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Background Platelets are involved in inflammatory reactions which play an important role in the development of atherosclerosis and its acute complications. The objective of this study was to test the ability of glycoprotein (GP) IIb-IIIa antagonist eptifibatide to suppress the increase of inflammatory markers in non-ST-segment elevation acute coronary syndrome (ACS). Methods Twenty-five patients with unstable angina and non-ST-segment elevation myocardial infarction received eptifibatide on admission (two 180 μg/kg boluses followed by infusion at 2.0 and 1.3 μg/kg/min for 24 and 48 h, respectively) and 25 were treated without GP IIb-IIIa antagonists. Plasma von Willebrand factor (vWF) and soluble P-selectin were determined at baseline, 48 h and 2 weeks after onset of ACS, and were also measured in a group of healthy volunteers. Serum C-reactive protein (CRP), tumor necrosis factor alpha (TNFα), and interleukin 6 (IL6) were measured at baseline, 48 h, 2 weeks and 6 months. Results P-selectin was increased at baseline and vWF at baseline, 48 h and 2 weeks in comparison with healthy donors. CRP, TNFα, but not IL6 were increased at baseline, 48 h and 2 weeks in comparison with their levels at 6 months. Maximal values of CRP, TNFα and vWF were detected at 48 h. At any time point eptifibatide failed to decrease the levels of all tested markers. Conclusion Eptifibatide does not suppress elevated levels of inflammatory markers in patients with non-ST-segment elevation ACS.

Nitroglycerin, isosorbide dinitrate and sodium nitroprusside, like nifedipine, were found to inhibit the receptor-provoked increase of cytosolic free calcium concentration in human platelets loaded with 2-[(2-amino-5-methylphenoxy)methyl]-6-methoxy-8-aminoquinoline- N,N,N′,N′ -tetraacetate. Sodium nitroprus-side and nitroglycerin induced elevation of cyclic guanosine 3′,5′-monophosphate content in platelets which correlated with their calcium-blocking activity. Methylene blue and epinephrine decreased the calcium-blocking effect and the influence of nitroglycerin on cyclic guanosine 3′-5′-monophosphate content, but failed to suppress the inhibitory effect of sodium nitroprusside. Ascorbic acid increased the calcium blocking effect of sodium nitroprusside and its influence on cyclic guanosine 3′,5′-monophosphate content, but did not alter the inhibitory effect of nitroglycerin. In order to evaluate the relationship between the mode of action of nitrates at cellular level and their vasodilatory effectiveness, we studied the circulatory response of the forearm to isosorbide dinitrate and the influence of nitroglycerin on free calcium concentration in the platelets in 10 patients with chronic heart failure. We established a significant positive correlation between the basal values for venous tone and its peak decrease after administration of the 10-mg dose of isosorbide dinitrate. A correlation was also found between the deviation of maximal decrease of venous tone by this dose of isosorbide dinitrate from the regression line (the relationship between the basal venous tone and its lowering by the drug) and mean inhibitory concentration values for nitroglycerin in blocking that proportion of the rise of calcium ion concentration in platelets due to blocking of the platelet-activating factor. Thus, nitrates, like calcium antagonists, inhibit the receptor-provoked calcium supply to the contractile system of the cells so neutralizing the effects of increased concentrations of vasoconstrictors. This suggests that the effectiveness of nitrates appears to be positively related to the contribution of receptor-induced increase of cytosolic free calcium concentration in vasoconstriction together with their capacity to raise cyclic guanosine 3′,5′-monophosphate.