Leila Najd-Hassan-Bonab, Maryam Moazzam-Jazi, Raziyeh Abooshahab, Shabnam Heydarzadeh, Maryam S Daneshpour, Mehdi Hedayati
Serial thoracic CT imaging demonstrated a statistically significant but small, progressive increase in mPA diameter during bevacizumab-based chemotherapy in this selected cohort. The change remained within the normal range, no patient crossed the threshold for probable pulmonary hypertension, and no association with OS was observed. In the absence of a non-bevacizumab comparator and of hemodynamic correlation, these changes cannot be attributed to bevacizumab; whether they carry clinical significance requires prospective validation with hemodynamic and echocardiographic correlation.
The global incidence of thyroid cancer (TC), particularly differentiated thyroid cancer (DTC), has increased substantially over recent decades, while cardiovascular disease (CVD) remains the leading cause of death globally. As advances in diagnosis and treatment have significantly improved long-term survival in thyroid cancer patients, attention has increasingly shifted toward non-cancer complications, especially cardiovascular morbidity and mortality. Current evidence indicates that TC survivors have a higher risk of atrial fibrillation (AF), coronary artery disease (CAD), stroke, heart failure, and other cardiovascular complications than the general population. This association appears to result from a complex interaction between shared cardiometabolic risk factors and biological pathways. Obesity, metabolic syndrome, diabetes, hypertension, and dyslipidemia promote chronic inflammation, endothelial dysfunction, and insulin/IGF signaling, which contribute to atherosclerosis and tumor progression. Thyroid hormone dysregulation provides an additional link between thyroid cancer management and cardiovascular risk. Long-term thyroid-stimulating hormone (TSH) suppression therapy may induce subclinical hyperthyroidism and increase susceptibility to atrial fibrillation, ischemic heart disease, cardiac remodeling, and vascular dysfunction. Treatment-related factors, including thyroidectomy, radioactive iodine therapy, and targeted therapies, may also contribute to cardiovascular toxicity and influence long-term cardiovascular outcomes. Importantly, cardiovascular risk is heterogeneous among thyroid cancer survivors and may vary according to thyroid cancer risk category and current disease status, the intensity and duration of TSH suppression, radioactive iodine exposure, and patient-level characteristics such as age, sex, and baseline cardiovascular risk. This review synthesizes epidemiological and mechanistic evidence linking TC and CVD, with particular emphasis on shared metabolic and inflammatory pathways, hormonal and treatment-related factors, and changes in cardiovascular risk across different phases of thyroid cancer survivorship. Recognizing these determinants may support individualized cardiovascular risk assessment and help balance the oncologic benefits of thyroid cancer treatment against its potential long-term cardiovascular consequences.