背景:甲状腺毒性心肌病是甲状腺毒症的一种罕见但严重的并发症,导致急性心力衰竭发作。该病例报告强调了一种罕见的甲状腺毒性心肌病伴低输出量心力衰竭,强调早期诊断和综合管理的重要性。该报告旨在提高临床医生对这种情况的潜在可逆性以及管理此类复杂病例的有效策略的认识。
方法:该患者出现呼吸困难和胸部收缩,没有任何先兆因素。随后,患者在门诊咨询期间突然表现出指示急性心力衰竭的症状。心电图显示快速房颤伴A型预激综合征,而心脏超声检查显示整体心脏增大,射血分数(EF)降低。
方法:经过全面评估,病人被诊断为甲状腺毒性心肌病,急性心力衰竭,和心房颤动伴预激综合征。
方法:立即干预包括利尿剂给药,氧疗,和抗心律失常药,解决急性心力衰竭伴随预激综合征。经过两周的综合治疗措施,病人出院了,开了口服药物的处方,尤其是甲氧咪唑。
结果:干预后,随着心力衰竭症状和呼吸困难的缓解,患者表现出显著的改善,恢复窦性心律,改善左心室射血分数(LVEF从36%提高到45%),和甲状腺功能正常化。这些结果强调了干预策略的有效性,并为类似病例提供了希望的预后。
结论:甲状腺毒症可能导致心力衰竭患者的心肌病,表现为心腔扩张。临床医生应仔细筛查患者的这种可逆情况。诊断需要对各种测试进行全面评估,治疗目标是恢复正常的甲状腺功能。
BACKGROUND: Thyrotoxic cardiomyopathy is a rare but severe complication of
thyrotoxicosis, leading to episodes of acute heart failure. This
case report highlights a rare presentation of thyrotoxic cardiomyopathy with low-output heart failure, emphasizing the importance of early diagnosis and comprehensive management. The report aims to increase awareness among clinicians about the potential reversibility of this condition and the effective strategies for managing such complex cases.
METHODS: This patient presented with dyspnea and chest constriction, without any antecedent predisposing factors. Subsequently, the patient abruptly manifested symptoms indicative of acute heart failure during outpatient consultation. Electrocardiography revealed rapid atrial fibrillation with type A preexcitation syndrome, whereas cardiac ultrasonography demonstrated global cardiac enlargement with a diminished ejection fraction (EF).
METHODS: After a comprehensive evaluation, the patient was diagnosed with thyrotoxic cardiomyopathy, acute heart failure, and atrial fibrillation with preexcitation syndrome.
METHODS: Immediate interventions comprised diuretic administration, oxygen therapy, and antiarrhythmic agents, addressing acute heart failure concomitant with preexcitation syndrome. Following a fortnight of comprehensive therapeutic measures, the patient was discharged with a prescription for oral medications, notably methimazole.
RESULTS: Following the intervention, the patient showed significant improvement with the resolution of heart failure symptoms and dyspnea, restoration of sinus rhythm, improved left ventricular ejection fraction (LVEF improved from 36% to 45%), and normalization of thyroid function. These outcomes underscore the efficacy of the intervention strategy and offer a hopeful prognosis for similar cases.
CONCLUSIONS: Thyrotoxicosis may cause cardiomyopathy in patients with heart failure that manifests as dilated cardiac chambers. Clinicians should carefully screen patients for this reversible condition. Diagnosis requires a comprehensive assessment of various tests, and the therapeutic goal is to restore normal thyroid function.