RadiationâInduced Cardiovascular Disease: Review of an Underrecognized Pathology
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It's Friday evening and time for another article from the "Radiation Induced xxxxx" series.
RadiationâInduced Cardiovascular Disease: Review of an Underrecognized Pathology
Background/relevance:
SARS-CoV-2 spike promotes inflammation and apoptosis through autophagy by ROS-suppressed PI3K/AKT/mTOR signaling (2021)
Mechanistically, SCV-2-S inhibited the PI3K/AKT/mTOR pathway by upregulating intracellular reactive oxygen species (ROS) levels, thus promoting the autophagic response.
https://pubmed.ncbi.nlm.nih.gov/34461258
Key excerpts.
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An increasing number of cancer survivors are seen with premature heart disease despite having no significant cardiovascular risk factors, often decades after completion of radiation treatments. The first data obtained regarding the effects of radiation on the cardiovascular system stem from the survivors of the Hiroshima and Nagasaki atomic bombings, which showed that nearly 10% of the observed group died of heart disease.2 Nowadays, among survivors of cancer, an increase of 1.7â to 2âfold in cardiovascular death is seen in patients who have undergone radiotherapy. An increase of 7.2âfold in cardiovascular death has been demonstrated in patients having received former radiation techniques before the 1970s.3 These patients present a therapeutic challenge as there is a paucity of data regarding the specific considerations in their management. In this article, we review the most important clinical effects of radiation therapy on the cardiovascular system, with a focus on recent data regarding its treatment.
Radiationâassociated cardiotoxicity appears to be delayedâtypically 10 to 30 years following treatment. In patients with prior Hodgkinâs lymphoma having undergone radiation therapy, the median time from diagnosis of malignancy to cardiac complications was 19 years
Pathophysiology
Many potential mechanisms have been hypothesized to explain the development of radiationâinduced coronary disease. Radiation leads to the formation of free radicals, which can cause molecular damage. Tissue malfunction ultimately occurs when the cellâs ability to repair itself is overwhelmed.14 Radiation initially causes an endothelial injury in the coronaries that leads to a proinflammatory state, which eventually damages blood vessels via oxidative stress, generation of reactive oxygen species, and cytokine release that disrupts DNA strands integrity.15 This inflammatory cascade leads to ruptured vessel walls, platelet aggregation, thrombosis, and replacement of the damaged coronary intima cells by myofibroblasts (Figure 1),16, 17 These changes ultimately accelerate vessel stenosis and atherosclerosis development, leading to CAD in unusually young patients.
Full paper: