ReviewFrontiers in cardiovascular medicine2026
Long-term TSH suppression in metabolically unhealthy survivors of differentiated thyroid cancer: a cardiovascular perspective.
Review in Frontiers in cardiovascular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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6 authors.
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Abstract
Differentiated thyroid cancer (DTC) is associated with favorable long-term survival in most patients, shifting clinical priorities from recurrence prevention alone toward survivorship care and competing cardiovascular risk. Thyroid-stimulating hormone (TSH) suppression with levothyroxine remains biologically plausible and clinically important in selected patients with high-risk disease, biochemical incomplete response, or persistent structural disease. However, prolonged exogenous subclinical hyperthyroidism may increase heart rate, atrial arrhythmogenicity, myocardial workload, vascular stress, and cardiovascular vulnerability. This issue is particularly relevant in metabolically unhealthy survivors, including those with obesity, insulin resistance, diabetes, hypertension, dyslipidemia, metabolic syndrome, chronic kidney disease, or established atherosclerotic cardiovascular disease. In these patients, TSH suppression may interact with a pre-existing pro-arrhythmic, pro-inflammatory, and pro-atherogenic substrate, although direct evidence that metabolic phenotype modifies suppression-related cardiovascular risk is currently lacking. This narrative review examines the evolving benefit-harm balance of long-term TSH suppression in DTC survivorship from a cardiovascular perspective. We discuss the oncologic rationale and uncertainty of persistent suppression, cardiovascular liabilities of chronic low TSH exposure, the potential role of cardiometabolic dysfunction as a modifier of treatment tolerance, treatment-related modifiers including radioiodine preparation and multikinase inhibitors, and a hypothesis-generating metabolism-informed framework for TSH target selection. The proposed framework integrates recurrence risk, dynamic response to therapy, cardiometabolic phenotype, cumulative suppression exposure, and cardiovascular reserve, but should be regarded as a hypothesis-generating model that requires prospective validation before it can guide TSH targets.
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