DNA and Cellular Damage Observed Following Cardiac CT Scans

July 22, 2015

STANFORD, CA — Low-dose radiation from cardiovascular computed-tomography (CT) angiography results in DNA and cellular damage, as well as increased expression of cells involved in the regulation of cell repair and apoptosis, according to the results of a new study. Most of the cells damaged by the CT angiogram were repaired, but a small percentage of cells died, according to researchers[1].

The results raise the possibility that radiation exposure from CT angiography can cause DNA damage that leads to cellular mutations if these damaged cells are not repaired or eliminated, according to lead investigator Dr Patricia Nguyen (Stanford University, CA) and colleagues. Moreover, the study suggests that cumulative cell death after repeated exposure to radiation from CT could be "problematic."

"It is well known that exposure of cells to therapeutic doses of radiation triggers a complex network of signal transduction pathways that induce changes in gene expression and protein structure, resulting in apoptosis, cell cycle arrest or progression, and DNA repair to minimize the risk of mutagenesis," the researchers explain in the article published online July 22, 2015 in JACC: Cardiovascular Imaging. "Whether radiation doses from medical imaging tests cause similar damage and activate these biological pathways is less certain."

The study included 67 patients undergoing cardiac CT angiography between 2012 and 2013 at two US medical centers. Patients included in the study were recruited with a wide range of radiation-dose exposure to determine the effects of dose on cellular damage. Those exposed to 20 mSv or more typically underwent CT angiography in a traditional scanner with older technology or had a scan performed of their entire aorta. The median radiation dose was 29.8 mSv.

DNA damage, assessed using protein biomarkers, increased 3.39% after radiation exposure. Overall, 70% of patients had a more than 2% increase in the phosphorylation of at least one protein biomarker of DNA damage following CT angiography (phosphorylation of ATM protein kinase was most commonly affected).

Importantly, in patients undergoing coronary angiography using a dual-source scanner where radiation doses were ≤7.5 mSv, there was no evidence of phosphorylation of the protein biomarkers. This finding supports the dose–response relationship between radiation and DNA damage. "Overall, these data are consistent with our hypothesis that higher radiation dose leads to more damage," state Nguyen and colleagues.

In addition to DNA damage, the group also observed a significant increase in cellular apoptosis in 15 of 25 patients with measured levels of apoptotic cell death before and after cardiac CT angiography. The median increase was a more than threefold surge in apoptosis, with at least 60% of patients experiencing a twofold increase. Cell death was highest in patients exposed to 20 mSv or more of radiation and was strongly correlated with the extent of DNA damage. As noted, the majority of damaged cells were repaired.

Regarding changes in biological pathways after radiation, the group reported changes in 39 transcription factors involved in the regulation of apoptosis, cell cycle, and DNA damage, as measured by whole-genome profiling. Researchers also observed significant changes after CT angiography in expression levels of DDB2, XRCC4, and BAX, genes known to play a role in response to DNA damage.

"Although cardiac CT angiography is a valuable clinical tool in the management of patients with cardiovascular disease, awareness among physicians and patients that DNA damage and apoptosis can occur even after diagnostic imaging may encourage greater adherence to dose-reduction strategies and perhaps further research to develop novel agents to protect patients from the potential adverse effects of radiation exposure from cardiac CT angiography," conclude the authors.

The authors reported no relevant financial relationships.


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