Sansone R, et al. - Researchers explored the link between endothelial microparticles (EMPs) and physicomechanical factors in stable arterial hypertension and hypertensive emergencies. The pattern of EMP release after mechanical endothelial injury was also examined. In hypertension, EMP release in complicated and could involve both physicomechanical endothelial injury and activation (CD144⁺, CD62e⁺) and decreased wall shear stress (CD31⁺/41^-).

Methods

• A pilot study was carried out with 41 subjects (50% hypertensives); flow-cytometry was used to discriminate EMPs (CD31⁺/41^-), CD62e⁺, CD144⁺).
• In addition to blood pressure measurements, pulse-wave-analysis was also carried out.
• Using ultrasonography, flow-mediated dilation (FMD), nitroglycerin-mediated dilation (NMD), and wall-shear-stress (WSS) were measured in the brachial artery; microvascular perfusion by laser-Doppler.
• Researchers examined patients with hypertensive emergencies before and 4 hours after BP lowering by urapidil (n = 12) and studied the release of EMPs due to mechanical endothelial injury after coronary angiography (n = 10).

Results

• Relative to normotensives, hypertensives exhibited increased EMPs (CD31⁺/41^-, CD144⁺, CD62e⁺).
• EMPs, univariately, were shown to be correlated with systolic BP (SBP), augmentation index, and pulse wave velocity and inversely with FMD.
• Data showed a correlation of CD31⁺/41^--EMPs with diameter and an inverse correlation of these with WSS and NMD.
• An inverse correlation of CD62e⁺ and CD144⁺-EMPs with microvascular function was observed.
• Relative to stable hypertensives, only CD62e⁺ and CD144⁺-EMPs were further elevated and FMD was decreased during hypertensive emergency.
• As a result of blood pressure lowering, decreased CD62e⁺and CD144⁺-EMPs and increased FMD were noted. No impact was seen on CD31⁺/41^—EMPs, diameter, and WSS.
• Like hypertensive emergency, only CD144⁺ and CD62e⁺-EMPs were found to be increased due to catheter-related endothelial injury.