Biomarkers Of Heart Disease Research Articles

Construction of Immune-Related circRNA-miRNA-mRNA Network and Identification of circRNAs as Biomarkers in Coronary Atherosclerotic Heart Disease

Circular RNAs (circRNAs) play crucial roles in the immune and inflammatory responses of many diseases by acting as competing endogenous RNAs (ceRNAs). However, the role of circRNAs as ceRNAs in the immune and inflammatory processes of coronary atherosclerosis heart disease (CHD) remains unclear. This study aimed to identify and validate the potential immune-related circRNAs as biomarkers for CHD. Firstly, we constructed a ceRNA regulatory network including 14 circRNAs, 24 miRNAs, and 15 genes through bioinformatics analysis. Four hub genes were identified and five candidate immune-related circRNAs were screened. Subsequently, the expression levels of these candidate circRNAs were detected by qRT-PCR. Notably, hsa_circRNA_101069 and hsa_circRNA_406053 showed significant up-regulation in CHD patients (p < 0.001). The value of these circRNAs as biomarkers for CHD was evaluated by the area under the ROC curve (AUC), net reclassification improvement (NRI), and integrated discrimination improvement (IDI) indexes. Adding circRNAs to a traditional CHD model significantly enhanced classification performance, with an IDI of 0.058 and an NRI of 0.280 for hsa_circRNA_101069 and an IDI of 0.051 and an NRI of 0.480 for hsa_circRNA_406053. Furthermore, hsa_circRNA_101069 was up-regulated in ox-LDL-induced THP-1 macrophages, and silencing hsa_circRNA_101069 significantly inhibited the apoptosis rates and the inflammatory cytokines levels. This study constructed an immune-related circRNA-miRNA-mRNA network and identified two circRNAs as biomarkers for CHD, with hsa_circRNA_101069 potentially contributing to the pathological basis of CHD.

Revealing alterations in heart rate fluctuations during the progression of Chagas disease.

The heart rate variability (HRV) continually evolves throughout life, reflecting modifications in the architecture of the sinoatrial node (SAN) and in the regulation of heart rate by the autonomic nervous system (ANS). Both can be considerably affected by Chagas disease, causing important changes in the complex nature of HRV. We aim to evaluate the ability of an index based on the false nearest neighbors method (FN10) to reflect these changes during disease progression. We perform a retrospective, descriptive, and cross-sectional study analyzing HRV time series of participants with Chagas disease. We determine the dependence of FN10 on age and sex in a healthy population, and then evaluate FN10 in individuals with Chagas disease. In the healthy population, FN10 has a scaling behavior with age, which is independent of sex. In Chagas disease, some individuals show FN10 values significantly above those seen in the healthy population. We relate the findings to the pathophysiological mechanisms that determine the progression of the disease. The results indicate that FN10 may be a candidate prognostic biomarker for heart disease.

BNP as a biomarker in adult congenital heart disease: help or hype?

BNP as a biomarker in adult congenital heart disease: help or hype?

Identification of necroptosis-related diagnostic biomarkers in coronary heart disease

BackgroundThe implication of necroptosis in cardiovascular disease was already recognized. However, the molecular mechanism of necroptosis has not been extensively studied in coronary heart disease (CHD). MethodsThe differentially expressed genes (DEGs) between CHD and control samples were acquired in the GSE20681 dataset downloaded from the GEO database. Key necroptosis-related DEGs were captured and ascertained by bioinformatics analysis techniques, including weighted gene co-expression network analysis (WGCNA) and two machine learning algorithms, while single-gene gene set enrichment analysis (GSEA) revealed their molecular mechanisms. The diagnostic biomarkers were selected via receiver operating characteristic (ROC) analysis. Moreover, an analysis of immune elements infiltration degree was carried out. Authentication of pivotal gene expression at the mRNA level was investigated in vitro utilizing quantitative real-time PCR (qRT-PCR). ResultsA total of 94 DE-NRGs were recognized here, among which, FAM166B, NEFL, POLDIP3, PRSS37, and ZNF594 were authenticated as necroptosis-related biomarkers, and the linear regression model based on them presented an acceptable ability to different sample types. Following regulatory analysis, the ascertained biomarkers were markedly abundant in functions pertinent to blood circulation, calcium ion homeostasis, and the MAPK/cAMP/Ras signaling pathway. Single-sample GSEA exhibited that APC co-stimulation and CCR were more abundant, and aDCs and B cells were relatively scarce in CHD patients. Consistent findings from bioinformatics and qRT-PCR analyses confirmed the upregulation of NEFL and the downregulation of FAM166B, POLDIP3, and PRSS37 in CHD. ConclusionOur current investigation identified 5 necroptosis-related genes that could be diagnostic markers for CHD and brought a novel comprehension of the latent molecular mechanisms of necroptosis in CHD.

Non-coding RNAs as therapeutic targets and biomarkers in ischaemic heart disease.

The adult heart is a complex, multicellular organ that is subjected to a series of regulatory stimuli and circuits and has poor reparative potential. Despite progress in our understanding of disease mechanisms and in the quality of health care, ischaemic heart disease remains the leading cause of death globally, owing to adverse cardiac remodelling, leading to ischaemic cardiomyopathy and heart failure. Therapeutic targets are urgently required for the protection and repair of the ischaemic heart. Moreover, personalized clinical biomarkers are necessary for clinical diagnosis, medical management and to inform the individual response to treatment. Non-coding RNAs (ncRNAs) deeply influence cardiovascular functions and contribute to communication between cells in the cardiac microenvironment and between the heart and other organs. As such, ncRNAs are candidates for translation into clinical practice. However, ncRNA biology has not yet been completely deciphered, given that classes and modes of action have emerged only in the past 5 years. In this Review, we discuss the latest discoveries from basic research on ncRNAs and highlight both the clinical value and the challenges underscoring the translation of these molecules as biomarkers and therapeutic regulators of the processes contributing to the initiation, progression and potentially the prevention or resolution of ischaemic heart disease and heart failure.

Discovery of circulating miRNAs as biomarkers of chronic Chagas heart disease via a small RNA-Seq approach

Chagas disease affects approximately 7 million people worldwide in Latin America and is a neglected tropical disease. Twenty to thirty percent of chronically infected patients develop chronic Chagas cardiomyopathy decades after acute infection. Identifying biomarkers of Chagas disease progression is necessary to develop better therapeutic and preventive strategies. Circulating microRNAs are increasingly reliable biomarkers of disease and therapeutic targets. To identify new circulating microRNAs for Chagas disease, we performed exploratory small RNA sequencing from the plasma of patients and performed de novo miRNA prediction, identifying potential new microRNAs. The levels of the new microRNAs temporarily named miR-Contig-1519 and miR-Contig-3244 and microRNAs that are biomarkers for nonchagasic cardiomyopathies, such as miR-148a-3p and miR-224-5p, were validated by quantitative reverse transcription. We found a specific circulating microRNA signature defined by low miR-Contig-3244, miR-Contig-1519, and miR-148a-3 levels but high miR-224-5p levels for patients with chronic Chagas disease. Finally, we predicted in silico that these altered circulating microRNAs could affect the expression of target genes involved in different cellular pathways and biological processes, which we will explore in the future.

Abnormal circulating steroids refine risk of progression to heart failure in ischemic heart disease.

