Association between thyroid cancer and cardiovascular disease risk: a nationwide observational study.

Analysis of the nationally representative cohort showed that thyroid cancer patients had a higher risk of developing CHD than the general population, although the results were not significant for IS and AF. The risk of coronary heart disease was higher in young thyroid cancer patients (< 65 years) and this risk persisted 5 years after cancer diagnosis, whereas the risk was the same in thyroid cancer patients (≥ 65 years) and in the general population.

The results of the present study are in agreement with the findings of a previous study.9 which showed that the risk of coronary heart disease events in patients with thyroid cancer is higher than in the general population. To our knowledge, no study has performed a SIR analysis for CHD risk among different age groups of thyroid cancer patients. A cohort study of 182,419 patients found a higher incidence of coronary heart disease in patients with thyroid cancer without subgroup analysis by age stratification9. A cohort study of 3706 thyroid cancer patients performed a subgroup analysis of CHD risk in cancer patients <40 and ≥40 years of age and a healthy control group. Although a higher incidence of coronary heart disease was observed among patients with thyroid cancer, the odds were higher in the younger group (< 40 años) que en la población de mayor edad (≥ 40 años) durante el seguimiento de 1 a 5 años y de 5 a 10 años. períodos, mientras que no se observó en los > 10-year follow-up12. Another cohort study of 6,900 patients, which performed a subgroup analysis of AF rather than CHD by age, reported that the risk of AF was higher among younger patients than among older patients. The SIR of AF was 2.67 (95% CI 1.61–4.41) in patients <45 years and 1.03 (95% CI 0.75–1.41) in patients ≥75 years10. These findings suggest that there is a higher long-term risk of CHD in younger patients than in older patients. Furthermore, our results showed that the incidence of AF in patients with thyroid cancer was similar to that in the general population, which is consistent with a previously published population-based study.12 and an overall result of the meta-analysis. However, in contrast to our findings, a previous study reported a significantly 1.66-fold increased risk of hospitalization for AF10.11. The discrepancy between the results of the current study and the previous study can be attributed to several factors. First, in our study, 90% of the participants had < 65 años, mientras que en el estudio anterior, un tercio de los pacientes tenían > 60 years. Young patients may better tolerate the effect of subclinical thyrotoxicosis, especially after thyroid-stimulating hormone suppression therapy. Second, the period of inclusion in the study was different in the two cohorts. Our study included patients with thyroid cancer diagnosed after 2011, whereas the previous study included those diagnosed between 1987 and 2013. Decades ago, prevailing guidelines suggested thyroid-stimulating hormone suppression therapy for life for all thyroid cancer patients. However, according to current recommendations, such as the American Thyroid Association guidelines, thyroid-stimulating hormone suppression therapy is not indicated for the treatment of low-risk recurrent thyroid cancer.14. Thus, the lower number of patients with subclinical thyrotoxicosis could have further reduced the incidence of AF in recent years. This suggests that the recent update of recommendations on the prevention of long-term AF during thyroid cancer treatment may have led to inconsistent results between the two studies that had different inclusion periods.

Although the pathophysiological reasons for the increased incidence of CHD in patients with thyroid cancer remain unclear, several factors could contribute to the increased risk. First, during thyroid cancer treatment, such as thyroidectomy, radioactive iodine therapy, and thyroid-stimulating hormone suppression therapy, adverse events of hypothyroidism and hyperthyroidism can develop. These events are implicated in the development of atherosclerosis, which is directly related to ischemic heart disease. For example, studies have reported that subclinical hyperthyroidism could contribute to enlargement of the left ventricle.15.16 and elevated systolic pressure, both of which reduce arterial elasticity and aggravate diastolic dysfunction17. Furthermore, hypercoagulability, a consequence of the prothrombotic effects of subclinical hyperthyroidism, can also lead to the development of atherosclerosis. Second, exposure to slow-release radioactive iodine could induce arterial atherosclerosis for several years. Animal studies have shown that radioactive iodine can cause atherosclerotic-like plaque formation through endothelial proliferation, chronic intimal and medial fibrosis, and occlusive changes in the vasa vasorum.18,19,twenty. Furthermore, intima-media thickness was significantly increased after radioactive iodine ablation in patients with hyperthyroidism, indicating the association of progressive atherosclerosis with radioactive iodine exposure.5. However, the discrepancy in the odds of incidence of CHD and IS in our study, which showed that patients with thyroid cancer had a significantly increased risk of fatal and non-fatal CHD, but a negligible risk of IS, may be attributed to the different etiologies of the disease. two conditions In contrast to the homogeneous pathophysiology of CHD, where atherosclerosis is the main cause of infarction, the etiology of SI is more complex. In addition to atherosclerosis, research has shown that cardioembolism, small-vessel occlusion, nonatherosclerotic vascular disease, hypercoagulable states, and hematologic disorders can lead to SI events.twenty-one. This heterogeneous etiology results in a more complex association between thyroid cancer and IS.

Our results support recent recommendations.14 and have important implications regarding the prevention of cardiotoxicity. From a public health perspective, viewing cancer as a chronic disease with safe long-term treatment rather than a fatal disease requiring aggressive intervention may provide pragmatic benefits to cancer patients. Regarding the pathophysiological reasons for the higher standardized incidence rate of coronary heart disease among patients with thyroid cancer, more evidence should be obtained for the association between radioactive iodine and thyroid-stimulating hormone suppressive therapies and coronary heart disease from additional epidemiological studies.


This study has several limitations. First, the relatively short follow-up period limited our ability to detect cardiovascular events and their association with thyroid cancer. However, the period of inclusion of the thyroid cancer diagnosis allowed for the inclusion of recent recommendations for the management of thyroid cancer, rather than recommendations prevailing decades ago. Second, although we performed a SIR analysis using age and sex stratification, residual confounders such as smoking and history of hypertension, diabetes, and hyperlipidemia might have been present in our study. To address this, we carried out stratified analyzes by SIR subgroups and the percentage of basic characteristics in our inclusion population. Third, there was a lack of sufficient evidence for the absence of waiting time bias in our investigation. Compared with the general population, thyroid cancer patients appear to visit outpatient clinics more frequently for their follow-up care, which could lead to a waiting time bias. However, this potential concern may be diminishing due to the increasingly convenient and affordable health care available in Taiwan, and the fact that similar medical resources are available for both thyroid cancer patients and the general population. Finally, the findings of this study are observational and cannot be used to establish causality; therefore, further investigation is warranted.

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