Correction: Gadolinium-enhanced cardiac MR exams of human subjects are associated with significant increases in the DNA repair marker 53BP1, but not the damage marker γH2AX.

[This corrects the article DOI: 10.1371/journal.pone.0190890.].

Gadolinium-enhanced cardiac MR exams of human subjects are associated with significant increases in the DNA repair marker 53BP1, but not the damage marker γH2AX.

Magnetic resonance imaging is considered low risk, yet recent studies have raised a concern of potential damage to DNA in peripheral blood leukocytes. This prospective Institutional Review Board-approved study examined potential double-strand DNA damage by analyzing changes in the DNA damage and repair markers γH2AX and 53BP1 in patients who underwent a 1.5 T gadolinium-enhanced cardiac magnetic resonance (MR) exam. Sixty patients were enrolled (median age 55 years, 39 males). Patients with history of malignancy or who were receiving chemotherapy, radiation therapy, or steroids were excluded. MR sequence data were recorded and blood samples obtained immediately before and after MR exposure. An automated immunofluorescence assay quantified γH2AX or 53BP1 foci number in isolated peripheral blood mononuclear cells. Changes in foci number were analyzed using the Wilcoxon signed-rank test. Clinical and MR procedural characteristics were compared between patients who had a >10% increase in γH2AX or 53BP1 foci numbers and patients who did not. The number of γH2AX foci did not significantly change following cardiac MR (median foci per cell pre-MR = 0.11, post-MR = 0.11, p = .90), but the number of 53BP1 foci significantly increased following MR (median foci per cell pre-MR = 0.46, post-MR = 0.54, p = .0140). Clinical and MR characteristics did not differ significantly between patients who had at least a 10% increase in foci per cell and those who did not. We conclude that MR exposure leads to a small (median 25%) increase in 53BP1 foci, however the clinical relevance of this increase is unknown and may be attributable to normal variation instead of MR exposure.

Statins are not associated with short-term improved aneurysm healing in a rabbit model of unruptured aneurysms.

BACKGROUND: Owing to their anti-inflammatory effects and ability to stimulate production of extracellular matrix and chemotactic migration of mesenchymal progenitor cells, statins could potentially improve aneurysm healing after endovascular treatment. OBJECTIVE: To test the hypothesis that systemic administration of simvastatin would improve aneurysm healing in a rabbit model of unruptured intracranial aneurysms. METHODS: Experimental aneurysms were created in female rabbits and were embolized with platinum coils. Six rabbits served as controls and six rabbits received oral administration of simvastatin. Digital subtraction angiography was used to evaluate stability after embolization. Subjects were euthanized 4 weeks after coil embolization. Histologic samples were examined with a grading system (0-12) based on neck and dome features. Aneurysm occlusion data were compared using a Student t test. RESULTS: No significant differences in the mean aneurysm size were found between groups. No coil compaction occurred in either group. All aneurysms in both the statin and control groups showed stable occlusion. There were no significant differences in the histologic grade of occlusion in either group (statin group 2.6±0.8 vs control group 2.7±3.2, p=0.94). CONCLUSIONS: Systemic statin administration after platinum coil embolization of unruptured aneurysms in a rabbit model does not improve aneurysm occlusion rates at 4 weeks.