To promote high quality neo tissue formation and inhibit pathological remodeling within engineered cardiovascular tissues, purinergic signaling must be inhibited. The P2Y12 receptor inhibitor called prasugrel, or Effient®, reduces the rate of thrombotic cardiovascular (CV) events (including stent thrombosis) in patients with acute coronary syndrome (ACS). Patients with unstable angina (UA) or non-ST-elevation myocardial infarction and patients with ST-elevation myocardial infarction should be managed with percutaneous coronary intervention (PCI) when managed with primary or delayed PCI. In tissue engineered vascular conduits, mural thrombi remodel into neo tissue and obstruct the lumen. Platelet-rich thrombi also contribute to pathological remodeling and may cause leukocytes might form neutrophil extracellular traps, or NETs. When the P2Y12 receptor is inhibited on platelets, it reduces its activation and recruitment, which also decreases the mural thrombus size. Macrophages and smooth muscle cells also express P2Y12 receptors, which enable chemotaxis towards the source of ADP. Although macrophages are essential for neo tissue formation, excess infiltration can increase inflammation and stenosis, which may impair high-quality neo tissue formation. Therefore, inhibiting purinergic signaling induced chemotaxis will inhibit macrophage recruitment to prevent TEVG stenosis and inflammation. Blocking the P2Y12 receptor may also block fibrosis by inhibiting the transition of macrophage to myofibroblast. Since smooth muscle cells also express the P2Y12 receptor, signaling through the receptor can stimulate cell proliferation and contraction. Like macrophages, these are essential processes, but an excess may lead to stenosis.