Published online Jul 26, 2025. doi: 10.4330/wjc.v17.i7.106561
Revised: April 9, 2025
Accepted: June 16, 2025
Published online: July 26, 2025
Processing time: 143 Days and 18.3 Hours
Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mor
Core Tip: A multiple-marker approach integrating traditional and novel cardiac biomarkers enhances early detection, prognosis, and risk stratification of cardiovascular diseases. This narrative review highlights emerging biomarkers, their pathophysiological significance, and their potential role in improving diagnostic accuracy and personalized treatment strategies.
- Citation: Bokhari SFH, Umais M, Faizan Sattar SM, Mehboob U, Iqbal A, Amir M, Bakht D, Ali K, Hasan AH, Javed MA, Dost W. Novel cardiac biomarkers and multiple-marker approach in the early detection, prognosis, and risk stratification of cardiac diseases. World J Cardiol 2025; 17(7): 106561
- URL: https://www.wjgnet.com/1949-8462/full/v17/i7/106561.htm
- DOI: https://dx.doi.org/10.4330/wjc.v17.i7.106561
The industrial revolution witnessed a dramatic shift from physically demanding labor to sedentary lifestyles, fueled by consumerism and technology. This paradigm shift, characterized by extended work hours, lengthy commutes, and reduced leisure time for physical activity, has demonstrably contributed to the global rise in cardiovascular disease (CVD) prevalence. A confluence of factors, including physical inactivity and diets rich in calories, saturated fats, and sugars, fosters the development of atherosclerotic burden, metabolic syndrome, diabetes mellitus (DM), and hypertension - all cardinal features of patients with CVD[1]. From 1990 to 2019, the global prevalence of CVD has nearly doubled, with related deaths soaring from 12.1 million to a staggering 18.6 million[2]. Despite advancements in CVD management strategies, the disease remains one of the leading causes of mortality worldwide, exerting a substantial economic and societal burden[3]. Early detection is paramount for effective disease management, as timely diagnosis can significantly improve treatment efficacy, mitigate disease progression, and ultimately reduce the overall healthcare and socioeconomic burdens[4,5].
Current diagnostic limitations in the field of cardiology are significant. Conventional invasive techniques such as coronary angiography and cardiac catheterization, while remaining prominent, carry inherent risks of bleeding, infection, limited access, and substantial cost[6,7]. Non-invasive imaging modalities, such as computed tomography and magnetic resonance imaging, although less invasive, are often expensive and potentially less effective for early detection[8,9]. Ultrasound, while widely available, suffers from limitations in resolution and failure to detect minor abnormalities, potentially hindering the detection of subtle abnormalities[10]. This highlights the critical need for the development of improved diagnostic tools.
In 1989, the idea of biomarkers emerged as a way to pinpoint specific, measurable biological indicators. These markers help evaluate the health and physiology of the patient, particularly in terms of disease risk and diagnosis[11]. The concept of biomarkers has revolutionized medical diagnostics by providing objective measures for predicting disease develop
Traditional cardiac biomarkers, including C-reactive protein (CRP), uric acid, troponin (Tn), and natriuretic peptides like B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP), have been instrumental in clinical practice for decades[12,15]. However, despite their widespread use, these traditional biomarkers have limitations. The diagnostic capabilities of established biomarkers are often limited by their inability to fully account for residual risk. Consequently, the accuracy of high-risk group identification, disease diagnosis, management strategies, and disease course prediction can be compromised[16]. It has been observed that a significant proportion of at-risk patients remain undetected when relying solely on traditional risk factors for identification[17]. This observation has catalyzed the pursuit of novel biomar
The emergence of novel cardiac biomarkers aims to address these limitations and offer enhanced diagnostic precision and prognostic value. Recent research has explored several promising new biomarkers, such as gamma-glutamyltransferase (GGT) and microRNAs (miRNAs), which hold promise for improving CV risk prediction and disease management[15]. These novel biomarkers are being investigated for their extended half-life, stability, and ability to reflect the complex pathophysiological processes involved in CVD development[16]. By enhancing sensitivity and specificity, they may facilitate the early detection of cardiac diseases, leading to improved patient outcomes[12]. The integration of these emerging biomarkers into clinical practice is expected to refine risk stratification algorithms, enable the development of more personalized treatment approaches, and ultimately lead to better management of cardiac diseases[14]. The ongoing pursuit of novel cardiac biomarkers signifies a critical evolution in the field of cardiology, aiming to overcome the limitations of traditional markers and improve overall healthcare outcomes for patients with CV conditions.
This narrative review performs a critical analysis of the dynamically evolving landscape of novel cardiac biomarkers. It also investigates the application of a multi-marker approach to enhance the early detection, prognostic evaluation, and risk stratification of patients with CVDs. The review delves into the pathophysiological mechanisms and clinical utility of these emerging biomarkers. By synthesizing contemporary research findings and current clinical applications, the review aims to elucidate the transformative potential of novel biomarkers in revolutionizing the field of cardiology. It empha
The multimarker approach involves assessing multiple biomarkers simultaneously from blood or other body fluids. This method understands the intricate nature of heart diseases (HDs) and its various underlying pathologies, such as myocardial injury, issues with blood vessel lining, inflammation, and oxidative stress. By evaluating a broad spectrum of biomarkers associated with different aspects of HD, this technique seeks to enhance the accuracy of diagnosis and the ability to stratify risk[18]. This approach not only identifies individuals at high risk who might be missed otherwise but also aids in the early intervention and treatment to decelerate cardiac disease progression[19]. By examining biomarkers related to stress, oxidative stress, endothelial dysfunction, inflammation, and myocardial damage, it provides valuable insights into the underlying pathological processes, allowing for tailored treatment strategies targeting specific mecha
Abboud et al[24] stated that a multimarker panel comprising NT-proBNP, hs-TnT, and insulin-like growth factor binding protein 7 offers valuable clinical, diagnostic, and prognostic insights for patients with acute dyspnea. They noted that variations in the number of elevated biomarkers at presentation could enhance clinical risk stratification for short-term mortality and HF rehospitalization. Similarly, various other studies have been conducted that state how hyper
Multiple biomarkers are valuable not only in detecting existing diseases but also in predicting the first CV event and death. In a study of about 3000 individuals followed up to 10 years, researchers evaluated the predictive value of 10 biomarkers for death and major CV events[27]. The most informative biomarkers for death were BNP, CRP, Hcy, renin, and the urinary ACR. BNP and the urinary ACR were most predictive for major CV events. High multimarker scores indicated a fourfold increased risk of death and nearly double the risk of major CV events compared to low scores. However, these biomarkers only moderately improved risk prediction over conventional factors, highlighting both the potential and limitations of the multimarker approach (Table 1).
| Biomarker | Pathophysiological role | Clinical application | Associated CVDs |
| MicroRNAs (miR-1, miR-133a, miR-208b, miR-499) | Gene regulation, myocardial injury & fibrosis | Diagnosis & prognosis, especially in MI and HF | MI, HF, HCM, CAD, myocarditis |
| Long non-coding RNAs (CHAST, MHRT) | Cardiac hypertrophy, fibrosis, gene expression | Biomarker & therapeutic target | HF, atherosclerosis, CAD |
| ST2 (soluble ST2) | Inflammation, fibrosis, IL-33 pathway | Prognosis, particularly in HF | HFpEF, HFrEF |
| Heart-type FABP | Myocardial injury, lipid metabolism | Early MI detection, prognosis in CAD & CKD | MI, CAD, CKD |
| Galectin-3 | Fibrosis, inflammation | Diagnostic and prognostic utility | HF, congenital heart disease, AF |
| OPG | Vascular calcification, inflammation | Risk stratification, prognostication | CAD, AMI, HF, atherosclerosis |
| GDF-15 | Inflammation, fibrosis, cellular stress | Prognostic tool, especially in MI and HF | MI, HF, PH, AF |
| MMP-2/MMP-9 | ECM remodeling, plaque rupture | Risk stratification, disease progression | ACS, HCM, KD, Chagas disease |
| OPN | Inflammation, fibrosis | Diagnostic and prognostic biomarker | HFpEF, myocarditis, CAD, RV failure |
| Adrenomedullin & copeptin | Vasodilation, fluid regulation | Early MI detection, HF prognosis | MI, HF, HTN |
| MPO | Oxidative stress, neutrophil activation | Prognosis, inflammation indicator | HF, MI, AF, cardio-oncology |
| PTX3 | Acute-phase response, inflammation | Early CVD detection, ACS diagnosis | MI, atherosclerosis |
| Placental growth factor | Angiogenesis, inflammation | MI prognosis, vascular remodeling | ACS, MI, CAD |
| EMP | Endothelial dysfunction, inflammation | Surrogate for vascular injury, prognosis | CAD, SIRS, stroke |
| ET-1 | Vasoconstriction, hypertrophy | Risk prediction, prognosis in HF | HF, CAD, MI, PAH, HTN |
| NRG-1 | Cardiomyocyte survival, angiogenesis | Prognostic and therapeutic implications | HF, MI, CAD |
| NGAL | Inflammation, renal dysfunction | Risk stratification in HF and MI | HF, MI, CRS |
| Cystatin C | ECM remodeling, renal marker | Predictor of MACE, mortality | MI, HF, metabolic syndrome |
| ADMA/SDMA | Nitric oxide inhibition, endothelial dysfunction | Prediction of MACE and CAD risk | MI, HF, HCM, CAD |
| Uromodulin | BP regulation, renal protection | Prognostic marker, especially in males | HF, CAD, CKD |
| sLOX-1 | Inflammation, plaque instability | Early diagnosis of ACS, CVD risk prediction | MI, CAD, psoriasis-associated CVD |
| AGEs | Oxidative stress, inflammation | Prognosis and early detection, especially in diabetes | HF, CAD, T2DM-related CVD |
The multiple-marker approach enhances sensitivity and specificity by integrating diverse pathophysiological indi
miRNAs are a group of non-coding, small RNAs (19 to 21 nucleotide-long oligonucleotides) that are endogenously produced from their genes. miRNAs interfere with or affect the transcription or translation of other genes, resulting in gene silencing or activation by a process known as RNA interference or RNA activation, respectively[28]. The miRNAs function as gene regulators that exert their function post-transcriptionally, which distinguishes them from classical epigenetic factors (e.g., DNA methylation, acetylation) that regulate gene expression at the chromatin level[29]. Their involvement in CVDs has particularly sparked interest due to their potential as diagnostic and prognostic biomarkers.
