A 49-year-old man with unremarkable past medical history presented to the emergency department for chest pain. Echocardiography showed biventricular severe dilatation and dysfunction (left ventricular ejection fraction [FEVS] 19%) with eccentric hypertrophy (Figure 1). ECG did not show acute ischemic issues (Figure 2). Serum biomarkers revealed raised Troponin-I, low NT-proBNP and no inflammation. An episode of sustained ventricular tachycardia was recorded during continuous ECG monitoring. Coronary angiography showed no coronary artery disease. Cardiac MRI was not performed due to patient’s claustrophobia. Anti-remodeling therapy for heart failure (HF) was started. Clinical examination revealed signs of acromegaly (prominent nose, protruding brow bones, macroglossia and enlarged hands and feet). Raised levels of Growth Hormone (GH) and Somatomedin were detected and brain MRI showed pituitary macroadenoma. A diagnosis of acromegaly was established, and specific treatment with first-generation somatostatin analog (SSA) was started (octreotide). A differential diagnosis of myocarditis versus acromegalic cardiomyopathy (AC) or an overlap condition was considered. A mild non-focal fluorodeoxyglucose (FDG) uptake in the myocardium was observed on a carbo-free-diet total-body computed-tomography positron emission tomography (Figure 3), thus, together with normalized troponin level, endomyocardial biopsy was deemed unnecessary. The patient was discharged with a wearable cardioverter defibrillator. Despite a 6-month course of optimized medical therapy for both HF and acromegaly, neither cardiac function (FEVS 25%) nor hormonal status improved. A subcutaneous cardioverter defibrillator was implanted and hormonal therapy was upgraded to second-generation SSA (pasireotide). AC is a frequent complication of acromegaly since GH cardiac toxicity involves multiple mechanisms. Differential diagnosis with other causes of cardiac dysfunction may be difficult since imaging features may be nonspecific. Our case shows abnormal myocardial FDG uptake, which may suggest GH-induced altered glucose metabolism or active myocardial inflammation, which could be considered possible pathways of GH-related cardiac damage, even though poor knowledge exists about nuclear imaging patterns in AC. Still, the efficacy of SSA on cardiac dysfunction reversal is unclear, posing significant diagnostic and prognostic challenges in the field of acromegaly and cardiac inflammatory diseases.
Associazione Nazionale Medici Cardiologi Ospedalieri
