Objective To retrospectively analyze the clinical effect of 131 I in the treatment of hyperthyroid heart disease.Methods 269 cases who received nuclear medicine 131 I therapy for hyperthyroid heart disease were selected.Clinical laboratory and related examinations,including determination of serum thyroid hormones and antibod-ies (FT3 ,FT4 ,TSH,TRAb,TGAb and TPOAb),biochemical indicators,analysis of blood,electrocardiogram,thyroid ultrasonography,thyroid 131 I uptake rate determination,static imaging and color Doppler ultrasound of the heart were condutced.After diagnosis clear integrated touch technique,thyroid color Super and the thyroid static imaging deter-mine thyroid weight.131 I dose by following formula calculation determine:131 I dose =(each grams thyroid plans vol-ume)×thyroid weight (g)/thyroid 24h or highest 131 I rate (%),each grams thyroid plans volume for 2.96-4.44MBq,calculation 131 I dose,application SPSS 17.0 statistics software for statistics,used paired t test to analyze serum hormone levels of FT3 ,FT4 ,sTSH before treatment,3,6 and 12 months after treatment.Results After 131 I treatment 3,6,12 months,serum FT3 ,FT4 ,sTSH levels significantly declined compared with before treatment (t =36.03,23.88,17.81,45.01,24.85,13.95,49.97,25.66,10.28,all P <0.01).Of 269 patients received 131 I treat-ment,hyperthyroidism cured in 220 cases (81.8%),improved in 42 cases (15.6%),invalid in 7 cases (2.6%);hyperthyroidism heart recovered in 226 cases (84.0%),effective rate was 97.0%(261 /269).Conclusion The treatment of hyperthyroid heart disease as soon as possible is the key to control hyperthyroid,reduced thyroid hormone in the peripheral circulation,131I can be fast and effective treatment of hyperthyroidism,hyperthyroid abnormal ECG and cardiac anomalies symptom relief for time is the ideal treatment of hyperthyroid heart disease recovery as soon as possible,with normal thyroid function,hyperthyroid can return to normal or part of normal.

The glymphatic system plays a pivotal role in maintaining cerebral homeostasis. Chronic cerebral hypoperfusion, arising from small vessel disease or carotid stenosis, results in cerebrometabolic disturbances ultimately manifesting in white matter injury and cognitive dysfunction. However, whether the glymphatic system serves as a potential therapeutic target for white matter injury and cognitive decline during hypoperfusion remains unknown. Here, we established a mouse model of chronic cerebral hypoperfusion via bilateral common carotid artery stenosis. We found that the hypoperfusion model was associated with significant white matter injury and initial cognitive impairment in conjunction with impaired glymphatic system function. The glymphatic dysfunction was associated with altered cerebral perfusion and loss of aquaporin 4 polarization. Treatment of digoxin rescued changes in glymphatic transport, white matter structure, and cognitive function. Suppression of glymphatic functions by treatment with the AQP4 inhibitor TGN-020 abolished this protective effect of digoxin from hypoperfusion injury. Our research yields new insight into the relationship between hemodynamics, glymphatic transport, white matter injury, and cognitive changes after chronic cerebral hypoperfusion.
Animals ; Brain Ischemia ; Carotid Stenosis/drug therapy* ; Cognitive Dysfunction/etiology* ; Digoxin ; Disease Models, Animal ; Mice ; Mice, Inbred C57BL ; White Matter