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Etiologies of coronary artery disease in cancer patients. [Review of CAD induced by cardiac metastases, radiotherapy, and chemotherapy]

Journal Article · · Int. J. Radiat. Oncol., Biol. Phys.; (United States)
The growing number of patient reports of angina and myocardial infarction during cancer management prompted this review of coronary artery disease (CAD) in cancer patients. There is no definite evidence that cancer per se nor any particular tumor type predisposes to coronary atherosclerosis. Cardiac metastases can cause CAD via tumor emboli, extrinsic compression, or ostial obstruction; in these patients the diagnosis of CAD as a result of cardiac metastases often is not made until death. The course of these patients usually is fulminant. Tumor-associated coagulation disorders and non-bacterial thrombotic endocarditis can cause coronary thromboemboli; treatment should be initiated early as these patients often are not in a terminal state when such CAD develops. Post-radiation CAD seen in experimental animals (via fibrosis and/or accelerated atherogenesis) can be extrapolated to the clinical situation. This is best evidenced by 10 young patients, with minimal coronary risk factors in most, who developed angina and/or myocardial infarction 2 to 100 months after chest radiotherapy; approximate mediastinal doses ranged from 1440 Roentgen to 5075 rad. In 5 patients there was no significant atherosclerosis beyond the radiation portals; 2 had successful saphenous vein bypass grafts. Lipid-lowering therapy may prevent post-radiotherapy atherogenesis in high risk individuals. Chemotherapy (acting directly or synergistically with radiotherapy) has caused angina and myocardial infarction within hours to days after the infusion of agents both classically cardiotoxic as well as others, although the exact mechanism(s) for coronary artery damage as a result of chemotherapy presently is unknown.
OSTI ID:
6858562
Journal Information:
Int. J. Radiat. Oncol., Biol. Phys.; (United States), Journal Name: Int. J. Radiat. Oncol., Biol. Phys.; (United States) Vol. 4:9/10; ISSN IOBPD
Country of Publication:
United States
Language:
English