Cardiac dysfunction in cancer survivors after thoracic irradiation: A necessary evil?
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Beverly B. and Daniel C. Arnold Distinguished Chair, Weill Cornell Medicine, Houston Methodist DeBakey Heart & Vascular Center, Houston Methodist Hospital, Houston, TX
Received Aug 4, 2020; accepted Aug 4, 2020 doi:10.1007/s12350-020-02348-1
See related article, https://doi.org/10.10 07/s12350-020-02255-5. It is well established that a wide range of cardiovascular complications could occur from radiation therapy for thoracic malignancies, such as breast cancer, Hodgkin’s lymphoma and non-small cell lung cancer. It is estimated that up to 60% of Hodgkin’s lymphoma survivors develop radiation therapy (RT)-induced coronary artery disease (CAD), whereas breast cancer survivors receiving RT experience higher odds of vascular death and a high likelihood of developing CAD particularly when subjected to left sided chest radiation (Table 1).1–3 While the risk of developing RT-related CAD is not disputed in patients with thoracic malignancies, there is a considerable temporal delay between radiation exposure and development of symptomatic disease making the detection of this phenomenon quite challenging. The risk of developing CAD is higher in patients subjected to RT at a younger age and also in patients with pre-existing traditional risk factors for atherosclerosis. Additionally, there appears to be a linear increase in risk with higher doses of RT as demonstrated in breast cancer patients, whereas one study found that for every 1 Gy (Gray) increase in mean heart dose a resultant 7.4% increase in major coronary events occurred.4 Similarly, a pooled analysis from dose-escalation studies in non-
Reprint requests: Mouaz H. Al-Mallah, MD, MSc, Beverly B. and Daniel C. Arnold Distinguished Chair, Weill Cornell Medicine, Houston Methodist DeBakey Heart & Vascular Center, Houston Methodist Hospital, 6550 Fannin Street, Smith-18, Houston, TX 77030; [email protected] J Nucl Cardiol 1071-3581/$34.00 Copyright Ó 2020 American Society of Nuclear Cardiology.
small cell lung cancer showed higher cardiovascular event rates in patients receiving higher radiation doses to the chest.5 Despite the development of image-guided radiotherapy and three-dimensional dosimetry which reduce the cardiac radiation doses delivered during therapy, the risk of RT-related CAD remains a concern for cancer survivors.6 The pathophysiology of radiation-related CAD is complex and has been hypothesized in several prior studies. At the ultrastructural level, the irradiated vasculature observes increased pro-inflammatory cytokines including interleukin-6, C-reactive protein, interferon gamma, and tumor necrosis factor-alpha, leading to a pro-thrombotic state and sustained inflammation.7,8 The alteration in vascular hemostasis with the loss of endothelium-derived vasodilators along with increased pro-thrombotic factors results in increased microvascular fibrosis, reduced vascular reserve, and myocardial ischemia.9 At the macrovascular level, radiotherapy results in direct myocardial and endothelial injury resulting in collagen deposition in the capillary lumen,
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