Subclinical Carotid Atherosclerosis and Early Vascular Aging From Long-Term Low-Dose Ionizing Radiation Exposure

Andreassi, Maria Grazia; Piccaluga, Emanuela; Gargani, Luna; Sabatino, Laura; Borghini, Andrea; Faita, Francesco; Bruno, Rosa Maria; Padovani, R.; Guagliumi, Giulio; Picaño, Eugenio

doi:10.1016/j.jcin.2014.12.233

Cited by 139 publications

(47 citation statements)

References 32 publications

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“…This is in line with a similar excess risk of cerebrovascular events after RAI among hyperthyroid and euthyroid patients ( 8 ), but in contrast to what others have found in population-based studies of healthy subjects ( 24 ). Further, findings from other studies were reproduced, namely that CIMT and presence of plaque depended on age ( 25 , 26 ), smoking status ( 27 ), whether patients were rendered hypothyroid by treatment ( 28 ), and whether CIMT differed from left to right (left > right) ( 3 ).…”

Section: Discussionmentioning

confidence: 81%

“…Increased risk of cardio- and cerebrovascular events after local radiotherapy of cancer has been described even within the first 0–4 years after exposure ( 2 ). Ionizing radiation has also been reported to increase carotid intima media thickness (CIMT) after low-dose exposure among catheterization laboratory workers ( 3 ). Therefore, all treatments that include radiation of arteries carry the potential to induce atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

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Radioiodine Therapy Does Not Change the Atherosclerotic Burden of the Carotid Arteries

Cour

Andersen

Sørensen

et al. 2016

Thyroid

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Background and aim: Atherosclerosis evolves or accelerates when arteries are exposed to ionizing radiation, both early and late after exposure. Radioiodine therapy of benign thyroid disease exposes the carotid arteries to 4–50 Gy, and may thereby increase the risk of atherosclerosis. Increased risk of cerebrovascular events has been reported after radioiodine therapy. This study aimed to examine whether atherosclerosis develops early or late after radioiodine therapy of benign thyroid disease.Method: Patients treated for benign thyroid disorders (nontoxic goiter, adenoma, and hyperthyroidism) were examined with ultrasound for the main outcome, carotid intima media thickness (CIMT), and for plaque presence (plaque presence only in late damage). Signs of early damage from radioiodine were studied in 39 radioiodine-treated patients, who were examined before treatment and at 1, 3, 6, and 12 months after treatment. Late changes were studied in a cross-sectional case-control design, with radioiodine-treated patients as cases (n = 193) and patients treated with surgery as controls (n = 95). Data were analyzed with repeated measurement for longitudinal data, and with multivariate regression for cross-sectional data. Results were adjusted for age, sex, cholesterol, smoking status, known atherosclerotic disease, and body mass index.Results: No changes in CIMT were found in the patients followed prospectively for one year after treatment with radioactive iodine for benign thyroid disease (p = 0.58). In the study on late effects, there was no difference in CIMT (p = 0.25) or presence of plaques (p = 0.70) between those treated with radioactive iodine and those treated with surgery (9.8 and 5.6 years since treatment, respectively). Furthermore, the level of thyrotropin (TSH) did not influence these atherosclerosis markers.Conclusion: No early changes in CIMT were detected in patients treated with radioactive iodine for benign thyroid disease. No signs of late effects of radioactive iodine on CIMT or plaque presence were found after 10 years of follow-up. The radiation to the carotid arteries by radioactive iodine therapy for benign thyroid disease may therefore have no or low effect on atherosclerotic burden of the carotid arteries in general.

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Section: Discussionmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Radioiodine Therapy Does Not Change the Atherosclerotic Burden of the Carotid Arteries

Cour

Andersen

Sørensen

et al. 2016

Thyroid

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“…Roguin et al [ 18 ] reported that the risk of cancer is increased when physicians who perform interventional procedures are exposed to ionizing radiation for long periods of time. Recent evidence suggests that even protracted low-dose radiation exposure could be associated with leukemia, carotid artery atherosclerosis, and early vascular aging [ 19 20 ].…”

Section: Main Bodymentioning

confidence: 99%

Radiation safety: a focus on lead aprons and thyroid shields in interventional pain management

