Other mechanisms may include plaque rupture resulting from cisplatin and vinca alkaloids (20), or coronary thrombosis due to pro-inflammatory and prothrombotic conditions associated with increased platelet aggregability induced by specific cancer therapies (e.g., cisplatin, vascular endothelial growth factor (VEGF) signaling pathway inhibitors and cyclophosphamide) (21). Here, VEGFA is linked to deep vein thrombosis.