Acute Heart Failure: Diagnostic-Therapeutic Pathways and Preventive Strategies-A Real-World Clinician's Guide

Abstract

Acute heart failure (AHF) is the most frequent cause of unplanned hospital admission in patients of >65 years of age and it is associated with significantly increased morbidity, mortality, and healthcare costs. Different AHF classification criteria have been proposed, mainly reflecting the clinical heterogeneity of the syndrome. Regardless of the underlying mechanism, peripheral and/or pulmonary congestion is present in the vast majority of cases. Furthermore, a marked reduction in cardiac output with peripheral hypoperfusion may occur in most severe cases. Diagnosis is made on the basis of signs and symptoms, laboratory, and non-invasive tests. After exclusion of reversible causes, AHF therapeutic interventions mainly consist of intravenous (IV) diuretics and/or vasodilators, tailored according to the initial hemodynamic status with the addition of inotropes/vasopressors and mechanical circulatory support if needed. The aim of this review is to discuss current concepts on the diagnosis and management of AHF in order to guide daily clinical practice and to underline the unmet needs. Preventive strategies are also discussed.

Keywords: acute heart failure; biomarkers; cardiac ultrasound; computer tomography; preventive strategies; therapeutic interventions.

Figure 2

Diagnostic workup of AHF. Abbreviations: ACS: acute coronary syndrome; ALT: alanine aminotransferase; AST: aspartate aminotransferase; BUN: blood urea nitrogen, BNP: brain natriuretic peptide; CT: computed tomography; ECG: electrocardiogram; TOE: transesophageal echocardiogram; TSH: thyroid-stimulating hormone.

Figure 6

Outpatient management. Abbreviations: BP: blood pressure; HF: heart failure; ICD: implantable cardiac defibrillator; PMK: pacemaker.

Figure 1

Triage. Abbreviations: AHF: acute heart failure; ED: emergency department; ICU/CCU: intensive cardiology unit/critical care unit; MCS: mechanical circulatory support; NIV: non-invasive ventilation; SBP: systolic blood pressure.

Figure 3

A 68-year-old female with history of dilated cardiomyopathy was admitted for shortness of breath, fatigue, and low-extremity edema. A diagnosis of acute pulmonary edema was made. TTE showed severe LV dilation (LVEDVi 86 mL/m²), severe reduction in ejection fraction (EF 25–30%), mildly dilated right ventricle (basal diameter 4 cm) (a), and moderate tricuspid regurgitation (TR) (b). Lung ultrasound showing B-lines in all sites explored (arrow) and pleural effusion (*) (c,d). Diastolic dysfunction with increased left ventricular end-diastolic pressures (LVEDP) and PAWP (E/A: 2.5, E/E’: 30 and S < D on pulmonary veins) (e–g) and estimated pulmonary artery pressure of 70 mmHg (h).

Figure 4

Use of CT in acute heart failure.

Figure 5

CT in different scenarios. Type B thoracic aortic dissection: post-contrast sagittal CT reconstruction of the aorta demonstrates a medio-intimal flap that begins below left subclavian arterial origin and extends up to diaphragmatic hiatus (A). Pulmonary thromboembolism: post-contrast axial CT reconstruction depicts linear contrast defects inside the lumen of main pulmonary arteries (arrows) due to thromboembolism (B). Volume rendering post-contrast CT of the left descending coronary artery depicts a brief stenosis of the medium segment (C). Coronal unenhanced chest CT shows ground glass opacities of the lungs, especially on the left side, due to interstitial COVID pneumonia (D). Post-contrast axial CT image of the pelvis demonstrates ileal loops ischemia with a stratified appearance of the ileal loop’s wall (arrows) due to intramural edema and low submucosal enhancement associated with mesenterial free fluid. (E).