Biomarkers of Importance in Monitoring Heart Condition After Acute Myocardial Infarction

Abstract

Despite notable advancements in cardiovascular medicine, morbidity and mortality rates associated with myocardial infarction (MI) remain high. The unfavourable prognosis and absence of robust post-MI protocols necessitate further intervention. In this comprehensive review, we will focus on well-established and novel biomarkers that can provide insight into the processes that occur after an ischemic event. More precisely, during the follow-up, it is of particular importance to monitor biomarkers that indicate an increase in myocardial stretch and stress, damage and death of cardiomyocytes, remodelling of the extracellular matrix, oxidative stress, and inflammation. This enables the identification of abnormalities in a timely manner, as well as the capacity to respond promptly to any changes. Therefore, we would like to highlight the importance of well-known markers, such as natriuretic peptides, high-sensitivity troponins, soluble suppression of tumorigenicity 2, galactin-3, C-reactive protein, and interleukins in post-MI settings, as well as biomarkers such as adrenomedullin, growth differentiation factor-15, insulin-like growth factor binding protein 7, amyloid beta, vitamin D, trimethylamine N-oxide, and advanced glycation end-products that recently emerged in the cardiovascular filed. The implementation of novel post-MI protocols, which encompass the monitoring of the aforementioned biomarkers deemed pertinent, in conjunction with adherence to established cardiac rehabilitation programmes, along with the already well-established therapeutic strategies and control of cardiovascular risk factors, has the potential to markedly enhance patient outcomes and reduce the elevated level of morbidity and mortality.

Keywords: biomarkers; heart failure; myocardial infarction; myocardial remodelling; patient monitoring.

Figure 1

Overview of emerging cardiovascular biomarkers. Vitamin D deficiency, Klotho downregulation, heightened FGF-23 levels, beta-amyloid, and TMAO accumulation lead to elevated levels of inflammation, oxidative stress, plaque formation, and destabilisation.

Figure 2

Endogenous production and exogenous sources of AGEs. On the one hand, the accumulation of AGEs leads to crosslinks with proteins contributing to tissue stiffening. On the other hand, AGEs enhance inflammation and oxidative stress after binding to RAGE. AGEs, advanced glycation end products; RAGE, receptors for advanced glycation end products.