Table 4.

Endogenous Causes of Acetylsalicylic Acid Antiplatelet Therapy Failure

Cellular	Genetic
Pathways not blocked by ASA (aggregation induced by erythrocytes, thrombin, collagen, adrenalin, ADP, cytokines)	Polymorphisms of COX-1 (alters the active site and inhibits acetylation by aspirin), COX-2, TxA2 synthase
Sensitivity of platelets to collagen and ADP	ADP polymorphisms of GP Ia/IIa, Ib/V/IX, IIb/IIIa receptors
COX-2 overexpression (rapid regeneration of platelets)	Polymorphisms of receptors for collagen GP VI, vWf GP Ia
Regenerated COX-1 (Mo, Ma, endothelial cells)	Polymorphism of f XIII (Val34Leu) leading to inhibition of factor XIII activation in ASA therapy
Resolvins
8-iso-PGF production

ADP, adenosine diphosphate; ASA, acetylsalicylic acid.