Risk of Ischemic Heart Disease in Women after Radiotherapy for Breast Cancer
ABSTRACT Radiotherapy for breast cancer often involves some incidental exposure of the heart to ionizing radiation. The effect of this exposure on the subsequent risk of ischemic heart disease is uncertain.
We conducted a population-based case-control study of major coronary events (i.e., myocardial infarction, coronary revascularization, or death from ischemic heart disease) in 2168 women who underwent radiotherapy for breast cancer between 1958 and 2001 in Sweden and Denmark; the study included 963 women with major coronary events and 1205 controls. Individual patient information was obtained from hospital records. For each woman, the mean radiation doses to the whole heart and to the left anterior descending coronary artery were estimated from her radiotherapy chart.
The overall average of the mean doses to the whole heart was 4.9 Gy (range, 0.03 to 27.72). Rates of major coronary events increased linearly with the mean dose to the heart by 7.4% per gray (95% confidence interval, 2.9 to 14.5; P<0.001), with no apparent threshold. The increase started within the first 5 years after radiotherapy and continued into the third decade after radiotherapy. The proportional increase in the rate of major coronary events per gray was similar in women with and women without cardiac risk factors at the time of radiotherapy.
Exposure of the heart to ionizing radiation during radiotherapy for breast cancer increases the subsequent rate of ischemic heart disease. The increase is proportional to the mean dose to the heart, begins within a few years after exposure, and continues for at least 20 years. Women with preexisting cardiac risk factors have greater absolute increases in risk from radiotherapy than other women. (Funded by Cancer Research UK and others.).
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ABSTRACT: Atherosclerosis is associated with DNA damage in both circulating and vessel-wall cells and DNA adducts derived from exposure to environmental mutagens are abundant in atherosclerotic vessels. Environmental chemical carcinogens identified as risk factor for atherosclerosis include polycyclic aromatic hydrocarbons (benzo(a)pyrene, dimethylbenz(a)anthracene, beta-naphthoflavone, pyrene, 3-methylcolanthrene), arsenic, cadmium, 1,3-butadiene, cigarette smoke. Accordingly, polymorphisms of genes encoding for phase I/II metabolic reaction and DNA repair are risk factor for cardiovascular diseases, although their role is negligible as compared to other risk factors. The pathogenic relevance of mutation-related molecular damage in atherosclerosis has been demonstrated in experimental animal models involving the exposure to chemical mutagens. The relevance of mutation-related events in worsening atherosclerosis prognosis has been demonstrated in human clinical studies mainly as referred to mitochondrial DNA damage. Atherosclerosis is characterized by the occurrence of high level of oxidative damage in blood vessel resulting from both endogenous and exogenous sources. Mitochondrial damage is a main endogenous source of oxidative stress whose accumulation causes activation of intrinsic apoptosis through BIRC2 inhibition and cell loss contributing to plaque development and instability. Environmental physical mutagens, including ionizing radiation, are a risk factor for atherosclerosis even at the low exposure dose occurring in case of occupational exposure or the high exposure doses occurring during radiotherapy. Conversely, the role of exciting UV radiation in atherosclerosis is still uncertain. This review summarizes the experimental and clinical evidence supporting the pathogenic role of mutation-related pathway in atherosclerosis examining the underlying molecular mechanisms. Copyright © 2015 Elsevier GmbH. All rights reserved.International Journal of Hygiene and Environmental Health 02/2015; 218(3). DOI:10.1016/j.ijheh.2015.01.007 · 3.28 Impact Factor
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ABSTRACT: The demand for breast cancer care has increased as cancer treatment innovations have proliferated. Adjuvant radiotherapy to the breast is considered to be part of the standard treatment in breast cancer. The role of radiotherapy in terms of reducing loco-regional recurrence and increased survival after conservative surgery, and also after a mastectomy in selected cases, has been previously shown in several randomized trials. Patterns of radiotherapy commonly used for breast cancer comprise a period of approximately five weeks, frequently with the addition of an additional 1–1.5 weeks of a radiation boost to the primary tumour area. In last years, there has been a renewed interest in hypofractionated and accelerated radiotherapy schedules that reduce the overall treatment time to barely three weeks, leading to an improvement in quality of life for patients and also optimizing workload of radiation oncology departments. However, despite the existing evidence supporting the use of hypofractionated treatment regimens, their widespread is still far from complete. Many questions have generated resistance among clinical oncologists for their regular use. The aim of this review is to answer those questions that may arise with the use of moderate hypofractionation in breast cancer.Breast (Edinburgh, Scotland) 08/2014; 23(4). DOI:10.1016/j.breast.2014.01.011 · 2.58 Impact Factor
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ABSTRACT: Within the context of radiotherapy our work investigates the feasibility of identifying changes in structural and biomechanical properties of pericardium resulting from exposure to penetrating photon irradiation. Collagen fibres extracted from bovine pericardium were chosen as a model of pericardium extracellular matrix as these form the main fibrous component of the medium. Tests of mechanical properties, controlled by the various structural elements of the tissues, were performed on frontal pericardium, including uni-axial tests and atomic force microscopy (AFM). While the irradiated collagen fibres showed no significant change in D-band spacing up to doses of 80 Gy, the fibre width was found to increase by 34±±9% at 80 Gy when compared with that for un-irradiated samples.Radiation Physics and Chemistry 03/2014; 96:176–180. DOI:10.1016/j.radphyschem.2013.09.017 · 1.19 Impact Factor