Acute Decompensated Heart Failure in an Elderly Patient: A Rare Presentation of Toxic Nodular Goiter

Introduction

Toxic nodular goiter (TNG) is a common cause of hyperthyroidism [1], particularly in older adults, but its association with heart failure is rare [2]. Epidemiological studies suggest that TNG is more prevalent in regions with iodine deficiency and that it increases in frequency with advancing age, especially among women. Hyperthyroidism exerts significant effects on the cardiovascular system, including increased heart rate, heightened myocardial contractility, and reduced systemic vascular resistance, which can exacerbate or precipitate heart failure in predisposed individuals. The mechanisms by which TNG leads to hyperthyroidism involve the autonomous functioning of thyroid nodules, resulting in excess hormone production independent of thyroid-stimulating hormone (TSH) regulation. This can significantly impact cardiac function by promoting arrhythmias, increasing myocardial oxygen demand, and causing structural remodeling of the heart.

Although thyroid function evaluation is a standard diagnostic procedure, it is not always included in routine assessments of unexplained heart failure exacerbations, potentially delaying the diagnosis of conditions like TNG. The rarity of TNG-induced cardiac complications underscores the need for heightened clinical vigilance, as these cases may highlight gaps in current diagnostic guidelines or common clinical oversights.

This case report highlights an 87-year-old woman with preexisting heart failure who experienced significant worsening of her condition due to TNG. It underscores the importance of thorough thyroid function evaluation in patients with unexplained exacerbation of heart failure, particularly in the elderly, to ensure timely diagnosis and management. Furthermore, by presenting this case, we aim to emphasize the broader clinical implications of TNG-induced heart failure and advocate for its consideration in similar clinical scenarios.

Case Report

We present the case of an 87-year-old woman, measuring 152 cm in height and weighing 73 kg, with a history of heart failure with preserved ejection fraction, atrial fibrillation, stage 4 chronic kidney disease, type 2 diabetes mellitus, and multinodular goiter. Her largest thyroid nodule measured 4 cm, and thyroid function tests conducted 6 months earlier were normal (Free T4: 1.37 ng/dL, TSH: 0.8 μIU/mL). She also did not report any symptoms of hyperthyroidism, such as palpitations, weight loss, heat intolerance, or tremors at that time. These observations suggested no evidence of active hyperthyroidism and no need for anti-thyroid medication. Her chronic heart failure was managed with spironolactone 25 mg and dapagliflozin 10 mg once daily to address fluid retention, along with bisoprolol 1.25 mg and ivabradine 5 mg twice daily for heart rate control. However, despite strict adherence to her heart failure treatment regimen, she experienced progressively worsening exertional dyspnea over the past week, necessitating further evaluation.

She presented with significant pitting edema and dyspnea during activities such as dressing and bathing, which improved with rest for 1 week. Upon admission, she was conscious with vital signs showing temperature 36.0°C, heart rate 83 beats per minute, blood pressure 129/76 mmHg, respiratory rate 19 breaths per minute, and oxygen saturation of 98% on 2 L/min nasal oxygen. Physical examination revealed irregular heartbeats, crackles over the bilateral lower lung field, significant bilateral pitting edema, and a visible neck mass. The echocardiogram revealed preserved left ventricular ejection fraction (57.9%) without chamber dilation or regional wall motion abnormalities. Additional findings included increased wall thickness, mild aortic and mitral regurgitation, moderate-to-severe tricuspid regurgitation, and no evidence of pericardial effusion or thrombus.

Laboratory investigations revealed a marked increase in NT-proBNP levels (6126 pg/mL compared to 2882 pg/mL 2 weeks earlier), indicative of worsened heart failure, alongside evidence of pulmonary edema on chest X-ray and atrial fibrillation confirmed by electrocardiogram. Notably, neither leukocytosis nor anemia was observed, and both sputum and pleural effusion cultures returned negative results, ruling out infection. Consequently, acute decompensated heart failure was diagnosed. Given the visible neck mass and unexplained worsening of heart failure symptoms, thyroid function tests were conducted. Elevated free T4 (3.77 ng/dL) and suppressed TSH (<0.01 μIU/mL) indicated new-onset hyperthyroidism, contrasting with normal thyroid function noted 6 months earlier. A Tc-99m thyroid scan demonstrated heterogeneous uptake, with higher uptake in the central portion of the thyroid gland, confirming the diagnosis of toxic multinodular goiter (Figure 1).

Importantly, repeat ultrasound confirmed that the 4-cm nodule had not increased in size compared with the previous examination 6 months prior, suggesting that linear growth was not a factor. Nonetheless, the patient did report mild compressive symptoms such as neck fullness and occasional difficulty swallowing. Fine needle aspiration of the nodule showed a benign lesion, ruling out malignancy. These findings support that the nodule’s transformation into a hyperfunctioning lesion likely stemmed from functional rather than structural changes.

