Adverse Cardiac Remodelling after Acute Myocardial Infarction: Old and New Biomarkers

Alexander E Berezin, Alexander A Berezin, Alexander E Berezin, Alexander A Berezin

Abstract

The prevalence of heart failure (HF) due to cardiac remodelling after acute myocardial infarction (AMI) does not decrease regardless of implementation of new technologies supporting opening culprit coronary artery and solving of ischemia-relating stenosis with primary percutaneous coronary intervention (PCI). Numerous studies have examined the diagnostic and prognostic potencies of circulating cardiac biomarkers in acute coronary syndrome/AMI and heart failure after AMI, and even fewer have depicted the utility of biomarkers in AMI patients undergoing primary PCI. Although complete revascularization at early period of acute coronary syndrome/AMI is an established factor for improved short-term and long-term prognosis and lowered risk of cardiovascular (CV) complications, late adverse cardiac remodelling may be a major risk factor for one-year mortality and postponded heart failure manifestation after PCI with subsequent blood flow resolving in culprit coronary artery. The aim of the review was to focus an attention on circulating biomarker as a promising tool to stratify AMI patients at high risk of poor cardiac recovery and developing HF after successful PCI. The main consideration affects biomarkers of inflammation, biomechanical myocardial stress, cardiac injury and necrosis, fibrosis, endothelial dysfunction, and vascular reparation. Clinical utilities and predictive modalities of natriuretic peptides, cardiac troponins, galectin 3, soluble suppressor tumorogenicity-2, high-sensitive C-reactive protein, growth differential factor-15, midregional proadrenomedullin, noncoding RNAs, and other biomarkers for adverse cardiac remodelling are discussed in the review.

Conflict of interest statement

The authors declare that there is no conflict of interest regarding the publication of this paper.

Copyright © 2020 Alexander E. Berezin and Alexander A. Berezin.

Figures

Figure 1
Figure 1
Adverse cardiac remodelling after AMI: the role of different triggers in development of cardiac architectonic disorders and heart failure. LV: left ventricular; HF: heart failure; HFpEF: HF with preserved ejection fraction; HFmrEF: HF with midrange ejection fraction; HFrEF: HF with reduced ejection fraction.
Figure 2
Figure 2
The factors preventing late adverse cardiac remodelling in AMI patients after successful reperfusion with PCI. IVUS-VH: intravascular ultrasound virtual-histology; BMS: bare metal stent; BES: biolimus eluting stent; OCT: optical coherence tomography; DAPT: dual antiplatelet therapy; ACE: angiotensin-converting enzyme; ARBs: angiotensin-II receptor antagonists; MCRA: mineralocorticoid receptor antagonists; IC: intracoronary.
Figure 3
Figure 3
The main pathogenetic mechanisms underlying the initiation and progression of late adverse cardiac remodelling in AMI patients after successful reperfusion with PCI. HF: heart failure; ECM: extracellular matrix; PCI: percutaneous coronary intervention.
Figure 4
Figure 4
The role of miRNAs in the pathogenesis of late adverse cardiac remodelling in AMI. VEGF: vascular endothelial growth factor; TGF: transforming growth factor; NO: nitric oxide; eNOs: endothelial NO synthase; MMP: matrix metalloproteinase; VCAM: vascular adhesive molecule.

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