Table 2 Summary of studies investigating the effect of different drug classes on radiation-induced vascular complications
Drug class | Potential mechanism | Animal study results | Real-world study observations | |||
|---|---|---|---|---|---|---|
Statin | Inhibits radiation-induced cell death, generates proinflammatory and profibrotic responses in different tissues, and inhibits extracellular matrix deposition in human fibrotic cells [40] | Radiation-induced atherosclerosis could not be circumvented by atorvastatin [31] | Statins were associated with a reduction in the combination of stroke and TIA (HR = 0.4; 95 % CI = 0.2–0.8; p = 0.01) [33] Statins were associated with a significant reduction of 32 % in stroke outcome alone (HR = 0.68, 95 % CI = 0.48–0.98, p = 0.04) [41] | |||
Antiplatelet | Anti-inflammatory and antithrombotic [30] | Radiation-induced atherosclerosis could not be circumvented by aspirin and clopidogrel [30, 31] | No significant difference in the risk of IS or TIA between patients on continuous oral antithrombotic agents and nonusers (adjusted HR = 0.81; 95 % CI = 0.20–3.31, p = 0.77) [34] | |||
Thyroxine | May attenuate fibrosis response [38] | NA | No significant difference in stroke risk among patients with euthyroid or hypothyroidism using or not using thyroxine supplement (p = 0.31; our study) | |||
ACE inhibitors | Reduces radiation-induced normal tissue damage [40] | NA | NA | |||
PPAR-γ agonist | Pioglitazone protects the artery wall against irradiation, with decreased plaque surface and less MMP expression [40] | NA | NA | |||
Pentoxifylline + α-tocopherol | Reduces radiation-induced fibrosis [40] | NA | NA | |||