Biomarkers in the management of acute heart failure: state of the art and role in COVID-19 era

Abstract

Acute heart failure (AHF) affects millions of people worldwide, and it is a potentially life-threatening condition for which the cardiologist is more often brought into play. It is crucial to rapidly identify, among patients presenting with dyspnoea, those with AHF and to accurately stratify their risk, in order to define the appropriate setting of care, especially nowadays due to the coronavirus disease 2019 (COVID-19) outbreak. Furthermore, with physical examination being limited by personal protective equipment, the use of new alternative diagnostic and prognostic tools could be of extreme importance. In this regard, usage of biomarkers, especially when combined (a multimarker approach) is beneficial for establishment of an accurate diagnosis, risk stratification and post-discharge monitoring. This review highlights the use of both traditional biomarkers such as natriuretic peptides (NP) and troponin, and emerging biomarkers such as soluble suppression of tumourigenicity (sST2) and galectin-3 (Gal-3), from patients' emergency admission to discharge and follow-up, to improve risk stratification and outcomes in terms of mortality and rehospitalization.

Keywords: Acute heart failure; Biomarkers; Diagnosis; Follow-up; Mortality; Risk stratification.

Figure 1

(A) Schematic representation of European HF guidelines and The American College of Cardiology guidelines regarding biomarkers coupled with classes of recommendations and level of evidence; (B) studies involving the biomarkers. AHF, acute heart failure; ADHERE, Acute Decompensated Heart Failure National Registry; ACC/AHA, American College of Cardiology/American Heart Association; BNP, B‐type or brain natriuretic peptide; CORONA, Controlled Rosuvastatin Multinational Trial in Heart Failure; COACH, Coordinating Study Evaluating Outcomes of Advising and Counselling Failure; ESC, European Society of Cardiology; Gal‐3, galectin‐3; HF, heart failure; NP, natriuretic peptides; N/A, not applicable; NT‐proBNP, N‐terminal pro B‐type natriuretic peptide; PRIDE study, Pro‐Brain Natriuretic Peptide Investigation of Dyspnoea in the Emergency Department; sST2, soluble suppression of tumourigenicity; RELAX‐AHF trial, Relaxin in Acute Heart Failure trial.

Figure 2

Schematic representation of NPs upon myocyte stretching. ANP, atrial natriuretic peptide; BNP, B‐type or brain natriuretic peptide; NP, natriuretic peptides; NT‐proBNP, N‐terminal pro B‐type natriuretic peptide.

Figure 3

Schematic representation of troponin I and T release into the circulation upon myocyte necrosis or damage.

Figure 4

Schematic representation of ST2 and sST2 and their involvement in fibrosis and hypertrophy. IL‐33, interleukin‐33; ST2, suppression of tumourigenicity; sST2, soluble suppression of tumourigenicity.

Figure 5

Schematic representation of Gal‐3 role in cardiac remodelling. Gal‐3, galactin‐3.

Figure 6

Flow diagram demonstrating remote monitoring and controlling for in‐home patients with HF risks. HF, heart failure; sST2, soluble suppression of tumourigenicity.

Figure 7

Flow diagram demonstrating the usefulness of multimarker approach for finer patient's management and decision‐making process in the ED. BNP, B‐type or brain natriuretic peptide; ED, emergency department; Gal‐3, galectin‐3; NT‐proBNP, N‐terminal pro B‐type natriuretic peptide; sST2, soluble suppression of tumourigenicity; VAD, ventricular assist device.