Radiation therapy (RT) has contributed to significant improvements with respect to the survival times
in many cancers, including Hodgkin"s Lymphoma (HL), breast cancer, lung cancer, and other thoracic
region tumors. In addition, the advances of anti-cancer therapies result in greater numbers of long-term
survivors after thoracic irradiation as well. Therefore, it has become more important to understand the
long-term complications of RT. Radiation-induced cardiovascular complications (RICC) have become
an increasingly recognized side effect of RT, which can cause non-malignant death in patients particularly
suffering from HL and breast cancer. The spectrum of RICC is broad, potentially involving any
component of the heart, including pericardium, myocardium, heart valves, coronary arteries, capillaries,
and conducting system that underwent RT, most often occurring decades after the treatment.
Numerous studies of RICC show that the injury of endothelial cells is the key point in most tissues that
ultimately leads to fibrosis or necrosis. Ionizing radiation directly modifies DNA, including single- and
double-strand breaks on a molecular level. Indirectly ionizing radiation also produces reactive oxygen
species, which can lead cellular stress and death. Radiation directly affects the vasculature by causing
endothelial cell apoptosis and senescence and by changing aspects of normal vascular homeostasis. The
mechanism of RICC has not been clearly defined yet. A better understanding of the biological mechanisms
of RICC is very important to clarify the exact pathogenesis of this important disease spectrum,
and it will also provide to develop novel treatment strategies.
Keywords: Cardiotoxicity; cardiovascular complications; inflammation; radiation therapy; radiation-induced heart disease
