Introduction: Advanced heart failure (HF) is commonly associated with hyponatremia which is associated to a worse prognosis. Furthermore, pathophysiological mechanisms of hyponatremia as well as therapeutic approach are challenging in settings of advanced HF. An inappropriate interpretation of hyponatremia, might lead to oversight of the important diagnostic clues.

Case presentation: We present the case of a 54-years-old male patient, heavy smoker, admitted for exertional dyspnea, left-side trepopnea and predominantly nocturnal coughing. Patient’s history reveals chronic HF with severely reduced left ventricular ejection fraction secondary to ischemic cardiomyopathy, three-vessel coronary artery bypass surgery associated with mitral valve replacement with mechanical prosthesis for severe ischemic mitral regurgitation (performed seven years earlier), followed by late occlusion of two of the grafts, and a relatively recent cardioverter defibrillator implantation for primary prevention. Additionally, re-cent history also reveals multiple hospital admissions in the previous three months for similar symptoms, interpreted as being part of HF decompensation and treated accordingly, with only transient improvement in clinical status. Physical examination revealed signs of peripheral and systemic congestion with peripheral edema and bibasal pulmonary crackles, audible sharp metallic clicks in the precordial area, and no neurolo-gical manifestations. Chest X-ray showed pulmonary interstitial edema and increased cardiothoracic ratio. Transthoracic echocardiography revealed a mildly dilated left ventricle, with a 30% ejection fraction, normally functioning metallic prosthesis, and increased left and right heart filling pressures. Laboratory workup show-ed moderately increased N-terminal pro B-type natriu-retic peptide, normal renal function, and severe hyponatremia (114 mmol/L) with reduced plasma osmola-lity and elevated urinary osmolality. Previous hospital admissions revealed the chronic state of the electrolyte imbalance, which appeared to be only mildly respon-sive to IV diuretics. Initial therapeutic strategy included high-dose intravenous diuretics and optimization of HF therapy. During the first week, euvolemic status and a 40% decrease in natriuretic peptides level were obtained, but without appropriate improvement of se-rum sodium concentration. Consequently, sodium was attempted using 5.85% hypertonic saline, which lead only to minor transient increases. Further workup reve-aled normal adrenal and thyroid function. A secondary cause of inappropriate antidiuretic hormone (ADH) secretion was considered. Contrast enhanced thoracic computed tomography revealed a left hilar mass with airway and vascular involvement. Subsequent exami-nations confirmed extensive stage small cell lung carcinoma.

Particular aspects of the case: Lung cancer is an im-portant comorbidity in HF patients. Inappropriate antidiuretic hormone secretion, as a paraneoplastic manifestation, is frequently missed, particularly when advanced HF is associated. Refined clinical judgement is necessary for proper interpretation of even commonly encountered clinical signs or electrolyte disorders.