Patients with ischemic heart disease (IHD) experience a high incidence of progression to heart failure (HF) despite current therapies. We speculated that steroid hormone metabolic disorders distinct adverse phenotypes and contribute to HF. We measured 18 steroids using liquid chromatography with tandem mass spectrometry in 2023 patients from the Registry Study of Biomarkers in Ischemic Heart Disease (BIOMS-IHD), including 1091 patients with IHD in a retrospective discovery set and 932 patients with IHD in a multicentre validation set. Our outcomes included incident HF after a median follow-up of 4 years. We demonstrated steroid-based signatures of inflammation, coronary microvascular dysfunction and left ventricular hypertrophy that were associated with subsequent HF events in patients with IHD. In both cohorts, patients with a high steroid-heart failure score (SHFS) (>1) exhibited a greater risk of incident HF than patients with a low SHFS (≤1). The SHFS further improved the prognostic accuracy beyond clinical variables (net reclassification improvement of 0.628 in the discovery set and 0.299 in the validation set) and demonstrated the maximal effect of steroid signatures in patients with IHD who had lower B-type natriuretic peptide levels (pinteraction = 0.038). A steroid-based strategy can simply and effectively identify individuals at higher HF risk who may derive benefit from more intensive follow-ups.

Tenascin-C: as a diagnostic biomarker for rheumatic heart disease

BackgroundRheumatic fever is a long-term inflammatory disease that can happen if group A beta-hemolytic streptococci bacteria are not treated well enough. Rheumatic fever is recognized globally as the leading cause of heart disease in the pediatric population. This disease destroys the heart muscle, progressively deteriorating its structure and impairing the function of its valves over time.AimThe aim of this study is to determine the role of serum tenascin-C in the diagnosis of acute rheumatic fever and chronic rheumatic heart disease.MethodsThis case–control study involved a group of 60 Egyptian children. Among them, 20 were diagnosed with acute rheumatic fever, identified using the updated Jones criteria from 2015. Another 20 children, who were suffering from chronic rheumatic heart disease, were also act as a part of the study. The remaining 20 participants, healthy children carefully matched in age and sex, served as the control group.ResultsSerum tenascin-C level was significantly increased in acute rheumatic fever (ARF) and highly significantly increased in chronic rheumatic heart disease (CRHD) groups when compared with control group (P = 0.04, 0.01), respectively. There were highly significant difference between and within the studied groups regarding the mean of serum tenascin-C. Serum tenascin-C mean of ARF, CRHD, and control was 4.82 ± 18.7, 5.46 ± 1.6, and 3.78 ± 2.4, respectively, P = 0.02. Level of serum tenascin-C was lower in cases with severe mitral valve insufficiency. No significant link was found between the level of serum tenascin-C and C-reactive protein (CRP), ESR, and ASO titer, with a P-value greater than 0.5. ROC curve for serum tenascin-C in ARF patients was area under the curve = 0.682 (P = 0.05) with optimal serum tenascin-C cut-off point (> 3.76 ng/ml); ROC curve for serum tenascin-C in CRHD patients was AUC = 0.73 (P = 0.01) with cut-off point level (73.76 ng/ml).ConclusionPatients with ARF and CRHD have increased level of serum tenascin-C. Serum tenancin-C is superior in the diagnosis of ARF in comparison to CRP, ESR, and ASOT. Tenascin-C level can be used as a diagnostic marker for ARF and CRHD.

Serum YKL-40 in coronary heart disease: linkage with inflammatory cytokines, artery stenosis, and optimal cut-off value for estimating major adverse cardiovascular events.

YKL-40, previously known as chitinase-3-like protein 1 (CHI3L1), is an inflammation-related glycoprotein that promotes atherosclerosis, but its application and optimal cut-off value as a prognostic biomarker in coronary heart disease (CHD) require more clinical evidence. Thus, this prospective study aimed to evaluate the linkage of serum YKL-40 with disease features, inflammatory cytokines, and major adverse cardiovascular events (MACEs) in CHD patients. A total of 410 CHD patients were enrolled for serum YKL-40 determination via enzyme-linked immunosorbent assay. Meanwhile, serum YKL-40 levels in 100 healthy controls (HCs) were also quantified. YKL-40 level was higher in CHD patients compared with that in HCs (P < 0.001). YKL-40 was positively linked with hyperlipidemia (P = 0.014), diabetes mellitus (P = 0.001), fasting blood glucose (P = 0.045), C-reactive protein (P < 0.001), the Gensini score (P < 0.001), and stenosis degree (graded by the Gensini score) (P < 0.001) in CHD patients. In addition, an elevated YKL-40 level was associated with increased levels of tumor necrosis factor alpha (P = 0.001), interleukin (IL)-1β (P = 0.001), IL-6 (P < 0.001), and IL-17A (P = 0.002) in CHD patients. The 1-/2-/3-year cumulative MACE rates of CHD patients were 5.5%, 14.4%, and 25.0%, respectively. Regarding the prognostic capability, YKL-40 ≥100 ng/ml (the median cut-off value) (P = 0.003) and YKL-40 ≥150 ng/ml (the third interquartile cut-off value) (P = 0.021) reflected an elevated accumulating MACE rate, whereas accumulating MACE was not different between CHD patients with YKL-40 ≥80 and <80 ng/ml (the first interquartile cut-off value) (P = 0.083). Serum YKL-40 is positively linked with inflammatory cytokines and the Gensini score, whose high expression cut-off by 100 and 150 ng/ml estimates a higher MACE risk in CHD patients.

Multifractal foundations of biomarker discovery for heart disease and stroke

Any reliable biomarker has to be specific, generalizable, and reproducible across individuals and contexts. The exact values of such a biomarker must represent similar health states in different individuals and at different times within the same individual to result in the minimum possible false-positive and false-negative rates. The application of standard cut-off points and risk scores across populations hinges upon the assumption of such generalizability. Such generalizability, in turn, hinges upon this condition that the phenomenon investigated by current statistical methods is ergodic, i.e., its statistical measures converge over individuals and time within the finite limit of observations. However, emerging evidence indicates that biological processes abound with nonergodicity, threatening this generalizability. Here, we present a solution for how to make generalizable inferences by deriving ergodic descriptions of nonergodic phenomena. For this aim, we proposed capturing the origin of ergodicity-breaking in many biological processes: cascade dynamics. To assess our hypotheses, we embraced the challenge of identifying reliable biomarkers for heart disease and stroke, which, despite being the leading cause of death worldwide and decades of research, lacks reliable biomarkers and risk stratification tools. We showed that raw R-R interval data and its common descriptors based on mean and variance are nonergodic and non-specific. On the other hand, the cascade-dynamical descriptors, the Hurst exponent encoding linear temporal correlations, and multifractal nonlinearity encoding nonlinear interactions across scales described the nonergodic heart rate variability more ergodically and were specific. This study inaugurates applying the critical concept of ergodicity in discovering and applying digital biomarkers of health and disease.

Measures of Aging Biology in Saliva and Blood as Novel Biomarkers for Stroke and Heart Disease in Older Adults.

The role of aging biology as a novel risk factor and biomarker for vascular outcomes in different accessible body tissues such as saliva and blood remain unclear. We aimed to (1) assess the role of aging biology as a risk factor of stroke and heart disease among individuals of same chronologic age and sex and (2) compare aging biology biomarkers measured in different accessible body tissues as novel biomarkers for stroke and heart disease in older adults. This study included individuals who consented for blood and saliva draw in the Venous Blood Substudy and Telomere Length Study of the Health and Retirement Study (HRS). The HRS is a population-based, nationally representative longitudinal survey of individuals aged 50 years and older in the United States. Saliva-based measures included telomere length. Blood-based measures included DNA methylation and physiology biomarkers. Propensity scores-matched analyses and Cox regression models were conducted. This study included individuals aged 50 years and older, who consented for blood (N = 9,934) and saliva (N = 5,808) draw in the HRS. Blood-based biomarkers of aging biology showed strong associations with incident stroke as follows: compared with the lowest tertile of blood-based biomarkers of aging, biologically older individuals had significantly higher risk of stroke based on DNA methylation Grim Age clock (adjusted hazard ratio [aHR] = 2.64, 95% CI 1.90-3.66, p < 0.001) and Physiology-based Phenotypic Age clock (aHR = 1.75, 95% CI 1.27-2.42, p < 0.001). In secondary analysis, biologically older individuals had increased risk of heart disease as follows: DNA methylation Grim Age clock (aHR = 1.77, 95% CI 1.49-2.11, p < 0.001) and Physiology-based Phenotypic Age clock (aHR = 1.61, 95% CI 1.36-1.90, p < 0.001). Compared with saliva-based telomere length, blood-based aging physiology and some DNA methylation biomarkers are strongly associated with vascular disorders including stroke and are more precise and sensitive biomarkers of aging. Saliva-based telomere length and blood-based DNA methylation and physiology biomarkers likely represent different aspects of biological aging and accordingly vary in their precision as novel biomarkers for optimal vascular health.

Proteome profiling of early gestational plasma reveals novel biomarkers of congenital heart disease

Prenatal diagnosis of congenital heart disease (CHD) relies primarily on fetal echocardiography conducted at mid‐gestational age—the sensitivity of which varies among centers and practitioners. An objective method for early diagnosis is needed. Here, we conducted a case–control study recruiting 103 pregnant women with healthy offspring and 104 cases with CHD offspring, including VSD (42/104), ASD (20/104), and other CHD phenotypes. Plasma was collected during the first trimester and proteomic analysis was performed. Principal component analysis revealed considerable differences between the controls and the CHDs. Among the significantly altered proteins, 25 upregulated proteins in CHDs were enriched in amino acid metabolism, extracellular matrix receptor, and actin skeleton regulation, whereas 49 downregulated proteins were enriched in carbohydrate metabolism, cardiac muscle contraction, and cardiomyopathy. The machine learning model reached an area under the curve of 0.964 and was highly accurate in recognizing CHDs. This study provides a highly valuable proteomics resource to better recognize the cause of CHD and has developed a reliable objective method for the early recognition of CHD, facilitating early intervention and better prognosis.

NT-proBNP as neuroendocrine tumor biomarker: beyond heart failure.

Neuroendocrine tumors (NETs) are rare neoplasms that occur in various locations throughout the body. Despite their usually benign character, they might manifest with distant metastases. N-terminal prohormone of brain natriuretic peptide (NT-proBNP) has previously been described as a useful biomarker in diagnosing carcinoid heart disease (CHD), a common advanced NETs manifestation. We observed plasma concentrations of NT-proBNP in metastatic midgut NETs over a 4-year period. We aimed to explore NT-proBNP concentrations in states of varying levels of cell proliferation and disease status. Our goal was to investigate NT-proBNP's role in predicting disease progression in relation to previous research and up-to-date scientific guidelines. We performed a retrospective multivariate analysis of NT-proBNP concentrations in 41 midgut NETs patients treated with somatostatin analogs, all with liver metastases. NT-proBNP concentrations were measured in every patient across 16 evenly distanced time points over a 48-month period and were compared to variables such as sex, age, grading, Ki-67, primary tumor location, and CT findings. NT-proBNP concentrations correlated positively with higher liver tumor burden, higher grading, high Ki-67 levels, and with progressive disease in CT. There were no differences in NT-proBNP levels with regard to primary location (ileum vs jejunum), sex, and age. We conclude that NT-proBNP is a useful analyte for monitoring NETs progression, due to its increased concentration in scenarios implying increased cellular proliferation. These long-term follow-up results align with previous findings and suggest an additional role for NT-proBNP in diagnostic algorithms, beyond a carcinoid heart disease biomarker.

VEGF-A related SNPs: a cardiovascular context.

Cardiovascular diseases (CVDs) are the leading cause of death worldwide. Currently, cardiovascular disease risk algorithms play a role in primary prevention. However, this is complicated by a lack of powerfully predictive biomarkers that could be observed in individuals before the onset of overt symptoms. A key potential biomarker for heart disease is the vascular endothelial growth factor (VEGF-A), a molecule that plays a pivotal role in blood vessel formation. This molecule has a complex biological role in the cardiovascular system due to the processes it influences, and its production is impacted by various CVD risk factors. Research in different populations has shown single nucleotide polymorphisms (SNPs) may affect circulating VEGF-A plasma levels, with some variants associated with the development of CVDs, as well as CVD risk factors. This minireview aims to give an overview of the VEGF family, and of the SNPs reported to influence VEGF-A levels, cardiovascular disease, and other risk factors used in CVD risk assessments.

Reduced Angiopoietin Factor 2 Levels Are Correlated with Better Cardiac Function and Prognosis in Valvular Heart Disease.

There are few circulating biomarkers for valvular heart disease. Angiopoietin (Ang) 1, Ang2, and vascular endothelial growth factor are important inflammation-associated cytokines. The aim of this study was to investigate the clinical significance and association of Ang1, Ang2, and vascular endothelial growth factor in valvular heart disease. This is a retrospective study; a total of 62 individuals (valvular heart disease patients [n=42] and healthy controls [n=20]) were included. Plasma levels of Ang1, Ang2, and vascular endothelial growth factor were detected by enzyme-linked immunosorbent assays. We retrospectively collected the baseline characteristics and short-term outcomes; logistic regression was performed to identify predictor for short-term mortality. Ang2 was significantly decreased in the valvular heart disease group compared with the healthy control group (P=0.023), while no significant difference was observed in the Ang1 and vascular endothelial growth factor levels. The Ang2 level of New York Heart Association (NYHA) I/II patients - but not NYHA III/IV patients - was significantly decreased compared with that of healthy control individuals (NYHA I/II: P=0.017; NYHA III/IV: P=0.485). Univariable logistic regression analysis indicated that Ang2 was a significant independent predictor for short-term mortality (odds ratio 18.75, P=0.033, 95% confidence interval 8.08-102.33). Ang1 was negatively correlated with Ang2 (P=0.032, Pearson's correlation coefficient =-0.317) and was positively correlated with vascular endothelial growth factor (P=0.019, Pearson's correlation coefficient = 0.359). Ang2 might serve as a therapeutic and prognostic target for valvular heart disease.

Correlation between HS-troponin I level and Brixia score in COVID-19 patients with diabetes mellitus at ICU of Dr. Moewardi Hospital, Indonesia

COVID-19 can cause disturbances in insulin production and worsen the clinical condition of patients with comorbid diabetes mellitus. In patients with diabetes mellitus, one of the complications is heart disease. Therefore, a study was conducted to determine the relationship between hs-Troponin I levels, which is a biomarker of heart disease, with the severity of COVID-19 patients as measured by the Brixia score in COVID-19 patients with comorbid diabetes mellitus in the ICU (Intensive Care Unit) of Dr. Moewardi Hospital, Surakarta. The study was conducted with a cross-sectional approach, the sample was COVID-19 patients with comorbid diabetes mellitus in the ICU, chosen by purposive sampling method. The dependent variable of this study was the Brixia score, and hs-Troponin I would be the independent variable. Data were analyzed by contingency coefficient test with p&lt;0.05 indicating statistical correlation. 44 patients hospitalized in ICU for COVID-19 were enrolled. The mean age was 61±8 years old. 27% of patients had normal hs-Troponin I levels, and 73% had elevated hs-Troponin I levels. 11% of patients had a low Brixia score, 43% had a moderate score, and 45% had a high score. Data were analyzed, and the result is the value of X2 count=2.804 &lt; X2 table=5.991 which means that there is no relationship between variables. The values of p=0,246 (p&gt;0,05) and r=0,245 showed that there is no significant relationship between hs-Troponin I and Brixia score. Hs-Troponin I level is negatively correlated to Brixia score in COVID-19 patients with diabetes mellitus.

