Acromegaly-induced dilated cardiomyopathy presenting with heart failure as the cardinal symptom: A case report

Abstract

Acromegaly is a rare endocrine disorder caused by excessive secretion of growth hormone, resulting in elevated serum levels of hepatic insulin-like growth factor-1 (IGF-1). With an estimated annual incidence of approximately three cases per million individuals, the condition is associated with a significantly increased risk of cardiovascular complications, such as arrhythmias and acromegaly-induced cardiomyopathy. Heart failure secondary to acromegalic cardiomyopathy occurs in approximately 3% of affected patients and is recognized as the leading cause of mortality in individuals with this condition. This case report describes a 53-year-old male diagnosed with acromegalic cardiomyopathy caused by a pituitary adenoma.

Introduction

Acromegaly is a chronic endocrine disorder with an insidious onset, characterized by excessive secretion of growth hormone (GH), which subsequently elevates insulin-like growth factor-1 (IGF-1) levels. This condition leads to progressive somatic deformities, predominantly affecting the face and limbs, as well as multi-system complications. ¹ In the vast majority of cases (>95%), this excessive GH secretion is attributable to a GH-secreting pituitary adenoma. ² The incidence of acromegaly ranges from 30 to 70 cases per million people, with an annual incidence of 3 to 8 new cases per million people. ³ The complications of acromegaly involve multiple systems, including the cardiovascular, respiratory and metabolic comorbidities.^1,4 Notably, cardiovascular disorders are the most prevalent complications, impacting over 50% of patients with acromegaly. ⁵ These include hypertension, arrhythmias, and acromegalic cardiomyopathy, which are also major contributors to mortality but are frequently underdiagnosed or misdiagnosed. ⁶ Consequently, early identification and effective management of cardiovascular complications are crucial for improving patient prognosis and quality of life. ⁷

Acromegalic cardiomyopathy refers to a myocardial structural and functional abnormality resulting from prolonged exposure to elevated GH and IGF-1 levels in the absence of other contributing risk factors. ⁸ Pathological features include progressive myocardial cell hypertrophy, interstitial fibrosis, and diastolic dysfunction, which may eventually progress to biventricular hypertrophy and impaired systolic function. ⁹ Notably, the early stages of this myocardial damage are often subtle, manifesting as mild dyspnea and fatigue, and are therefore frequently overlooked. However, without timely intervention, approximately 20%–30% of patients may progress to irreversible heart failure. ⁶ To date, treatment strategies for this condition remain controversial. While some studies suggest that cardiac remodeling may improve following normalization of GH and IGF-1 levels, ¹⁰ the prognosis for advanced-stage cases remains generally unfavorable.

We present a case of a patient with acromegaly in whom heart failure was the initial clinical manifestation. The diagnosis of acromegalic cardiomyopathy was established based on findings from echocardiography, cardiac magnetic resonance (CMR), and additional investigations. Following multidisciplinary deliberation involving cardiology, endocrinology, and neurosurgery, it was determined that surgical resection of the pituitary adenoma was essential. Postoperatively, the patient’s GH and IGF-1 levels decreased significantly.

Case presentation

In May 2025, a 53-year-old male patient presented to the clinic with complaints of chest tightness, exertional dyspnea, and productive cough lasting over 1 month. The patient had undergone hernia repair surgery in 2014. Notably, he did not have a history of smoking or excessive alcohol consumption. On admission, the patient’s vital signs were stable: temperature 36.9°C, blood pressure 136/89 mmHg, heart rate 88 beats per min, and respiratory rate 21 breaths per min. Physical examination revealed acromegalic features, including enlarged hands and feet, coarse facial features, prominent superciliary arches, and enlargement of the nose and forehead (Figure 1). Cardiac examination demonstrated an enlarged cardiac silhouette with regular rhythm and no pathological murmurs in the valve areas. Jugular venous distention was absent, and there was no evidence of lower extremity edema. Pulmonary examination showed no adventitious sounds, such as moist rales.

Figure 1.

Physical examination findings (a) Coarse facial features, prominent superciliary arches, and enlargement of the nose and forehead (b) Comparison of the patient’s hands with those of a normal adult male.

