Early Coronary Artery Calcification Progression over Two Years in Breast Cancer Patients Treated with Radiation Therapy: Association with Cardiac Exposure (BACCARAT Study)

SIMPLE SUMMARY: Radiotherapy for breast cancer can induce radiation-induced coronary artery diseases many years after RT. Long before the onset of clinical signs of these diseases, increase in coronary artery calcium (CAC) score is a good predictor of the risk of coronary disease in patients who may be asymptomatic. In order to improve knowledge for the prevention of radiation-induced coronary artery diseases, our study aimed to evaluate whether there was an association between early CAC increase and cardiac exposure. Based on a population of 101 breast cancer patients with CAC score measured before and 2 years after RT, CAC increase was observed in 28 patients presenting higher cardiac exposure than others. Calcifications were mainly localized in the left anterior descending coronary, the most exposed coronary artery. This study suggests that minimizing cardiac exposure could limit the risk of early CAC increase and therefore the longer-term risk of coronary artery diseases. ABSTRACT: Background: Radiotherapy (RT) for breast cancer (BC) can induce coronary artery disease many years after RT. At an earlier stage, during the first two years after RT, we aimed to evaluate the occurrence of increased coronary artery calcium (CAC) and its association with cardiac exposure. Methods: This prospective study included 101 BC patients treated with RT without chemotherapy. Based on CAC CT scans performed before and two years after RT, the event ‘CAC progression’ was defined by an increase in overall CAC score (CAC RT+ two years—CAC before RT > 0). Dosimetry was evaluated for whole heart, left ventricle (LV), and coronary arteries. Multivariable logistic regression models were used to assess association with doses. Results: Two years after RT, 28 patients presented the event ‘CAC progression’, explained in 93% of cases by a higher CAC score in the left anterior descending coronary (LAD). A dose–response relationship was observed with LV exposure (for Dmean LV: OR = 1.15, p = 0.04). LAD exposure marginally explained increased CAC in the LAD (for D2 LV: OR =1.03, p = 0.07). Conclusion: The risk of early CAC progression may be associated with LV exposure. This progression might primarily be a consequence of CAC increase in the LAD and its exposure.