In the context of CV health, miRNAs have been extensively studied for their role as biomarkers, reflecting both normal physiological conditions and pathological states. Circulating miRNAs have shown promise in diagnosing MI and HF, two prevalent conditions with significant morbidity and mortality rates worldwide[30,31]. These miRNAs are released into circulation from cardiac tissues and other cells under stress or injury, making them accessible and detectable biomarkers for cardiac injury and dysfunction[32]. They play a crucial role in CVDs by regulating various pathological processes and serving as promising biomarkers for diagnosis and prognosis. In type 2 DM (T2DM) and coronary artery disease (CAD), dysregulated miRNAs such as miR-92a are elevated, correlating with increased CAD risk, making them potential prog
The miRNAs are detectable not only in cardiac tissue but also in circulating blood, enabling less invasive diagnostic tests. For instance, miR-1, miR-133a, miR-208, and miR-499 are abundantly expressed in cardiac tissue and are critical in cardiogenesis and myocardial function; their dysregulation is associated with various HDs, including acute MI (AMI)[29]. In AMI, specific miRNAs such as miR-133a and miR-208b exhibit higher expression levels, particularly in ST-elevation MI (STEMI) cases, highlighting their potential as diagnostic markers[29]. Furthermore, miRNAs like miR-21, miR-22, and miR-132 are implicated in HF pathophysiology, correlating with disease severity and New York Heart Asso
Long non-coding RNAs (lncRNAs) have emerged as pivotal regulators in CVD, offering diverse roles as diagnostic and prognostic markers across various conditions. Initially dismissed as transcriptional noise, lncRNAs are now recognized for their regulatory functions in gene expression and cellular processes crucial to cardiac health[35]. In HF, specific lncRNAs such as cardiac hypertrophy-associated transcript (CHAST) and myosin heavy-chain-associated RNA tran
In CAD, the lncRNA CoroMarker demonstrates promise as a stable plasma biomarker, distinguishing patients with CAD from controls based on differential expression in plasma and monocytes[39]. This underscores the potential utility of lncRNAs in non-invasive diagnostic strategies for CVDs. Diabetic vascular complications further illustrate the multi
Suppression of tumorigenicity 2 (ST2), initially identified as an “orphan” receptor in 1989, is a family of interleukin 1 (IL-1) receptors. It is encoded by the ST2 gene, which is present on chromosome 2 and is part of the IL-1 gene cluster. ST2 exists in two forms in the body: A cellular form called ST2 ligand (ST2L) and a soluble form (sST2) that has no trans-membranous or cytoplasmic domain. These two forms exist because of alternate splicing of ST2 mRNA. ST2 is the receptor for IL-33. When IL-33 binds to ST2L, the ST2L/IL-33 complex produces cardioprotective effects such as pre
Cardiac TnT (cTnT) has emerged as a cornerstone biomarker in CV medicine due to its sensitivity and specificity in detecting myocardial injury. Defined by concentrations above the 99th percentile upper-reference limit of a healthy cohort, cTnT serves as the preferred biomarker for identifying myocardial injury[51]. Its clinical utility extends beyond acute conditions to encompass chronic CV risks, making it invaluable in prognostic and diagnostic applications. The elevated levels of cTnT, particularly assessed using high-sensitivity assays (hs-cTnT), has been associated with increased incidence of HF, independent of traditional risk factors such as early menopause[52]. Moreover, hs-cTnT levels predict major CV events across a spectrum of left ventricular EFs (LVEFs), highlighting its role in risk stratification and manage
In population studies, hs-cTnT has demonstrated its predictive power in incident CAD, emphasizing its value in preventive medicine and population health strategies[54]. This biomarker also facilitates the efficient evaluation of patients with acute chest pain, where historical data combined with initial levels aid in rapid ruling out of MI[55]. Fur
H-FABP, also known as FABP-3, plays a crucial role as a cardiac biomarker due to its specific distribution in cardiac myocytes and its rapid response to myocardial injury. Initially identified as a member of the lipid-binding protein superfamily, H-FABP functions in both membrane-bound and cytoplasmic forms, facilitating the intracellular transport of long-chain FAs essential for cardiac metabolism[59].
H-FABP has garnered attention for its diagnostic utility in detecting early MI. Studies highlight its superiority over traditional markers like creatinine kinase-MB (CK-MB) and high-sensitivity CRP in providing sensitive and prognostic information for young patients experiencing MI[60]. Its rapid release into circulation from cardiomyocytes following ischemic damage makes it particularly effective for early diagnosis and monitoring of myocardial injury[60]. In the con
Moreover, the combination of H-FABP with hs-TnT in a dual marker approach has shown promise in enhancing diagnostic accuracy for AMI in emergency settings, reducing the need for serial testing and expediting patient manage
Galectin-3 (Gal-3), a β-galactoside-binding lectin encoded by the LGALS3 gene on chromosome 14, plays multifaceted roles in inflammation, fibrosis, and tissue repair within the heart. The diverse body of research surrounding Gal-3 underscores its potential as both a diagnostic and prognostic marker in various cardiac conditions[64].
Gal-3 has been implicated in myocardial fibrosis, a key factor in cardiac remodeling and HF progression[65,66]. Studies have consistently showed elevated Gal-3 levels in patients with chronic HF (CHF), indicating its potential utility in diagnosing and monitoring this condition[67,68]. Its role extends beyond diagnosis; Gal-3 levels have also been associated with predicting outcomes in congenital HDs, where higher levels correlate with an increased risk of adverse cardiac events (CEs) post-surgery[69]. This predictive ability highlights Gal-3 as a tool for stratifying patient risk and guiding therapeutic interventions early in disease progression. Furthermore, Gal-3 shows promise in identifying cardiac dys
In the clinical context, Gal-3 has been explored as a potential marker for complications post-cardiac surgery, particularly in predicting atrial fibrillation (AF) development. While current evidence suggests its association with AF occurrence, further research is needed to solidify its prognostic role in this context[70]. The mechanistic insights into the involvement of Gal-3 in cardiac pathology underscore its potential as a therapeutic target. Studies have demonstrated that Gal-3 inhibition could mitigate adverse cardiac remodeling and improve outcomes in HF models, suggesting a dual role as both marker and therapeutic avenue[65]. However, challenges remain, particularly regarding its specificity in certain clinical scenarios. For instance, Gal-3 has shown limitations as a marker of acute cardiac damage in patients with polytrauma[71], emphasizing the need for further refinement in its clinical application.
Osteoprotegerin (OPG), known for its role in bone protection, is encoded by the tumor necrosis factor (TNF) receptor superfamily member 11b (TNFRSF11B) gene. OPG belongs to the TNF receptor superfamily and is also referred to as an osteoclastogenesis inhibitory factor[73]. In clinical research, elevated OPG levels have consistently correlated with markers of inflammation, endothelial dysfunction, oxidative stress, and CVD[73]. This association underscores the potential utility of OPG in diagnosing and monitoring CV pathologies, ranging from stable CAD to AMI. Studies have demonstrated that higher plasma OPG levels predict adverse CV events, including all-cause death, CV death, and HF hospitalization in patients with CAD, suggesting its role in risk stratification and prognosis[74].
Moreover, OPG levels have shown promise in acute settings such as AMI, where they not only aid in identifying AMI in patients presenting with acute chest pain but also correlate with the severity of coronary artery occlusion and predict mortality risk during hospitalization[75]. This dual diagnostic and prognostic capability highlights OPG's potential for guiding acute clinical management and post-event prognostication. Beyond acute conditions, OPG has been implicated in chronic CV risks. Meta-analyses have linked higher OPG levels with an increased risk of coronary artery calcification, a marker of early atherosclerosis and CV risk[76]. This finding suggests that OPG could serve as a tool for early detection and intervention in individuals prone to developing CVD.
In both HFrEF and HF with preserved EF (HFpEF), OPG levels have demonstrated associations with disease severity and outcomes. In HFrEF, elevated OPG correlates with arterial stiffness, a critical factor in disease progression and CV morbidity[77]. Similarly, in patients with CKD in the pre-dialysis stage, OPG elevation is linked to LV diastolic dysfunc
Growth differentiation factor 15 (GDF-15), a member of the transforming growth factor-beta superfamily, is encoded by the GDF15 gene and is involved in various physiological and pathological processes within the CV system[81]. In HF, GDF-15 has shown promising utility as an independent predictor of all-cause mortality, offering valuable prognostic information beyond traditional risk factors[82]. Its ability to stratify risk in patients with post-MI for both HF and mortality underscores its potential in enhancing clinical decision-making and patient management[83]. Additionally, GDF-15 plays a crucial role in assessing myocardial fibrosis, particularly in conditions like AF and rheumatic HD. Elevated levels of GDF-15 have been associated with the development and maintenance of atrial fibrosis, suggesting its use as a novel biomarker for evaluating fibrotic remodeling in these patient populations[84]. In acute settings such as AMI, high levels of GDF-15 have been linked to increased risk of major adverse CEs (MACEs) and sudden cardiac death (SCD) within the first 24 hours of incident MI[85,86]. This rapid prognostic insight highlights the potential of GDF-15 for early risk stratification and intervention in acute cardiac care.
Furthermore, GDF-15 demonstrates its versatility across systemic conditions beyond HF and MI. In pulmonary hypertension (PH), it serves as a biomarker of right ventricular (RV) dysfunction, aiding in the assessment of disease severity and progression[83]. Combining GDF-15 with other biomarkers like sST2 has been proposed to enhance pre
Matrix metalloproteinases (MMPs) constitute a family of protease enzymes crucial for the maintenance of extracellular matrix (ECM) integrity and are involved in various physiological and pathological processes in CVDs. Structurally, MMPs feature a conserved catalytic zinc-binding domain essential for their enzymatic activity, which operates optimally at neutral pH[90]. In HCM, MMP-2 plays a pivotal role in cardiac remodeling. Activation of MMP-2 contributes to myocardial hypertrophy and fibrosis, exacerbated by chronic inflammation and oxidative stress. This process leads to detrimental effects on cardiac function, including decreased contractility and increased susceptibility to arrhythmias[91]. MMP-2 levels in patients with HCM reflect the severity of ECM remodeling and serve as a potential biomarker for disease progression and therapeutic response monitoring[91]. Similarly, in hypertrophic obstructive cardiomyopathy (HOCM), altered MMP-2/tissue inhibitor of MMP-1 (TIMP-1) ratios are indicative of myocardial remodeling due to microvascular rarefaction. These ratios independently predict adverse outcomes in HOCM, highlighting their role in ECM dysregulation and subsequent cardiac dysfunction[92].
In ACS, MMP-9 emerges as a significant biomarker associated with plaque instability and rupture. Elevated MMP-9 levels correlate with increased risk of adverse CV events post-ACS, underscoring its utility in risk stratification and clinical management[93]. MMPs also contribute to the pathogenesis of Kawasaki disease (KD), where MMP-2 and MMP-9 levels are elevated in patients with coronary artery lesions. The upregulation of MMPs in KD suggests their involvement in vascular inflammation and remodeling, thereby serving as potential diagnostic markers for disease progression and treatment efficacy[94]. Furthermore, MMPs are implicated in chronic conditions like Chagas disease cardiomyopathy, where MMP-2 and MMP-9 levels, along with Gal-3 and TIMP-2, reflect disease severity and prognosis. Elevated Gal-3/TIMP-2 expression correlates with progression to the cardiac form of Chagas disease, highlighting their role as prognostic biomarkers[95].
In the context of HF, MMP-2 is associated with ECM remodeling dynamics after a heart transplant. Elevated MMP-2 levels correlate with adverse hemodynamics and pulmonary vascular disease, indicating its potential as a marker for disease severity and therapeutic response in patients with HF[96]. Moreover, MMPs contribute to atherosclerosis by promoting ECM degradation and smooth muscle cell migration, thereby influencing plaque stability and vulnerability to rupture. MMP-1, MMP-7, and MMP-12 are potential biomarkers for coronary artery calcification and atherosclerotic plaque instability, emphasizing their role in CV risk assessment and management[97,98].
Osteopontin (OPN), initially recognized for its pro-inflammatory actions, functions as a matricellular protein of the ECM, susceptible to proteolytic cleavage by ECM-associated proteases[99]. In inflammatory HDs like myocarditis, OPN expre
Interestingly, OPN demonstrates diagnostic potential even in patients with low CV risk factors, independently associating with CAD. This unexpected finding underscores the pleiotropic activities of OPN beyond traditional risk factors, suggesting its utility as a novel biomarker for CAD risk assessment[102]. In victims of SCD with DM and HFpEF, OPN levels are significantly elevated alongside related proteins like low-density lipoprotein (LDL) receptor (LDLR) and fibronectin-1, implicating OPN in the pathological processes of diabetic HD. This supports OPN's role as a diagnostic marker for specific cardiac phenotypes associated with metabolic disorders[103]. Furthermore, OPN serves as a biomar
In atherosclerotic vascular disease, OPN acts as a multi-modal marker and mediator, influencing the progression of atherosclerosis through its interactions with integrins and participation in plaque development[105]. Additionally, OPN levels above 38.25 ng/mL are proposed as an early diagnostic marker and independent predictor of PH in patients with chronic obstructive pulmonary disease and concomitant ischemic HD, highlighting its role in cardiopulmonary diseases[106]. Moreover, OPN shows promise as a prognostic marker for LV hypertrophy regression following surgical aortic valve replacement, indicating its potential in predicting post-operative outcomes and therapeutic response[107].
Adrenomedullin (AM) is a peptide molecule that was first discovered by Kitamura et al[108] in 1993 when he was studying a tumor called pheochromocytoma located in the adrenal medulla. MR-proAM plasma concentrations can also be used as biomarkers to screen for the hypertrophy of cardiac ventricles in patients of hypertension and estimate the severity of MI as well post- recovery complications[108-115]. As discussed previously, AM has its therapeutic potential limited due to physiological properties, but studies have shown that intravenous infusion of AM is associated with improved LV function, increased heart rate (HR), and cardiac output (CO), and decreased pulmonary and systemic blood pressure levels[111,116]. Similarly, sacubitril, which is an inhibitor of neprilysin, can be used to increase the levels of AM in patients with HF[110-121]. Studies have shown that copeptin levels rise quickly in AMI even when cTnT levels are undetectable. Moreover, cTnT cannot differentiate between ischemic and non-ischemic causes of chest pain, and a rise in copeptin is not related to the necrosis of myocytes. Hence, copeptin can be added with cTnT to improve the accuracy of AMI diagnosis or to exclude it. Similarly, copeptins can also be used as a prognostic indicator in patients with HF, as higher levels are associated with an increased rate of hospitalization and mortality. Copeptin can augment the role of BNP and NT-proBNP, as its levels are not related to age[119-136]. The levels of BNP can also be used to estimate LV dysfunction, which can supplement the diagnosis of this condition by echocardiography as the level of 75 pg/mL was 98% specific for the diagnosis of LV dysfunction by echocardiography or in some cases may rule out the need for echocardiography altogether[137-141]. Additionally, the soluble cluster of differentiation (CD) ligand (sCD40L) levels in smokers are greater than healthy individuals during the acute stages of MI, putting smokers at a greater risk of developing thrombotic complications[142]. This increase can be alleviated by timely administration of glycoprotein llb/Illa antago
Myeloperoxidase (MPO) is a heme-containing peroxidase enzyme, which is mainly released by the activated neutrophils, monocytes and macrophages. Under normal conditions, it present in lysosomes where it is responsible for the breakdown of phagocytosed microbes by production of hypohalous acid and hypochlorous acid. Hence, it is an important component of cell immunity, and its deficiency results in immune deficiency. When it is released from these cells, it is sequestered in the ECM. Here it is responsible for producing reactive oxygen species (ROS)-mediated damage to tissues[143-145]. Similarly, MPO and underlying neutrophil activation were also implicated in AF due MPO-mediated modification of proteins and fibrosis of myocytes, both of these are associated with AF. Pericardial MPO is also involved in prediction the post-operative AF[1]. The role of MPO in HF has also been studied extensively. Hage et al[143] reported that increased plasma levels of MPO were found in patients of HF with HFpEF showing oxidative stress to be involved in underlying mechanism in the disease. Other studies have reported that MPO is related to HFrEF. In the domain of cardiac oncology, MPO can add to Tns in the estimation of negative outcomes. Administration of doxorubicin and trastuzumab is asso
Pentraxin-3 (PTX3) is a member of the long PTX family, which is part of the PTX superfamily and also includes PTX4, neuronal PTX1, neuronal PTX2, and neuronal PTX receptor. It is encoded by the PTX3 gene, which is located on chromosome 3q25. The PTX3 gene contains three exons and produces a 381-amino acid sequence, which includes a long signal peptide of 21 amino acids. The carboxy terminal region of PTS, including short PTXs like CRP and serum amyloid P, contains the characteristic PTX signature pattern of amino acids (HxCxS/TWxS) that is common to all PTXs. Conversely, the amino terminal region of long PTXs (such as PTX3) is distinct and unrelated to the C-terminal PTX domain or other known protein structures.
Similar to other PTXs, PTX3 primarily exists as a multimer, specifically an octamer, where individual molecules are linked by disulfide bonds. Unlike short PTXs, which are produced exclusively in the liver under the influence of IL-6, PTX3 is produced in a wide variety of cells including fibroblasts, and epithelial, endothelial, mesangial, and smooth muscle cells under the influence of IL-1β, TNF-α, and microbial components[154-162]. De Jager et al[163] reported that increased levels of macrophage inflammatory protein 1 alpha are associated with ACS such as MI; hence, it can also be used as a diagnostic marker. It is an acute phase protein that is present in many mammals including humans. The principal site of its production is hepatocytes[164-169]. The concentration of serum amyloid A (SAA) in circulation is remarkably increased during the inflammatory process and endothelial injury[170]. During the acute phase response, the concentration of SAA can increase by up to 1000 times within 24 hours[168]. It may also promote thermogenesis and atherothrombosis. Its increased levels at the site of coronary occlusion indicate that it may be produced by cells of the atherosclerotic vessel wall or white blood cells trapped in the thrombus[171]. Acute infections can produce fast inflammation in the coronary arteries. This potentially results in plaque rupture and the development of ACS[172]. As SAA has pro-inflammatory properties it is suggested to play a role in these conditions.
Recently, investigations have been conducted to predict the diagnostic role of SAA in the early detection of cardiac disease. There is a positive link between SAA and ACS, as well as several cardiac disorder risk factors including meta
A clinical study comparing CRP and SAA concluded that a higher SAA concentration is related to worse 30-day outcomes in patients with NSTEMI-ACS, indicating that SAA is a stronger predictor of clinical outcome than CRP in these patients[175]. A large cohort study on individuals with high CV risk showed that SAA concentration was significantly correlated with all-cause and CV mortality. It was also established that high SAA was not only correlated with CVD but also with its risk factors such as CAD, DM, smoking, aging, and kidney impairment[176]. Thus, the positive association of SAA concentration with various cardiac diseases hints at the diagnostic value of SAA. It can play a pivotal role as a biomarker for early diagnosis and the risk stratification of heart ailments.
Placental growth factor (PlGF), a polypeptide hormone, is essential for immunological response, vascular homeostasis, angiogenesis, and cellular metabolic activities. It promotes angiogenesis and encourages the growth and survival of endothelial cells[177,178]. PlGF is a member of the vascular endothelial growth factor family and is predominantly expressed in the placenta. Other sources include cardiac and lung tissues. Various factors such as hypoxia-inducible factor 1, nuclear factor kappa B (NF-kB), nitric oxide (NO), inflammation, and oxidation stress control the expression of this polypeptide. PlGF plays a significant role in the regulation of hypertrophy[179]. It is also involved in the processes of angiogenesis and arteriogenesis[180]. Increasing concentrations of PlGF have been linked to vascular inflammation and a worse prognosis in patients with ACS[181]. Hypoxia and cardiac damage cause PlGF production. This causes increased angiogenesis, atherosclerotic plaque formation, and inflammation (by monocyte induction to produce IL-1 and TNF-α). These factors, along with coronary artery spasm and plaque rupture, lead to MI with non-obstructive coronary arteries[180].
Current findings have also shown that PlGF levels rise rapidly in patients with MI. The blood concentration of this protein also has a reported positive correlation with LV function improvement[182]. A clinical trial found reduced myocardial work in asymptomatic heavy alcoholics, and showed that global work efficiency was inversely correlated with PlGF (β = 0.493, 95% confidence interval [CI]: 1.010-0.230, P = 0.004). It was concluded that PlGF may play a role in alcohol-induced cardiac dysfunction[183]. A study demonstrated a significant association between PlGF and ACS, particularly unstable angina (OR = 0.78, 95%CI: 0.64-0.94, P = 0.008) and MI (OR = 0.83, 95%CI: 0.72-0.95, P = 0.007) and suggested that it is a potential biomarker of ACS[184]. Other studies have also suggested PlGF as a significant predictor for CVD. PlGF levels have been found to be significantly higher in patients with CVD compared to healthy individuals[185]. A prospective cohort study demonstrated that a 1-standard deviation increase in the natural logarithm of PlGF concentration increased CVD mortality by 21%. It was inferred that it can be an independent prognostic factor for 10-year CVD mortality in that general population[186]. Overall PlGF can be a useful diagnostic biomarker for all-cause mortality and non-fatal MI in ACS cases. It has proven predictive value in short-term and long-term follow-up studies[187,188].
Endothelial activation and dysfunction play a significant role in atherosclerosis and CVD including CAD, carotid artery disease, peripheral artery disease, and ischemic stroke[189,190]. Recently, there has been growing evidence that endo
EMPs affect endothelial function by releasing vasoactive compounds, controlling vascular tone, and regulating permeability, angiogenesis, vascular remodeling, and hemostasis. Thus, it is implicated in different CVDs[191]. They carry endothelial proteins such as cadherin and adhesion molecules, which may be recognized by the presence of certain cell surface CD proteins. These cell surface antigens are identified using particular antibodies and are frequently dis
The commonly studied cell surface antigens are CD31, CD62e, and CD144. Present data support the concept that the CD31+ EMP is a sensitive marker for CAD[202]. In one study, CD144+ EMPs were analyzed using a flow cytometer in samples obtained with 1500 g, 3000 g, and 3000 g post protocols. The modified protocol produced 5-fold more CD144+ EMPs than the standard protocols and 3000 g. In the 3000 g post protocol group, patients with CAD had levels that were 30%-40% higher than healthy controls. However, there was no significant difference in 1500 g post EMP (CD144+). These findings indicate that new MPs might serve as a biomarker for vascular damage in patients with CAD and provide a distinctive therapeutic target in CAD[203]. EMP can also serve as biomarkers of inflammatory response after sutureless valve implantation because increased circulating EMPs has been linked to triggering systemic inflammatory response syndrome (SIRS). A clinical study reported that after 24 hours of surgery, the plasma levels of EMP (MP CD31+, CD42b-, CD144+) increased significantly compared to preoperative levels, which indicated the development of SIRS[204]. Hence, it has been proposed that assessing EMP levels as biomarkers might be a simple and useful technique to measure endothelium function. This may aid in early diagnosis and patient stratification with various CVDs[191,193,205,206].
Endothelins (ETs) belong to a family of polypeptides containing 21 amino acids. This family consists of three members: ET-1, ET-2, and ET-3. These isoforms are encoded separately by different genes. Of these, ET-1 is the most studied, most abundant, and most potent vasoconstrictor[207-210]. It is produced from a propeptide called big ET-1. ET-1 is transcribed from the gene, Edn1, which is present on chromosome 6[211]. Furthermore, ET-1 is the only member produced by endothelial cells. It is an autocrine/paracrine hormone with a short plasma half-life of less than 2 minutes[212]. Other than endothelial cells, it can also be produced from various cell types including cardiac myocytes, vascular smooth muscle cells, renal epithelial cells, inflammatory cells, neurons, and hepatocytes[212]. It acts on three receptors, namely, ETA, ETB, and ETC. ETA receptors are located in vascular smooth muscle tissue and produce vasoconstriction. ETBs are found in the lining of blood vessels and are linked to the release of vasodilators such as NO and prostacyclin. The role of ETC is currently being investigated[213].
ET-1 plays many roles in the body, namely, vasoconstriction, maintaining vascular tone, controlling ion transport in the gut, and recruiting immune cells to sites of inflammation[214]. It controls the overall basal tone of the systemic, coronary, and pulmonary vasculature and imparts vascular resistance. It also has mitogenic actions, which promote vascular smooth muscle growth heart enlargement and myocardial fibrosis. Also, ET-1 levels may be associated with CV re
ET-1 levels have been studied in various CVDs including hypertension, atherosclerosis, HF, CAD, AMI with LV systolic dysfunction, HCM, DCM and pulmonary arterial hypertension[215,217,218]. A recent clinical trial analyzed the diagnostic value of ET-1 along with other factors for CAD. They found that ET-1 was very reliable for the diagnosis of CAD with a sensitivity of 1.0 and specificity of 0.8[219]. In an investigation of about 3048 patients with HFrEF were analyzed for clinical outcomes correlation with their ET-1 levels. Interestingly, those with high concentrations of ET-1 were independently associated with the worst outcomes (CV death or worsening HF) and rapidly declining kidney function[220]. An analytic observation study with a cohort design was conducted to assess ET-1 as a predictor of MACE in 63 patients with chronic coronary syndrome (CCS) undergoing coronary intervention. The authors determined that ET-1 successfully detected MACE occurrence with a sensitivity of 83.3%, specificity of 75.4%, and accuracy of 76.2% and concluded that it can be utilized effectively to predict MACE in patients with CCS receiving coronary intervention. Furthermore, Big ET-1 has a high concentration and longer half-life and has also recently been used to predict various CV ailments. Recent findings have demonstrated the independent association of increased Big ET-1 levels with LV reverse remodeling, prognosis in patients with DCM, and poor short-term outcomes in patients with acute decompensated HF[218,221]. Hence both ET-1 and big ET-1 can be used as biomarkers for early prediction, prognosis, and risk stratification.
Neuregulin-1 (NRG-1) is a member of the epidermal growth factor family. It is secreted by the proteolytic cleavage from endothelial cells in the microvasculature of multiple tissue types including the myocardium[222-225]. It is released in response to inflammation, adrenergic stimulation, ischemia, and oxidative stress. Its production occurs through the tran
Various studies have been conducted on NRG-1 that have shown its various beneficial prospects. NRG-1 has been proven to alleviate HF in multiple animal models and is currently being investigated as a possible therapy in a Phase 3 clinical trial[236,237]. Ebner et al[238] discovered that remote injection of recombinant NRG-1β protected the heart against early reperfusion damage without altering hemodynamics. Hedhli et al[239] found that NRG-1 secreted by endothelial cells is essential for arteriogenesis and angiogenesis, and that exogenous NRG-1 can boost both processes. Haller et al[240] analyzed the relationship between NRG-1 and STEMI. A small RCT showed that NRG-1 plasma levels dropped considerably after percutaneous coronary intervention (PCI)/remote ischemic conditioning and remained low for up to 1 month after MI. They concluded that NRG-1 may be independently influenced by MI.
Hage et al[241] examined the plasma levels of NRG-1 in 86 patients with HFpEF, 86 patients with HFrEF, and 21 healthy volunteers. The NRG-1 levels in the healthy persons were higher 29.0 ng/mL (23.1-24.3 ng/mL) than the 3.6 ng/mL (2.1-7.6 ng/mL) in the HFrEF group and the 6.5 ng/mL (2.1-11.3 ng/mL) in the HFpEF group. They observed that higher NRG-1β was associated with worse outcomes in HFrEF, regardless of ischemia. However, In HFpEF, in patients with ischemia (patients with CAD), higher NRG-1β was associated with worse outcomes, while better outcomes were associated with NRG-1β levels in cases without ischemia. The levels of NRG-1β were low in ischemic HFpEF and HFrEF, while they were high in non-ischemic HFpEF as a compensatory cardioprotective mechanism[241]. A statistically signi
Neutrophil gelatinase-associated lipocalin (NGAL), also called human neutrophil lipocalin, is a 25-kDa acute-phase protein with 178 amino acids. It was first derived from human neutrophils. It may be synthesized in the bone marrow and stored in mature neutrophil granules[247-249] and other cell types such as endothelial cells, hepatic cells, cardiomyo
NGAL plays a role as an inflammatory modulator and early and sensitive marker of acute kidney injury[255-258]. Moreover, it plays a role in apoptosis, carcinogenesis, cell differentiation, and proliferation. Its concentration increases considerably in conditions involving damage to epithelial cells like acute and chronic renal disorders, following cardiac procedures, CVD, cancer, and contrast-induced nephropathy[259]. It can be assessed in urine and plasma. NGAL can be found in arterial plaques, injured myocardium, and atherosclerotic plaques[260,261].
The severity of CAD is correlated with elevated plasma NGAL levels[262]. It has been observed that patients with AMI have increased plasma NGAL levels[263]. NGAL levels are higher in compensatory cardiomyocytes following MI in an animal investigation[264]. Urinary NGAL levels in the early phase of AMI can be used to efficiently predict it[265]. In recent research, individuals with STEMI had considerably greater NGAL levels than those with stable angina or control participants[266]. Higher NGAL concentration can be correlated with inflammation-related cardiac injuries, as there is evidence of increased NGAL expression following inflammatory stimuli[264,267,268], which can indicate a decline in renal function in acute HF (AHF) and thus is a significant predictor of poor clinical outcomes. The prognostic mortality factor is higher than cystatin C (CysC) levels and estimated GFR (eGFR) in patients with HF, both with and without chronic renal disease[267,269]. Another study analyzed 177 people with major adverse cardiac and cerebrovascular events (MACCE). They found that elevated serum NGAL concentrations were significantly related to the risk of MACCE[270]. Phan et al[271] studied 139 patients with AHF and concluded that elevated plasma NGAL concentrations along with raised creatinine levels could predict the onset of cardiorenal syndrome type 1. In short, NGAL has been related to different cardiac diseases and is proven to be a reliable biomarker of these CV events.
CysC is a protein containing 122 amino acids. It is an endogenous cysteine protease inhibitor. It is encoded by the CST3 gene. It is an effective inhibitor of lysosomal proteinases. Almost all nucleated cells in mammals produce CysC. In humans, it is present in body fluids and tissues[272]. It is a low molecular weight protease (13 kDa) that is freely filtered by the glomeruli and reabsorbed and metabolized by proximal tubules[273]. CysC plays an important role in the regu
Classically, CysC had been used for estimation of renal function. Recently, there has been an increasing trend among researchers to evaluate its implications in CVD. Many epidemiologic studies have demonstrated that the increased circulating CysC levels were related to worse outcomes in patients with ACS[276-280]. Rothenbacher et al[281] found out that CysC-based CKD provides accurate risk estimation and better prognostic value for CVD as compared to creatinine. Another study observed that CysC is an efficient predictor of MACE. MACE includes MI, death from CV reasons, and hospitalization due to HF[282]. Wasyanto et al[283] determined that CysC can identify MACE with 80.0% sensitivity, 86.7 specificity, and 85.0% diagnostic by setting the cut-off point at 1.21. They concluded that CysC levels are independent predictors of MACE in patients with AMI without cardiogenic shock or renal impairment following PCI. Song et al[284] assessed CysC for the predictor of long-term, all-cause, and CV mortality in United States adults with metabolic syndrome. During the median follow-up of 15.3 ± 5.4 years, they observed that CysC had the highest predictive efficacy for mortality outcomes, followed by eGFR, which surpassed urea nitrogen, creatinine, uric acid, and CRP. CysC alone had a significant predictive value for all-cause and CVD mortality. When it was combined with age, its predictive value further increased. It was inferred that patients with metabolic syndrome with higher CysC levels are at greater risk of all-cause, CVD, and cancer death. CysC may help predict metabolic syndrome all-cause and CVD mortality[284].
The eGFR calculated with cystatin (eGFRcys) has a strong and more linear correlation with CV outcome and mortality[285]. It can predict the risk of CVD efficiently even before the appearance of clinically significant CKD. It can identify CVD at eGFRcys < 90 mL/minute/1.73 m2[285]. Thus, both the eGFR and traditional biomarkers should be used in clinical settings together to improve risk prediction and primary CVD prevention.
Symmetric dimethylarginine (SDMA) is a derivative of L-arginine formed by the posttranslational methylation of argi
These are known to be markers of renal function and progression of CVD. ADMA is known to be associated with atherosclerosis and CVD. High levels of circulating SDMA plasma levels are a risk factor for renal diseases and may also be associated with CVDs[292-296]. ADMA predicts future lesions, MI, and stroke[297]. A study found that cases with cardiometabolic diseases had higher ADMA and SDMA concentrations and decreased citrulline levels compared to healthy controls[298]. A study examined the predictive capacity of ADMA and SDMA for hospital and 3-month mortality in patients with AHF. They discovered a significant positive association between ADMA and SDMA concentrations and hospital and 3-month mortality. Their concentrations were further increased by venous volume overload in patients with AHF[299].
In one study, the plasma concentrations of NO-related pathway metabolites were measured in patients with AMI (n = 60) and healthy controls (n = 27). The authors determined the predictive value of these metabolites for post-AMI MACE development over a median of 3.5 years. Patients with AMI had greater plasma concentrations of both SDMA and ADMA than healthy participants. One interesting finding was that the SDMA was an independent predictor of MACE during a 3.5-year follow-up period following AMI. SADMA predicted MACE with 80% sensitivity, 85% specificity, 33% positive predictive value, and 98% negative predictive value[300]. Szabo et al[301] analyzed SDMA and ADMA in patients with CAD referred for stress/rest myocardial perfusion scintigraphy. Their finding suggests that SDMA concentrations in conjunction with poor myocardial perfusion should be considered in addition to traditional risk factors in individuals receiving elective cardiac assessment. Pre-stress serum SDMA concentrations with a cut-off value of about 0.592 mmol/L predicted CV mortality with a sensitivity of 83% and specificity of 76% in long-term follow-up in their study. Cordts et al[302] found that elevated ADMA concentrations were associated with the severity of diastolic dysfunction in HCM. The reason may be diminished NO production due to ADMA. This results in altered myocardial relaxation patterns. Overall, both dimethylarginines have shown promising prospects in the prediction and risk stratification of various CVDs.
Uromodulin (UMOD) is a kidney-specific glycoprotein. It is mostly secreted from the thick ascending limb (85%-90%) and early distal tubules (10%-15%). It is released both into urine and interstitial fluid[303]. It is also called Tamm-Horsfall protein, which is a key component of hyaline casts. It is encoded by the UMOD gene located on chromosome 16. It activates monocytes and granulocytes (proinflammatory) and inhibits T lymphocytes (anti-inflammatory). This protein plays an important role in protection against urinary tract infections, immunomodulation, blood pressure control, urinary concentration (by activation of the Na-K-Cl cotransporter and renal outer medullary potassium channel), and protection against kidney stone formation[303-305]. The concentrations of UMOD are altered with tubular dysfunction, age, sex, diabetes, and metabolic syndrome[306-309]. Various findings have shown that high salt intake increases UMOD secre
Garimella et al[315] found that in non-diabetic patients with CKD, the incidence rate of CVD events declined with increasing concentrations of UMOD. They observed that elevated UMOD levels were independently associated with a lower risk of HF and CVD mortality. Similar findings were discovered by subsequent investigations. Then et al[316] analyzed 1079 participants (age 62-81 years) for the relationship of serum UMOD with CV morbidity and total mortality in the population-based KORA F4 study, stratified by sex. After adjustment for age, BMI, diabetes, and eGFR, it was observed that there was a significant inverse relation of serum UMOD with total mortality and CV mortality (hazard ratio [HR]: 0.70; 95% confidence interval [CI]: 0.52-0.93) in men, but not in women. They concluded that serum UMOD was an independent biomarker for total and CV mortality in males aged 62 years or above[316].
Another study assessed a cohort of 529 patients undergoing coronary angiography for the evaluation of established or suspected stable CAD with follow-up periods of up to 8 years. Serum UMOD level predicted the overall mortality even after controlling for eGFR, current smoking status, diabetes, and CAD status (adjusted HR = 0.57; 95%CI: 0.37-0.89; P = 0.014). They also found that low UMOD concentrations can significantly identify and predict CV events (HR = 1.45; 95%CI: 1.04-2.02; P = 0.027). Also, the creatinine to UMOD ratio significantly predicted the incidence of CV events[317]. Hence, UMOD has in various ways demonstrated that it can be a valuable addition to existing techniques for the eva
Lectin-like low oxidized LDL receptor 1 (LOX-1) is a transmembrane scavenger receptor from oxidized LDLs. It is commonly present in endothelium but is also expressed by macrophages, smooth muscle cells, cardiomyocytes, platelets, and fibroblasts[318,319]. Its production is low under normal circumstances. It is upregulated by oxidatively modified LDL (ox-LDL), proinflammatory cytokines, pro-oxidative, and biomechanical stimuli. LOX-1 receptor is considered to be involved in atherosclerotic and pro-inflammatory processes. It is overexpressed in various pathological conditions like atherosclerosis, hypertension, MI, stable CAD, and diabetes. It is also associated with endothelial dysfunction, fibroblast development, hypertrophy of vascular smooth muscles, and myocardial remodeling[320]. In the presence of pro-inflammatory stimuli, the receptor is converted into soluble LOX-1 (sLOX-1) by proteolytic cleavage. sLOX-1 is present in the circulation and can be easily measured in serum to assess various inflammatory and CV conditions[321,322]. The inflammatory stimuli can be oxidized-LDL, CRP, TNF-α, and IL-8[323,324]. sLOX-1 levels may represent activation of the LOX-1 receptor and the overall inflammatory burden of the body.
Multiple studies have been conducted to evaluate the implications of sLOX-1 in various CVDs. A study included 107 subjects with acute NSTEMI, 223 with acute STEMI, and 107 healthy subjects. Patients with NSTEMI and STEMI showed a substantial increase in plasma sLOX-1 levels, with area under the curve values of 0.92 and 0.925, respectively. They inferred that increased plasma sLOX-1 concentrations may be employed as a clinical biomarker for early identification of patients with NSTEMI and STEMI[325]. Florida et al[326] assessed the association of sLOX-1 with coronary plaque progression in 327 patients with psoriasis. Patients with high levels of sLOX-1 and high-sensitivity CRP had elevated high-risk coronary plaques. They were associated with atherosclerotic plaque progression irrespective of biological or systemic therapy. It was concluded that sLOX-1 can be used as a reliable biomarker for CAD risk assessment. Stinson et al[327] identified that sLOX-1 levels were associated with worsened cardiometabolic profiles in pediatric obesity and can be used as a marker for their early detection. Elevated sLOX-1 levels were found to be associated with elevated risks of first-time MI in another prospective population study. In the highest tertile of sLOX-1, there was a 77% statistically significant increased risk of MI and a significant relation between sLOX-1 with all CV risk factors excluding male sex and high BMI[328]. In another study, the predictive value of sLOX-1 was much higher in the subgroup of individuals without any of the standard modifiable CV risk factors (SMuRFs). sLOX-1 was associated with CAD severity. It was the first reliable biomarker for risk assessment in the SMuRFless population[329]. Hence, sLOX-1 can be a reliable risk predictor and early identification of cardiac diseases.
