Thyroid Hormones, Brain, and Heart

Cerebrovascular disorders (CVDs) remain the leading cause of morbidity and mortality worldwide. Neuropsychiatric symptoms (such as depression and fatigue) and cognitive impairment are common complications in CVD patients which are associated with worse patient-centered health status, adverse clinical outcomes, and worse CVD prognosis. Impairment of normal functioning of the hypothalamic–pituitary–thyroid (HPT) axis (as in the low triiodothyronine syndrome) is also commonly observed in patients with CVDs and is linked to greater neuropsychiatric symptom severity, cognitive impairment, worse quality of life, and shorter survival. However, there are no studies examining whether treatment of subclinical HPT axis dysfunction can improve patient-centered health status of CVD patients. Further studies should attempt to elucidate if treatment of subclinical thyroid dysfunction could improve neuropsychiatric and cognitive symptom severity of CVD survivors and possibly translate into better patient-centered outcomes and longer survival. Evaluation of possible association between genetic polymorphisms of enzymes involved in thyroid hormone transport and metabolism with patient-centered health status could help to more accurately identify high-risk CVD patients and provide with personalized treatment approaches.