Heart failure (HF) is a chronic and progressive clinical syndrome resulting from structural or functional abnormalities of the heart. The most common symptoms and signs of HF are dyspnea, fatigue, pulmonary and peripheral congestion or edema and jugular vein distension. The prevalence of HF continuously increases due to improved treatment and reduced short-term mortality in patients with acute coronary syndromes, congenital heart disease, population aging and improved survival of patients with already developed heart failure by the widespread application of modern disease-modifying medications and devices.

Acute heart failure (AHF) is recognized when symptoms of HF appear in the patient without the history of previous HF (de novo HF) or when symptoms and signs are rapidly exacerbating in a patient with previously recognized HF (decompensated HF). Acute heart failure is the most common cause of unplanned hospital admissions in older patients. The pathophysiology of both conditions is similar, but de novo HF requires a more detailed diagnostic approach to find the underlying pathology. The initial treatment of AHF includes intravenous diuretics and short-acting vasodilators. The minority of patients with AHF present with cardiogenic shock associated with low blood pressure and severely compromised perfusion of peripheral tissues; the cardiogenic shock is associated with much higher mortality than AHF without shock. Whereas the treatment of chronic HF has substantially improved survival rates, the outcome of AHF is still poor, with high mortality and hospital readmission rates. Currently used therapy is directed to reduce the pre and afterload of the heart and does not target the specific underlying pathology in a given patient, which may explain unsatisfactory progress of clinical outcomes. Therefore, individualized therapy is highly appreciated, requiring establishing specific markers.^,

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