Advanced glycation end products (AGEs) are heterogeneous compounds formed by nonenzymatic reactions between reducing sugars and other biomolecules such as lipids, proteins, and nucleic acids. In healthy individuals, AGEs are present in moderate amounts but their concentration increases dramatically in hyperglycemic states[330]. AGEs interact with the receptor for AGE (RAGE), which are present in endothelial cells, monocytes, and macrophages. By binding these receptors, AGEs can influence cellular functions and metabolism by enhancing inflammation, apoptosis, and oxidative stress[331,332]. AGEs accumulate within the body (plasma, vessels, skin, and cardiac tissue) with poor glycemic manage
Multiple findings have indicated that elevated concentrations of AGEs are associated with the progression of complications related to diabetes, including CVD. The AGEs were identified to be present at higher levels in diabetics with CVD as compared to those without CVD[333,335,336]. Many studies have demonstrated the role of AGEs in the prevalence and pathophysiology of CVD in T2DM[337-339].
Considering endothelial dysfunction and intima-media thickness of the common carotid arteries (IMT-CC) as subclinical indicators of atherosclerotic CVD (ASCVD), De la Cruz-Ares et al[340] conducted a cross-sectional study in 540 people. AGE levels and IMT-CC were consistently reported to be greater in patients with CVD with T2DM. A recent study showed that the lower the level of AGE, the lesser the risk of CVD in patients with poorly controlled diabetes. The authors assessed the levels of serum methyl-glyoxal-hydroimidazoline (MG-H1) twice in 138 patients with diabetes whose mean glycated hemoglobin was 10.1%. The continuous low levels of AGEs (MG-H1) were associated with a reduced risk of CVD (HR: 0.50; 95%CI: 0.28-0.87; P = 0.02)[341]. Arshi et al[342] measured AGE levels with SAF to assess their association in patients with prevalent HF. They discovered that higher AGE concentrations were associated with a greater risk of prevalent HF. One unit increase in SAF was associated with a 0.98% lower LVEF in patients without HF. The relationship was observed to be greater among those with diabetes compared to non-diabetes. CV complications are one of the most observed complications of diabetes. Measurement of AGE levels can be an efficient marker for identifying these complications.
Ceramides is a central molecule in a sphingolipid structure, consisting of a fatty chain linked with amides and sphingo
Several studies have recently been conducted to assess the correlation and effectiveness of ceramide levels in predicting CVD risk and associated adverse outcomes. Burrello et al[352] observed that ceramide levels in extracellular vesicles (EVs) were considerably higher before reperfusion in individuals with STEMI. A recent study analyzed different ceramide species in 581 patients for the same cause. They found that ceramide species were linked with necrotic core tissue type and lipid core load in coronary angiography. They also observed that ceramides successfully predicted the risk of 1-year all-cause death in individuals with ACS or stable CVD[353].
Vasile et al[354] analyzed 1131 subjects to assess the predictive value of ceramide score in the general population. A significant relationship between ceramide ratios and MACE was observed independent of LDL-cholesterol and other CAD risk factors. The patients with the highest quantile of ceramide score were at around 1.5-fold increased risks of MACE. They observed a dose-response association across different levels of ceramide ratios and MACE. It was concluded that a higher ceramide score was an efficient predictor of CVD and MACE in the community[354]. Another finding showed that a high ratio of Cer (d18:1/24:1) to Cer (d18:1/24:0) was associated with more severe coronary artery stenosis[355]. A study further showed that ceramides and sphingomyelins containing palmitic acid were linked to an increased risk of AF compared to those with very long-chain saturated FAs[356].
Another study investigated the relationship between ceramide with heart function in 2652 Framingham offspring participants. They discovered that greater levels of C16:0/C24:0 ratio are linked to worse LVEF, poor overall circumferential strain, and higher LV end-systolic volume. They concluded that a higher ceramide ratio had adverse effects on cardiac remodeling[357]. A study conducted in Shanghai, China demonstrated that distinct plasma ceramides can be used as independent predictors of ACS in patients with chest pain. Further, when combined with hs-cTn and conventional factors, ceramide efficiently diagnoses ACS in individuals with chest discomfort[358]. Hence, ceramides have shown pro
Lipoprotein-associated phospholipase A2 (Lp-PLA2), also known as platelet-activating factor acetylhydrolase, belongs to the phospholipase A2 superfamily and is primarily synthesized by monocytes and macrophages[16,359-361]. This enzyme catalyzes the hydrolysis of the ester bond at the sn-2 position of phospholipids, liberating free fatty acids (FFAs) and generating lysophospholipids (LPLs)[362,363]. FFAs, such as arachidonic acid (AA) and oleic acid (OA), serve as critical energy substrates. AA can undergo further metabolism by enzymes like cyclooxygenases, lipoxygenases, and cytochrome P450, yielding eicosanoids, potent mediators of inflammation, cellular signaling, and carcinogenesis[364]. Meanwhile, lysophospholipids contribute to phospholipid (PL) remodeling, membrane integrity, and cell signaling, and are precursors to lysophosphatidic acid, crucial for cellular proliferation, survival, and migration.
Moreover, Lp-PLA2 significantly alters the surface characteristics of LDL particles via PL hydrolysis, rendering them more susceptible to oxidation[365]. Upon oxidation, Lp-PLA2 releases lyso-phosphatidylcholine and oxidized FAs, triggering an inflammatory cascade. Accumulation of these oxidized products in the sub-intimal space promotes the formation of plaque lipid cores and facilitates macrophage transformation into foam cells, pivotal in the genesis of vulnerable plaques and ACS[366,367].
Lp-PLA2 plays a pivotal role in atherosclerotic plaque formation and inflammation[368]. The landmark West of Scotland Coronary Prevention Study initially linked elevated Lp-PLA2 levels with increased CV events[369]. Subse
However, despite the association between elevated Lp-PLA2 levels and heightened CV risk, the clinical utility of this biomarker remains contentious. Significantly, recent large-scale randomized trials failed to demonstrate clinical benefit from Lp-PLA2 inhibition in patients with stable or unstable CAD[372,373]. These outcomes challenge the potential use of Lp-PLA2 in predicting CV risk. Therefore, further research is crucial to elucidate the causal role of Lp-PLA2 in CV events and to ascertain its genuine value in clinical practice.
The metabolite trimethylamine N-oxide (TMAO), synthesized by gut microbes, has garnered considerable attention as a potential biomarker for various CVDs. TMAO, originally noted for its protective role in deep-sea organisms against protein damage under high hydrostatic pressure, has prompted extensive research into its implications for human CV health[374]. TMAO is derived from dietary sources like choline, carnitine, and phosphatidylcholine, which gut microbiota metabolizes into trimethylamine (TMA). Hepatic flavin monooxygenases then oxidize TMA into TMAO[375].
Endothelial dysfunction, pivotal in atherosclerosis pathogenesis, is exacerbated by acute TMAO exposure, as demonstrated by Seldin et al[376], who found that TMAO induces vascular inflammation and endothelial dysfunction through NF-κB activation both in vivo and in vitro. A study by Ma et al[377] corroborated these findings, highlighting the role of TMAO in impairing endothelial function. Furthermore, Sun et al[378] identified that TMAO triggers inflammation and endothelial dysfunction via activation of the ROS-thioredoxin-interacting protein-NLR family pyrin domain containing 3 inflammasome[378]. TMAO also heightens risks associated with atherosclerosis by increasing monocyte adhesion, platelet activity, and thrombotic tendencies[379]. Moreover, the accumulation of ox-LDL in macrophages pro
Professor Tang et al[381] from the Cleveland Medical Center (Cleveland, OH, United states) was the first to link elevated TMAO levels with MACE such as MI, stroke, and mortality. Subsequent studies have consistently demonstrated that higher levels of TMAO and its precursors (L-carnitine, choline, and betaine) correlate with increased risks of CV events and mortality[382,383]. A community-based cohort study by Lee et al[384] in older adults in the United States fur
Retinol-binding protein 4 (RBP4), belonging to the lipocalin family, adopts a tertiary structure known as the ‘lipocalin fold,’ facilitating the binding of small hydrophobic molecules such as lipids. Primarily synthesized in the liver and also produced in adipose tissue, RBP4 circulates in the bloodstream bound to vitamin A and transthyretin[386-392]. This suggests that elevated RBP4 levels may contribute to vascular complications in T2DM. Additionally, RBP4 shows a strong association with atherogenic apolipoprotein B-containing lipoproteins, particularly triglycerides, suggesting its potential role in CVD pathogenesis. However, the link between circulating RBP4 and CVD diminishes after adjusting for triglyceride levels[393,394]. Moreover, the inverse relationship between mean IMT and the retinol/RBP4 ratio persists even after accounting for established CV risk factors[395]. This indicates that the retinol/RBP4 ratio, indicative of RBP4 satu
Adipocyte FABP (also known as FABP4), is part of the cytoplasmic FABP multigene family, and is predominantly expressed in adipocytes and macrophages[397]. Initially recognized for its role as a lipid buffer, recent studies have un
Elevated levels of cardiac-FABP have been associated with altered myocardial substrate utilization, insulin resistance, adverse lipid profiles, and other cardiometabolic risk factors, suggesting a potential role in early CV risk assessment[401,402]. Experimental evidence supports that blocking or genetically removing FABP4 prevents the formation of atherosclerotic lesions in conditions of severe hypercholesterolemia and accelerated atherosclerosis[403]. Additionally, research by Zhang et al[404] indicates that heart-type FABP serves as a valuable predictor for CV events in patients with stable CAD, underscoring its potential as an early biomarker. Moreover, elevated plasma FABP4 levels have been modestly linked to a higher risk of HF in older individuals, suggesting its utility in risk stratification[405]. However, studies such as those by Reiser et al[406] suggest that circulating FABP4 serves as a prognostic biomarker in patients with ACS but not in asymptomatic individuals. Furthermore, the exploration of FABP4 antagonists as potential pharmaceutical interventions to mitigate atherosclerotic disease progression is supported by findings from studies like that of Peeters et al[407]. None
The superfamily of phospholipase A2 (PLA2) encompasses several major families of isoenzymes, including secretory PLA2 (sPLA2), cPLA2, calcium-independent PLA2, lipoprotein-associated PLA2, lysosomal PLA2, and adipose tissue-specific PLA2[408]. Among these, the sPLA2 family stands out as the largest subgroup, comprising 10 low molecular mass, disulfide-rich isoenzymes: SPLA2-IB, SPLA2-IIA, SPLA2-IIC, SPLA2-IID, SPLA2-IIE, SPLA2-IIF, SPLA2-III, SPLA2-V, SPLA2-X, and SPLA2-XIIA, each with distinct biological functions[363].