Laboratory investigations revealed markedly elevated levels of brain natriuretic peptide (BNP) at 623 pg/mL, glycated hemoglobin (HbA1c) at 7.9%, and alanine aminotransferase at 61 U/L. Blood gas analysis indicated a reduced partial pressure of oxygen at 61.9 mmHg. A comprehensive lipid profile demonstrated elevated triglyceride levels at 2.25 mmol/L. Fasting growth hormone (GH) level was significantly increased at 3.520 ng/mL (reference range: 0.003–0.971 ng/mL), and IGF-1 level was substantially elevated at 621.57 ug/L (reference range: 76.44–244.1 ug/L). Oral glucose tolerance test results showed fasting glucose at 7.58 mmol/L and 2-h postprandial glucose at 14.30 mmol/L. Routine blood tests, myocardial enzymes, coagulation function, renal function, thyroid function, IGF binding protein, and markers for infectious diseases showed no significant abnormalities. Pulmonary function tests revealed a decrease in mid-to-late expiratory flow rate, mild reduction in maximum minute ventilation, and a negative bronchodilator test. Polysomnography confirmed severe obstructive sleep apnea-hypopnea syndrome. A 12-lead electrocardiogram (ECG) performed upon admission demonstrated sinus rhythm with ST-segment depression and T-wave inversion (Figure 2). Ambulatory ECG monitoring revealed occasional monomorphic premature ventricular contractions, with a total burden of 227 beats over a 24-h period. No sustained or non-sustained ventricular tachycardia was observed.

Figure 2.

ECG on admission.

Transthoracic echocardiography (Figure 3) revealed left heart enlargement, aortic root dilation, moderate mitral regurgitation, the interventricular septum and left ventricular posterior wall exhibit normal thickness, accompanied by a diffuse reduction in wall motion amplitude, and reduced left ventricular systolic function with an EF value of 24%. Upon detailed inquiry by the attending physician, the patient’s wife reported a notable observation: the patient’s hands and feet had progressively enlarged over time, rendering his previous footwear too small. Given the clinical suspicion of acromegaly, a pituitary magnetic resonance imaging (MRI) scan was ordered, which identified a pituitary tumor measuring 15 mm × 13 mm × 6 mm (Figure 4). Consequently, the diagnosis included acromegaly complicated by heart failure with reduced ejection fraction (HFrEF), commonly referred to as acromegalic cardiomyopathy. Subsequent CMR confirmed the diagnosis: left ventricular enlargement, markedly diminished wall motion of the left ventricle, predominantly affecting the interventricular septum, the thickness of the middle segment of the interventricular septum is about 10–12 mm, and the thickness of the lateral wall is about 6.6 mm, along with patchy delayed enhancement in the apical segment of the inferior left ventricular wall on late gadolinium enhancement imaging (Figure 5).

Figure 3.

Echocardiograms on admission (a) Parasternal long-axis view showing a LVDd of 71 mm (b) Parasternal long-axis view showing a LAD of 45 mm (c) M-mode echocardiography showing an ejection fraction of 24%.

Figure 4.

MRI for pituitary adenoma.

Figure 5.

CMR images showing the presence of LGE in the apical segment of the left ventricular (arrow).

The globally recognized primary treatment for pituitary adenoma is surgical resection. However, considering the patient’s significantly compromised left ventricular function and untreated severe sleep apnea, surgery was deemed to pose a substantial risk. Therefore, in alignment with current guidelines, ¹¹ we implemented a meticulous management strategy for heart failure through the administration of diuretics, sodium-glucose cotransporter 2 inhibitors, angiotensin receptor-neprilysin inhibitors, β-blockers, and spironolactone. Collaborative consultations were conducted with the Endocrinology and Neurosurgery departments. Ultimately, Neurosurgery agreed to proceed with transsphenoidal resection of the pituitary adenoma. Four days after surgery, the repeat GH level was 0.47 ng/mL and IGF-1 level was 240.00 ng/mL. Three months after surgery, a follow-up transthoracic echocardiogram demonstrated a reduction in left cardiac chamber dimensions and an improvement in left ventricular systolic function, with the EF increasing to 42% (Figure 6).

Figure 6.

Follow-up echocardiograms 3 months after surgery (a) Parasternal long-axis view showing a LVDd of 56 mm (b) Parasternal long-axis view showing a LAD of 38 mm (c) M-mode echocardiography showing an ejection fraction of 42%.

A structured, multidisciplinary follow-up plan will be implemented for this patient to comprehensively manage the primary endocrine disorder and its associated cardiovascular complications. The plan is organized into three distinct phases. Short-term follow-up (every 3–6 months) will focus on monitoring response to heart failure management and endocrine control. Cardiovascular assessment will include clinical evaluation of symptoms, measurement of NT-proBNP levels, and echocardiography to monitor LVEF, ventricular structure, and diastolic function. Endocrine evaluation will involve assessment of serum IGF-1 and random GH levels to evaluate biochemical control following interventions such as surgery or medical therapy. Medium-term assessment (6–12 months post-treatment) may include repeat CMR imaging, which is considered the gold standard for evaluating myocardial fibrosis and extracellular volume remodeling. Early CMR establishes a baseline, while imaging performed approximately 1 year after treatment enables a more objective assessment of the potential reversibility of myocardial abnormalities. Long-term follow-up (annual) will consist of comprehensive risk stratification, including continued cardiovascular monitoring, ambulatory electrocardiographic recording (given the presence of ventricular premature beats and associated arrhythmia risk), and screening for acromegaly-related comorbidities such as colorectal polyps and obstructive sleep apnea.