Cheon

Kim

et al. 2018

Korean J Pain

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C-arm fluoroscopy is useful equipment in interventional pain management because it helps to guide correct needle targeting for the accurate injection and drug delivery. However, due to increased use of C-arm fluoroscopy in various pain procedures, the risk of radiation exposure is a significant concern for pain physicians. The harmful biological effects of ionizing radiation on the human body are well known. It is therefore necessary to strive to reduce radiation exposure. Lead aprons with thyroid shields are the most fundamental radiation protective devices for interventional procedures, and are very effective. However, the operator's radiation safety cannot be guaranteed because pain physicians seem to lack sufficient interest, knowledge, and awareness about radiation safety. Also, inappropriate care and use of radiation protective devices may result in a higher risk of radiation exposure. The purpose of this article was to review the literature on radiation safety with a focus on lead aprons and thyroid shields and present recommendations related to those devices during C-arm fluoroscopic-guided interventions by pain physicians.

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“…In turn, it has been established that there is an association between radiation exposure and indicators of accelerated vascular aging, coronary artery disease and stroke in occupationally exposed groups. Andreassi et al observed that long-term, low level radiation exposure is positively correlated to early atherosclerosis, as identified by increased subclinical cIMT (carotid intima media thickness), and to telomere shortening, an indicator for genomic instability [ 34 ]. This study also concluded that subjects with the Thr241Met polymorphism in the XRCC3 gene (gene coding for X-ray repair cross-complementing protein 3) have a greater susceptibility to radiation-induced vascular effects.…”

Section: Genomic Instability As a Causal Factor In Vascular Aging:mentioning

confidence: 99%

DNA Damage: A Main Determinant of Vascular Aging

Bautista-Niño

Portilla‐Fernandez

Vaughan

et al. 2016

IJMS

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Vascular aging plays a central role in health problems and mortality in older people. Apart from the impact of several classical cardiovascular risk factors on the vasculature, chronological aging remains the single most important determinant of cardiovascular problems. The causative mechanisms by which chronological aging mediates its impact, independently from classical risk factors, remain to be elucidated. In recent years evidence has accumulated that unrepaired DNA damage may play an important role. Observations in animal models and in humans indicate that under conditions during which DNA damage accumulates in an accelerated rate, functional decline of the vasculature takes place in a similar but more rapid or more exaggerated way than occurs in the absence of such conditions. Also epidemiological studies suggest a relationship between DNA maintenance and age-related cardiovascular disease. Accordingly, mouse models of defective DNA repair are means to study the mechanisms involved in biological aging of the vasculature. We here review the evidence of the role of DNA damage in vascular aging, and present mechanisms by which genomic instability interferes with regulation of the vascular tone. In addition, we present potential remedies against vascular aging induced by genomic instability. Central to this review is the role of diverse types of DNA damage (telomeric, non-telomeric and mitochondrial), of cellular changes (apoptosis, senescence, autophagy), mediators of senescence and cell growth (plasminogen activator inhibitor-1 (PAI-1), cyclin-dependent kinase inhibitors, senescence-associated secretory phenotype (SASP)/senescence-messaging secretome (SMS), insulin and insulin-like growth factor 1 (IGF-1) signaling), the adenosine monophosphate-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR)-nuclear factor kappa B (NFκB) axis, reactive oxygen species (ROS) vs. endothelial nitric oxide synthase (eNOS)-cyclic guanosine monophosphate (cGMP) signaling, phosphodiesterase (PDE) 1 and 5, transcription factor NF-E2-related factor-2 (Nrf2), and diet restriction.

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Subclinical Carotid Atherosclerosis and Early Vascular Aging From Long-Term Low-Dose Ionizing Radiation Exposure

Abstract: Long-term radiation exposure in a cath lab may be associated with increased subclinical CIMT and telomere length shortening, suggesting evidence of accelerated vascular aging and early atherosclerosis.

Cited by 139 publications

References 32 publications

Radioiodine Therapy Does Not Change the Atherosclerotic Burden of the Carotid Arteries

Radioiodine Therapy Does Not Change the Atherosclerotic Burden of the Carotid Arteries

Radiation safety: a focus on lead aprons and thyroid shields in interventional pain management

DNA Damage: A Main Determinant of Vascular Aging

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