sPLA2, particularly sPLA2-IIA, is noteworthy for its involvement in inflammatory and CV processes. It plays a crucial role in PL hydrolysis, leading to the generation of pro-inflammatory mediators. sPLA2-IIA, sPLA2-V, and sPLA2-X are detected in atherosclerotic plaques and ischemic myocardial tissue, suggesting their potential roles in atherogenesis and inflammation through mechanisms such as enhancing lipoprotein retention in vascular proteoglycans, activating platelets via the prostanoid pathway, and promoting LDL oxidation[409-414].
Observational studies have linked elevated sPLA2-IIA levels and increased sPLA2 activity with a heightened risk of initial and recurrent CV events, including CV death, AMI, and stroke[362,364,368]. Consequently, sPLA2 has been considered a promising biomarker for CVD and a potential target for therapeutic intervention. However, clinical trials investigating the sPLA2 inhibitor darapladib did not demonstrate a reduction in the risk of recurrent CV events in patients with ACS and even suggested an increased risk of MI[415].
Moreover, evidence from Mendelian randomization studies and Phase 3 randomized controlled trials (RCTs) has cast doubt on the causal role of sPLA2 in CV events[371]. Therefore, the clinical utility of measuring sPLA2 levels remains uncertain, and further research is necessary to elucidate its value in CV risk assessment and management.
Fibroblast growth factor 23 (FGF23) is an endocrine hormone primarily secreted by osteocytes, crucial for maintaining phosphate homeostasis by enhancing renal phosphate excretion and suppressing the renal production of 1,25-dihydroxy vitamin D, thereby accelerating its degradation[416]. This mechanism collectively reduces the efficiency of intestinal phosphate absorption in response to dietary intake, maintaining serum phosphate levels within a narrow normal range[417]. However, in CKD, FGF23 levels rise progressively early in the disease course as a compensatory response to declining renal phosphate excretion capacity, aiming to sustain a neutral phosphate balance[418,419].
Despite its apparent compensatory roles, prospective studies have identified independent associations between elevated FGF23 levels and increased risks of CV events and mortality[420,421]. Potential mechanisms linking elevated FGF23 to CV risk include its contribution to LV hypertrophy, leukocyte dysfunction, and chronic inflammation[422]. In vitro studies have also demonstrated that FGF-23 enhances calcium influx and promotes cardiomyocyte hypertrophy, suggesting direct effects on cardiac function[423,424].
FGF-23 has emerged as a promising biomarker candidate for CV risk assessment[425]. The Heart and Soul Study highlighted a positive correlation between FGF-23 levels and recurrent CV events[421,426]. Similarly, the Cardiovascular Health Study found associations between higher FGF-23 levels and increased risks of incident HF and total CV events[427]. Moreover, the Uppsala Longitudinal Study of Adult Men reported a positive link between FGF-23 and CV mortality[428]. FGF-23 has also been independently associated with long-term mortality following STEMI, suggesting its potential utility in managing patients with STEMI and as a target for future therapeutic strategies[429].
Myoinositol plays a pivotal role as a fundamental component of membrane-bound phosphatidylinositol and exerts diverse biological functions in various forms, including free molecules, isomers, and phosphate derivatives, thereby significantly influencing cellular metabolic balance and stress responses[430]. In an experimental model of MI in rabbits, elevated serum myoinositol levels were observed alongside varied decreases in myocardial tissue signals. This pattern mirrors findings in both patients with HF and animal models, where increased plasma myoinositol levels correlate with the severity of cardiac dysfunction[431,432].
The elevated plasma myoinositol levels observed in HF may be attributed to heightened renal synthesis compensating for reduced tissue concentrations, altered myoinositol metabolism, or increased release from tissues[431]. Conversely, reduced myocardial tissue myoinositol levels observed in MI rabbit model suggest disruptions in lipid metabolism[430]. In failing hearts, decreased energy production is partly due to a metabolic shift away from mitochondrial oxidative metabolism towards glycolysis, with impaired FFA oxidation playing a significant role in this metabolic reprogramming[433,434].
Furthermore, this study delineated distinct lipid metabolism alterations in the MI model: Decreased glycerol and palmitoleic acid in the interventricular septum, increased linolenic acid in the LV free wall, and elevated stearic acid levels in the serum. Cholesterol levels were elevated in the RV of MI rabbits, indicating altered lipid substrates and meta
Klotho protein, identified in 1997, plays a pivotal role in aging and various physiological processes, primarily known for its anti-aging properties and its impact on pathways related to longevity, cognition, and metabolism. Recent research has revealed additional roles of Klotho beyond its initial discovery. For instance, studies have elucidated its neuroprotective effects, demonstrating that Klotho expression in the brain correlates with enhanced cognitive function and reduced neurodegenerative pathology[436]. The aging suppressor gene Klotho encodes a single-pass transmembrane protein predominantly found in the distal tubule cells of the kidney, parathyroid glands, and choroid plexus of the brain[437]. In mice lacking klotho expression, aging-related phenotypes such as atherosclerosis, endothelial dysfunction, reduced bone mineral density, sarcopenia, skin atrophy, and impaired cognition have been observed[438].
Klotho protein also exerts a protective role in the CVS by enhancing endothelium-derived NO production through humoral pathways[439]. Reduced serum soluble Klotho levels have independently been associated with markers of vascular dysfunction, including arterial stiffness, in patients with CKD[440]. This association is considered pivotal in the pathogenesis of CVD and serves as a significant risk factor for its progression[440].
Furthermore, Klotho deficiency has been implicated in cardiac aging due to its impact on the nuclear factor erythroid 2-related factor 2-glucocorticoid receptor pathway. The administration of exogenous secreted Klotho is emerging as a promising therapeutic approach for addressing age-related cardiomyopathy and HF[441]. In a recent study involving community-dwelling adults, higher plasma concentrations of Klotho were independently associated with a reduced likelihood of CVD [442]. Recent findings suggest that increasing Klotho levels or enhancing its function could offer benefits in managing age-related conditions such as CKD, CVD, and diabetes[443].
The urea cycle, also referred to as the ornithine cycle, is a crucial biochemical pathway primarily active in the liver. Its principal function is to detoxify ammonia, a toxic byproduct of amino acid metabolism, by converting it into urea for safe elimination. This process involves key metabolites such as ornithine, citrulline, arginine, and aspartate, which play essential roles in the production and regulation of urea[444,445]. Understanding the dynamics of these metabolites provides valuable insights into metabolic health and ensures the proper functioning of the urea cycle. Disruptions in this cycle can lead to severe metabolic complications, underscoring the importance of effective diagnostic and therapeutic approaches.
In the context of CVDs, urea cycle metabolites play significant roles, particularly in the production of NO by endothelial cell NO synthase (eNOS). The availability of L-arginine, a critical substrate for eNOS, is crucial for normal CV function. Insufficient L-arginine supply has been strongly linked to various CV conditions, including hypertension, atherosclerosis, diabetic vascular disease, hyperhomocysteinemia, HF, and ischemia-reperfusion injury[446,447]. Oral supplementation with L-arginine reportedly prevents endothelial dysfunction and restore endothelium-dependent vasodilation in conditions such as diabetes, hypertension, reperfusion injury, and HF[448-450].
In conditions where L-arginine supplementation has shown therapeutic benefits, supplementation with L-citrulline should also be considered. Both L-citrulline and L-arginine have demonstrated efficacy in improving various CV dysfunctions, including systemic hypertension, HF, diabetes, and ischemia-reperfusion injury. For example, in sickle cell disease, administration of L-arginine and L-citrulline has been shown to reduce plasma peroxidase levels, attenuate leukocyte activation, alleviate red blood cell sludging, mitigate vaso-occlusion and PH, and improve sensory-motor deficits[447,451].
Prostaglandin D2 synthase (PGD2S) plays a critical role in catalyzing the biosynthesis of PGD2 by converting PGH2, a precursor of various prostanoids. PGD2, a potent lipid mediator, is synthesized from AA via the cyclooxygenase pathway and exerts its effects through G-protein-coupled receptors DP1 and DP2. Known for its diverse physiological and pathological roles, PGD2 is involved in inflammation, allergic responses, and regulation of sleep-wake cycles[452].
PGD synthase (PGDS) encompasses two primary types: Lipocalin-type PGDS (L-PGDS) and hematopoietic PGDS. L-PGDS, part of the lipocalin superfamily, is predominantly expressed in the CNS and CVS[453]. Its presence has also been documented in the human heart, with extensive studies on its cellular localization in various mammalian tissues[454]. L-PGDS can be detected in biological fluids like serum, CSF, and urine, indicating its systemic distribution and potential roles across diverse physiological contexts[455].
