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Endocrine Abstracts (2024) 100 P12 | DOI: 10.1530/endoabs.100.P12

1Royal Blackburn Hospital, Blackburn, United Kingdom; 2NHS Greater Glasgow and Clyde, Glasgow, United Kingdom


Introduction: Thyrotoxicosis, characterized by excessive production of thyroid hormones, can precipitate a spectrum of cardiovascular complications, including heart failure and valvulopathy. This case study highlights a case where effective management of thyrotoxicosis precipitated the reversal of heart failure and valvulopathy.

Case Presentation: A 44-year-old woman presented at the emergency department with complaints of dyspnea, palpitations, and fatigue. She reported a recent history of weight loss, heat intolerance, and tremors. Physical examination unveiled signs of perspiration, tachycardia, and a distinct systolic murmur audible at the apex. Furthermore, bilateral lower limb edema was noted.

Investigations: Thyroid function tests indicated markedly elevated levels of serum free thyroxine (T4) and triiodothyronine (T3), and suppressed thyroid-stimulating hormone (TSH) in conjunction with positive TRAB levels confirming a diagnosis of Graves’ disease. Echocardiography revealed biventr icular failure with reduced ejection fraction, accompanied by moderate mitral and tricuspid regurgitation, and mild pulmonary regurgitation, suggestive of valvulopathy secondary to thyrotoxicosis. Atrial fibrillation was detected by ECG.

Results and Treatment: Treatment initiation involved the administration of antithyroid medications (Carbimazole) and beta-blockers to address Atrial fibrillation. Additionally, standard heart failure therapy, including diuretics, was instituted. Regular monitoring of thyroid function and echocardiography ensued to evaluate treatment efficacy.

Outcome: With aggressive management directed at thyrotoxicosis, the patient’s symptoms exhibited gradual amelioration. Subsequent echocardiography displayed notable enhancement in ventricular function, with ejection fraction restoration to normal levels and resolution of pulmonary, mitral and tricuspid regurgitation. Consequently, manifestations of heart failure resolved, precluding the necessity for diuretic therapy. Subsequent ECGs confirmed the resolution of atrial fibrillation.

Discussion: This case underscores the intricate nexus between thyroid dysfunction and cardiovascular sequelae, underscoring the imperative of promptly identifying and managing thyrotoxicosis in individuals concurrently presenting with heart failure and valvulopathy. Effective management of thyrotoxicosis holds the potential for reversing cardiac abnormalities and ameliorating symptoms.

Conclusion: In conclusion, this case serves as a testament to the successful management of heart failure and valvulopathy secondary to thyrotoxicosis through timely recognition and intervention targeting thyroid dysfunction. It accentuates the potential for holistic cardiac recovery with judicious medical intervention, advocating for a collaborative, multidisciplinary approach in addressing such clinical scenarios. Early recognition and management of thyrotoxicosis emerge as pivotal in mitigating cardiovascular complications in patients with heart failure and valvular abnormalities.

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