelial dysfunction in patients with coronary heart disease

S D Robinson, S A Harding, P Cummins, J N Din, J Sarma, I Davidson, K A A Fox, N A Boon, D E Newby

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Platelet-monocyte binding and surface P-selectin expression are sensitive markers of platelet activation. Endothelium-derived factors are known to inhibit platelet activation and may confer important anti-atherothrombotic effects. We assessed the relationship between platelet activation and endothelium-dependent vasomotion in patients with coronary heart disease (CHD). Twenty male patients with stable CHD were compared with 20 healthy men. Platelet-monocyte binding and platelet surface expression of P-selectin were assessed using two-colour flow cytometry on whole blood. Forearm blood flow was assessed in patients using venous occlusion plethysmography during intra-arterial infusions of substance P, acetylcholine and sodium nitroprusside. Platelet activation was higher in patients than healthy men (platelet-monocyte binding, 27 +/- 3 vs. 20 +/- 1%; P <0.05). In patients with CHD, there was an inverse correlation between maximal substance P induced vasodilatation and both platelet-monocyte binding (P = 0.003) and P-selectin expression (P = 0.02). A similar correlation was observed between platelet-monocyte binding and the vasomotor response to acetylcholine (P = 0.08) but not with sodium nitroprusside. In patients with stable coronary heart disease, there is a strong inverse relationship between markers of platelet activation and endothelium-dependent vasomotor function. This may explain the pathophysiological mechanism linking endothelial vasomotor dysfunction and the risk of acute atherothrombotic events.
Original languageEnglish
Pages (from-to)158-62
Number of pages5
Issue number3
Publication statusPublished - 2006


Dive into the research topics of 'Functional interplay between platelet activation and endothelial dysfunction in patients with coronary heart disease'. Together they form a unique fingerprint.

Cite this