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Table 2 Summary of studies investigating the effect of different drug classes on radiation-induced vascular complications

From: Hypothyroidism and risks of cerebrovascular complications among patients with head and neck cancer after radiotherapy

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
  1. ACE angiotensin converting enzyme, CI confidence interval, HR hazard ratio, IS ischemic stroke, MMP matrix metalloproteinase, NA not available, PPAR-γ peroxisome proliferator-activated receptor-gamma, TIA transient ischemic attack