Discussion

We report a case of acromegaly presenting with clinical symptoms and signs suggestive of heart failure, which was attributed to acromegaly-induced dilated cardiomyopathy. Following transsphenoidal resection of the pituitary adenoma, there was a significant reduction in GH and IGF-1 levels. This case highlights the critical importance of thorough clinical evaluation and timely diagnosis.

Acromegaly exerts a profound impact on the cardiovascular system. Heart failure secondary to acromegalic cardiomyopathy is one of the leading causes of mortality in patients with acromegaly and has gained increasing recognition.^12–14 Chronic exposure to elevated GH and IGF-1 levels in acromegaly leads to adverse effects on the myocardium, including diffuse myocardial cell hypertrophy, mononuclear lymphocyte infiltration, increased collagen fiber content, interstitial fibrosis, and disordered myocardial fiber arrangement, ultimately progressing to cardiomyopathy. ¹⁵ The hallmark features of acromegalic cardiomyopathy encompass diastolic dysfunction, concentric hypertrophy of both ventricles, and myocardial fibrosis. ¹⁶ Cardiac functional changes in patients with acromegaly can be categorized into three distinct stages: In the early stage, the primary manifestations include elevated heart rate and increased cardiac output, which may be reversible upon normalization of GH and IGF-1 levels through surgical or medical treatment. ¹⁷ As the disease advances, myocardial hypertrophy intensifies, resulting in diastolic dysfunction of the ventricles. Without effective treatment, the ventricles progressively enlarge, leading to contractile dysfunction. ¹⁸ Even with therapeutic intervention, advanced acromegalic cardiomyopathy is often irreversible, significantly reducing the life expectancy of affected individuals. ¹⁹

In this case, the patient’s wife provided valuable insights regarding the observed changes in his physical appearance, which further substantiated our clinical suspicion of acromegaly and prompted appropriate investigations leading to a definitive diagnosis. The management principles for acromegalic cardiomyopathy primarily involve controlling the excessive secretion of GH and IGF-1, as well as managing heart failure effectively. ⁷ Normalizing serum GH and IGF-1 levels through surgical or medical interventions is critical for alleviating clinical symptoms and reducing mortality risk. ²⁰ Transsphenoidal resection of the pituitary adenoma remains the primary treatment modality due to its reportedly high cure rate.^3,21 A previous case report documented a 56-year-old male with acromegalic cardiomyopathy whose left ventricular systolic function remained severely impaired despite adherence to guideline-directed medical therapy for 3 months but significantly improved following the resection of a pituitary microadenoma and normalization of IGF-1 levels. ²² In our case, the patient exhibited a high surgical risk owing to severely compromised left ventricular systolic function. We initially managed the severe heart failure to optimize his condition for tolerating the transsphenoidal resection of the pituitary adenoma, which was successfully performed, resulting in postoperative GH and IGF-1 levels returning to normal. Given the favorable initial response to treatment, the patient’s cardiac function has the potential for improvement if adherence to the therapeutic regimen is maintained.

This case report has several limitations that should be acknowledged. First, the relatively short follow-up duration precluded a comprehensive evaluation of the long-term effects of GH and IGF-1 control on myocardial remodeling. Second, the absence of a myocardial biopsy limited the provision of histological-level pathological evidence, such as the extent of myocardial cell hypertrophy and collagen deposition. Finally, given that the patient has diabetes and HFrEF with ST-T abnormalities, ischemic causes should be systematically excluded. Despite these limitations, this case underscores the critical importance of early cardiac evaluation in patients with acromegaly, even in the absence of overt symptoms. Future studies involving larger cohorts and employing advanced imaging techniques are essential to elucidate the natural history of acromegalic cardiomyopathy.

Conclusion

Acromegaly is a complex and multifaceted disease characterized by significant cardiovascular comorbidities, which contribute to increased morbidity and mortality. This case highlights the necessity for routine cardiovascular surveillance in patients with acromegaly. Early intervention aimed at normalizing GH and IGF-1 levels, coupled with personalized heart failure management, may enhance clinical outcomes. Further research is imperative to establish standardized screening protocols and investigate the utility of advanced imaging modalities in disease monitoring.

Take-home message

This case illustrates that severe, new-onset heart failure with reduced ejection fraction may represent the sole initial manifestation of occult acromegaly, even in the absence of classic phenotypic features or left ventricular hypertrophy. It underscores the importance of considering endocrine etiologies in the evaluation of idiopathic dilated cardiomyopathy, as early diagnosis and dual-targeted management of both the myocardial dysfunction and the underlying hormonal excess may lead to the reversal of cardiac impairment.