Oxidative Stress and Inflammation in Heart Disease: Do Antioxidants Have a Role in Treatment and/or Prevention?

Figure 4

Oxidative stress mediates abnormal platelet function and dysfunctional endothelium-dependent vasodilation. Oxidative stress is an important mediator of both abnormal platelet function and dysfunctional endothelium-dependent vasodilation in the setting of cardiovascular disease. Superoxide anion is an important source of oxidative stress, has direct effects, and limits the biological activity of NO. Excessive vascular superoxide production drives further platelet activation and recruitment leading to greater thrombus formation. The occurrence of superficial intimal injury caused by endothelial denudation and deep intimal injury caused by plaque rupture expose collagen and Tissue Factor (TF) to platelets. Local platelet activation stimulates further thrombus formation and additional platelet recruitment by supporting cell-surface thrombin formation and releasing potent platelet agonists such as adenosine diphosphate (ADP), serotonin, and thromboxane A2. A thrombus forms as platelets aggregate via the binding of bivalent fibrinogen to GP IIb/IIIa. Platelet NO release influences platelet recruitment to the growing thrombus and impaired platelet-derived NO release is likely associated with acute coronary and stroke syndromes. Antioxidants may indirectly inhibit platelets through scavenging of reactive oxygen species, many of which alter platelet function. Despite the different subcellular locations of water- and lipid-soluble antioxidants, these antioxidant pathways in platelets are closely linked. Antioxidants may also indirectly inhibit platelets through the metabolism of reactive oxygen species, many of which alter platelet function. Inflammation is linked with the evolution of cardiovascular disease and acute coronary syndromes, adapted from [15].