The patient was started on carbimazole 10 mg once daily in addition to her heart failure therapy. Carbimazole was chosen over other antithyroid medications due to its long-term efficacy and favorable adherence profile in elderly patients. During hospitalization, her symptoms improved significantly, and her heart failure management was adjusted to account for the metabolic effects of hyperthyroidism, including careful monitoring of fluid status and rate control to maintain cardiovascular stability. One month later, follow-up revealed stabilized thyroid function. The long-term management plan included continued carbimazole therapy to sustain euthyroid status and regular cardiac and thyroid function monitoring to prevent further exacerbations. This case underscores the necessity of thyroid function testing in elderly patients presenting with unexplained worsening of heart failure symptoms, as well as the challenges in balancing heart failure and hyperthyroidism treatment in such complex clinical scenarios.

Discussion

TNG typically presents with more subtle symptoms compared with Graves’ disease [3]. It is characterized by heterogeneous thyroid enlargement and the presence of autonomously hyperfunctioning thyroid nodules, leading to a persistent hyperthyroid state in the absence of thyroid autoimmunity [4]. Advancing age, lower iodine intake, and prior radiation exposure are recognized risk factors for TNG. It is more commonly observed in women than in men [1,5]. Compared with previous cases reported in the literature [6], our case highlights the unique presentation of TNG-induced cardiac complications in the elderly, emphasizing the necessity of recognizing TNG as a potential exacerbating factor in heart failure. Unlike other studies that primarily associate TNG with mild hyperthyroid symptoms [7,8], our case underscores the condition’s significant impact on cardiovascular health, contributing to the growing body of evidence linking TNG to acute cardiac events.

While the standard diagnosis of TNG involves clinical evaluation, laboratory testing, and imaging studies [8], our case presented unique challenges that deviated from typical presentations. Notably, the patient initially had normal thyroid function and no hyperthyroid symptoms, complicating the diagnostic process. The confirmation of TNG through elevated free T4, suppressed TSH, and a Tc-99m thyroid scan underscores the necessity of integrating thyroid evaluation into unexplained heart failure workups.

In this particular case, the nodule’s size remained stable over 6 months, yet it transitioned from a non-functioning state to an autonomously functioning lesion. Potential reasons for this functional change include intrinsic alterations such as TSH receptor or G-protein mutations within the thyroid tissue, an age-related decline in regulatory mechanisms, or other local microenvironmental factors within the thyroid gland. While compressive symptoms were present due to the nodule’s size, there was no evidence of malignant transformation on fine needle aspiration. Therefore, the most plausible explanation is that the nodule gradually acquired autonomy over time – a phenomenon that can occur in longstanding multi-nodular goiters, especially in the elderly.

Additionally, while her pre-existing atrial fibrillation could contribute to her symptoms, the new diagnosis of hyperthyroidism likely exacerbated her cardiovascular condition [9]. This conclusion is supported by the significant clinical improvement observed after initiating antithyroid therapy with carbimazole in addition to her optimized heart failure treatment. The disproportionate worsening of her symptoms compared with her previous atrial fibrillation-related baseline also pointed towards hyperthyroidism as a critical contributing factor [10,11].

Cardiac complications associated with TNG are less frequently documented than those associated with Graves’ disease [12]. Previous reports, such as a case involving a 48-year-old woman with dilated cardiomyopathy secondary to TNG, highlight its potential impact on cardiac function [13]. Although limited research has explored the prevalence of TNG in elderly patients with heart failure, a study indicated that cardiothyreosis was observed in 6.5% of patients hospitalized for overt hyperthyroidism. The risk factors for developing cardiothyreosis included age over 50 years and multinodular toxic goiter as the underlying cause of hyperthyroidism [14].

Autoimmunity is not involved in the development of TNG. Consequently, definitive treatment options such as thyroidectomy and radioiodine therapy are regarded as suitable approaches for managing TNG. However, the 2016 American Thyroid Association guidelines recommend that for elderly patients with comorbidities that increase surgical risk or shorten life expectancy, as well as for those who are not ideal candidates for ablative therapy, antithyroid medication may be a more suitable treatment option [15]. Also, a recent study indicated that prolonged low-dose methimazole therapy, administered over 60 to 100 months, is a safe and effective approach for managing TNG and is not inferior to radioiodine therapy [7]. Thus, we chose antithyroid medication with carbimazole instead of radioiodine for both short- and long-term control of hyperthyroidism in this case, after considering our patient’s old age and medical comorbidities.

Conclusions

TNG was diagnosed in this case through elevated thyroid function tests, ultrasound imaging, and Tc-99m thyroid scan findings, which confirmed its role in acute decompensated heart failure. Key diagnostic markers included elevated free T4 and suppressed TSH, alongside imaging that revealed autonomously functioning nodules. Following treatment with carbimazole and optimized heart failure therapy, the patient demonstrated significant clinical improvement. This case underscores the critical importance of considering TNG in the differential diagnosis of acute decompensated heart failure in elderly patients, particularly those with thyroid abnormalities. Early recognition and intervention, as evidenced by the patient’s positive treatment response, can significantly improve outcomes. Furthermore, stability in nodule size, benign cytology findings, and mild compressive symptoms over the prior 6 months highlight that functional changes in multinodular goiter can occur without overt structural progression. Future research should focus on understanding the prevalence of TNG in similar populations and developing diagnostic protocols that integrate thyroid function testing into the evaluation of unexplained heart failure.