Circular RNAs as a promising biomarker for heart disease

Heart-related diseases account for a high proportion of deadly pathologies, so a large number of studies have been conducted to discover potential biomarkers for the early detection of heart disease. Circular RNAs (circRNAs) are known to be involved in various human diseases, and several circRNAs associated with heart disease have been reported recently. However, there is a lack of literature summarizing the potential of circRNAs as biomarkers of heart disease and suggesting future research prospects. In this review, the history of circRNA research and important studies on circRNAs are described. In addition, the biogenesis process of circRNAs and the applicability of circRNA as a biomarker of heart disease are introduced, and select studies that monitored circRNAs circulating in human blood as biomarkers of heart disease are summarized. The contents of this review may help the researchers interested in the detection and prevention of heart disease at an early stage.

Review on cardiovascular disease and antihypertensive drugs effect on the circulating biomarkers of heart disease

Cardiovascular diseases (CVD), a group of diseases that affect the heart and blood vessels have posed high morbidity rate to humans, with the second-high mortality rate after cancer. These diseases include hypertension, coronary artery disease, cardiac dysrhythmias, cerebrovascular disease, valvular heart disease, cardiomyopathies, peripheral vascular disease, and congenital cardiac abnormalities. These diseases have been observed to affect people of older age and have higher susceptibility in male than the female counterparts. Some circulating biomarkers such as C-reactive protein, cardiac troponin I, myostatin, homocystein, dimethylarginine, e.t.c have been found to be indispensable in the diagnosis and prediction of possible occurrence of CVD. It has been postulated that C-reactive protein rises in acute inflammation and may contribute to further atherosclerosis by stimulating macrophage uptake of low density lipoprotein cholesterol (LDL-C). Antihypertensive drugs are used to combat these diseases and they come in different forms with variable mechanisms of action. Antihypertensive drugs have been postulated to have lowering effect on circulating biomarkers of CVD. However, prophylactic measures are highly recommended.

Review on cardiovascular disease and antihypertensive drugs effect on the circulating biomarkers of heart disease

Review on cardiovascular disease and antihypertensive drugs effect on the circulating biomarkers of heart disease

Circulating miRNA Fingerprint and Endothelial Function in Myocardial Infarction: Comparison at Acute Event and One-Year Follow-Up.

MicroRNAs (miRNA) are major regulators of intercellular communication and key players in the pathophysiology of cardiovascular disease. This study aimed to determine the miRNA fingerprint in a cohort of 53 patients with acute myocardial infarction (AMI) with non-ST-segment elevation (NSTEMI) relative to miRNA expression in healthy controls (n = 51). miRNA expression was initially profiled by miRNA array in the serum of patients undergoing cardiac catheterization during NSTEMI (n = 8) and 1 year past the event (follow-up, n = 8) and validated in the entire cohort. In total, 58 miRNAs were differentially expressed during AMI (p < 0.05), while 36 were modified at follow-up (Fisher’s exact test: p = 0.0138). Enrichment analyses revealed differential regulation of biological processes by miRNA at each specific time point (AMI vs. follow-up). During AMI, the miRNA profile was associated mainly with processes involved in vascular development. However, 1 year after AMI, changes in miRNA expression were partially related to the regulation of cardiac tissue morphogenesis. Linear correlation analysis of miRNA with serum levels of cytokines and chemokines revealed that let-7g-5p, let-7e-5p, and miR-26a-5p expression was inversely associated with serum levels of pro-inflammatory cytokines TNF-α, and the chemokines MCP-3 and MDC. Transient transfection of human endothelial cells (HUVEC) with let-7e-5p inhibitor or mimic demonstrated a key role for this miRNA in endothelial function regulation in terms of cell adhesion and angiogenesis capacity. HUVEC transfected with let-7e-5p mimic showed a 20% increase in adhesion capacity, whereas transfection with let-7e-5p inhibitor increased the number of tube-like structures. This study pinpoints circulating miRNA expression fingerprint in NSTEMI patients, specific to the acute event and changes at 1-year follow-up. Additionally, given its involvement in modulating endothelial cell function and vascularization, altered let-7e-5p expression may constitute a therapeutic biomarker and target for ischemic heart disease.