PGDS, particularly L-PGDS, has emerged as a novel marker in cardiac disease, offering insights into its roles and implications for CV health. Recent research highlights its involvement in conditions such as asthma, allergic rhinitis, and various CVDs, positioning PGD2S as a promising target for therapeutic interventions[455-457]. Understanding the enzymatic activity and regulation of PGD2S is pivotal for developing treatments that effectively modulate PGD2 levels. Further research into the enzymatic activity and regulation of PGDS is crucial for fully understanding its mechanistic roles in CV health. This understanding could pave the way for innovative diagnostic strategies, risk stratification me
Growth arrest specific-6 (Gas6) is a vitamin K-dependent protein that is found in the uterus, ovary, heart, and kidney. It plays roles in platelet function, phagocytosis, and reducing inflammation and has been implicated in several diseases including rheumatologic (systemic lupus erythematosus, rheumatoid arthritis), cirrhosis of the liver, and venous throm
PAI-1 is a serine protease inhibitor glycoprotein produced by endothelial cells, fibroblasts, smooth muscle cells, monocytes, macrophages, adipocytes, endometrium, peritoneum, mesothelial cells, liver cells, and cardiac myocytes. It is involved in suppression of fibrinolysis as well as the regulation of cell replication and angiogenesis. PAI-1 is associated with a number of pathologies like MI, peripheral arterial disease, deep vein thrombosis, and disseminated intravascular coagulation[461]. High levels of PAI-1 have implicated in CAD and metabolic syndrome[462]. Also, an acute rise in the levels of PAI-1 has been associated with worse outcomes in patients with STEMI[463]. Jung et al[464] demonstrated that low levels of PAI-1 are associated with unplanned revascularization for late stent complications.
Soluble urokinase plasminogen activator receptor (suPAR) is an inflammatory biomarker and being non-specific, is released in various inflammatory states. It is a type of urokinase receptor that is soluble and it functions as a leukocyte chemoattractant. It also plays role in tissue remodeling. suPAR is present in the inactive membrane-bound state on cells like leukocytes, fibroblasts, macrophages, endothelial cells, cardiac myocytes, and renal tubular cells.
Elevated levels of suPAR have been found in patients with MI and also is associated with an increased risk of MI, worse prognosis, and increased CV mortality[465]. Moreover, rising suPAR levels are associated with a decrease in eGFR values in patients with advanced HFrEF, suggesting its prognostic utility in HFrEF[466]. Chew-Harris et al[467] demon
TNF-α has two main receptors on cells: TNFR1 and TNFR2. TNFR1 is expressed ubiquitously and has role in apoptosis. TNFR2 is primarily expressed in T cells activating the NF-κB pathway. Both receptors exist as transmembrane and soluble forms. Soluble forms compete for binding of ligand with transmembrane ones, thereby inhibiting TNF-α action. TNFR1 is proinflammatory while TNFR2 is anti-inflammatory. High levels of sTNFR1 and sTNFR2 are associated with an increased risk of adverse clinical outcomes in patients with STEMI, especially HF[468]. Also, circulating levels of sTNFR1 and sTNFR2 have been shown to predict worse prognosis and mortality in patients with HF[469].
Syndecan-1 (SDC-1) is a proteoglycan that functions through the TGF-β pathway with protective effects on short-term inflammation post-MI through minimal remodeling. In the long run, however, it causes remodeling through the renin-angiotensin-aldosterone system worsening the prognosis. The ectodomain of SDC-1 has been found to be shed in plasma, and is therefore measurable. Tromp et al[470] showed that SDC-1 is a predictor of prognosis in patients with HFpEF and not in those with HFrEF. It also has been linked to fibrosis and remodeling after HF. Animal models have shown an association of SDC-1 levels with inflammation in AMI[470]. Increased SDC-1 levels have also been associated with in
Chromogranin A (CgA) is a prohormone produced by many cells of the body including neuroendocrine and myocardial cells and its levels are associated with prognosis in patients with ACS, HF, and severe sepsis. CgA is hyperglycosylated in HF and a low CgA to catestatin conversion is associated with worse prognosis in patients with HF[472]. It is also an important marker for the diagnosis and predicting the prognosis in patients with carcinoid syndrome and carcinoid HD[473].
Fibulin-1 is a calcium-binding ECM glycoprotein that plays role in fibrinogen (FBN) crosslinking. Elevated levels of fibulin-1 have been shown in patients with aortic stenosis. An association has been found between fibulin-1 and suPAR suggesting some crosslinking between plasminogen and fibrotic pathways within the ECM[474]. Holmager et al[475] have shown elevated levels of Gal-3 and fibulin-1 in patients with HFrEF and altered glucose metabolism compared to those with normal glucose tolerance.
EVs are transport vehicles meant for transferring contents from cells of origin to target cells and tissues and serve as mediators of intercellular communication. These are composed of a lipid bilayer with the cellular content packaged within the vesicle. Endothelial injury is associated with release of EVs. Levels of EVs are increased in CVDs, including both stable chronic and unstable ACS. Hence EVs may have diagnostic and prognostic applications in patients with CVDs[476]. Levels of small EVs (sEVs) are increased in hypoxia and cardiac ischemia. In addition, heat shock protein 47 (HSP47) and hERG1 levels, found on the surface of sEVs, are increased in HF. Thus, sEV-human ether-a-go-go-related gene 1 (hERG1) and sEV-HSP47 serve as markers of CVDs[477]. The levels and sizes of exosomes have been found to be increased in patients with STEMI as opposed to those with CCS. Analysis of the protein contents of exosomes have revealed that ceruloplasmin increases and transthyretin decreases in patients with STEMI compared to those with CCS, similar to the trend of these two proteins when their concentrations are measured in the plasma of patients with acute inflammation like STEMI.
Moreover, variation in protein expression was found in the exosomes of patients who had undergone coronary artery bypass graft surgery or heart valve surgery before and after the procedure. Also, patients with out-of-hospital cardiac arrest secondary to STEMI can be characterized by higher expression of oligodendrocyte proteolipid protein-1 in their circulating exosomes compared to those with uncomplicated STEMI due to the increased release of exosomes from hypo
Ceruloplasmin is a hepatically synthetized glycoprotein that primarily transports copper acquired mainly from the diet. It is also an acute phase reactant released in inflammatory states and may function as an antioxidant; however, it can contribute to free radical production, which can exacerbate various conditions, particularly those involving iron imba
The proprotein convertase subtilisin/kexin type 9 (PCSK9) gene, located on human chromosome 1, encodes the enzyme PCSK9. It activates other proteins and is the ninth member of the proprotein convertase family. Numerous species share orthologs, or similar genes. A section of peptide chains that prevent PCSK9 from being active at first causes it to be produced in an inactive form. Proprotein convertases cut this region off of PCSK9 to activate it. Throughout the body, PCSK9 is expressed in a variety of tissues and cell types. It attaches to LDL and breaks down their receptor. The liver and other cell membranes include the LDLR, which attaches to LDL particles to facilitate their uptake into cells and send them to lysosomes where they are destroyed. The LDL-LDLR complex splits during trafficking when PCSK9 is inhibited, allowing the LDLRs to be recycled back to the cell surface and the LDL to be broken down in the lysosome. The ability to extract more LDL particles from the extracellular fluid is enhanced by this recycling. So, in essence, PCSK9 is associated with increased amount of LDL-cholesterol in blood[481].
A study conducted on 1031 individuals reported that even after controlling for confounding variables, plasma PCSK9 levels were higher in patients with CAD. PCSK9 levels increased with CAD severity as measured by the Gensini Score in both crude and adjusted models. Plasma PCSK9 levels were significantly correlated with circulating inflammatory and lipid-related markers. Also, mediation analysis revealed that lipid and inflammation pathways partially mediated the effect of PCSK9 levels on CAD, with effect sizes for lipid at 17% and for severity at 18%, respectively. These results provide an understanding of the mechanisms behind the association between CAD and plasma PCSK9[482]. Another study suggested that PCSK9 level is associated with coronary lesion severity and high PCSK9 level is associated with severe coronary lesion. The cut-off value of 70.35 ng/mL of PCSK9 exhibited a 75% sensitivity and a 78% specificity when utilizing area under the receiver operating characteristic analysis to forecast a severe coronary lesion. This study shows that among patients with CAD, PCSK9 level has a moderate sensitivity and specificity for predicting the severity of coronary lesions[483]. A meta-analysis on the predictive role of PCSK9 showed that PCSK9 levels are modestly but significantly associated with increased risk of total CV events[484].
Angiopoietin-like 3 (ANGPTL3) is a member of the secreted factor family that resembles angiopoietin. It is mostly expressed in the liver and has a structure similar to that of ANGPTs, including a signal peptide, a coiled-coil domain at the N-terminus, and a FBN-like domain at the C-terminus. ANGPTL3 protein's FBN-like domain interacts with alpha-5/beta-3 integrins to facilitate endothelial cell adhesion and migration. It is possible that this protein controls angiogenesis as well. In mice and humans alike, ANGPTL3 functions as a dual inhibitor of LPL and endothelial lipase (EL), raising plasma levels of triglycerides, LDL-cholesterol, and HDL-cholesterol. Moreover, it prevents EL from hydrolyzing HDL-PL, which raises HDL-PL levels. The ability of circulating PL-rich HDL particles to efflux cholesterol is strong.
It is believed that ANGPTL8, a hepatokine generated by feeding, activates ANGPTL3 to greatly enhance the absorption of circulating triglycerides into white adipose tissue during the fed state. According to the ANGPTL3-4-8 model, this mechanism decreases postprandial LPL activity in the skeletal and cardiac muscles[485]. In a study of 90 patients with CAD, over the course of a 54-month median follow-up, 33 CV incidents occurred. Individuals who experienced these episodes had lower statin use, more severe baseline CAD, and higher levels of ANGPTL3 and CRP. The high ANGPTL3 group had a greater incidence of CV events, according to Kaplan-Meier analysis. Even after controlling for a number of variables, ANGPTL3 levels remained a significant predictor of elevated CV risk, with a greater hazard ratio for CV events being linked to every 1 ng/mL increase in ANGPTL3[486]. In another study, ANGPTL3 was shown to be a risk factor for CAD by univariate analysis. Furthermore, even after controlling for confounding variables, multivariate analysis showed that ANGPTL3 was independently linked with the existence of CAD. Additionally, circulating ANGPTL3 levels showed no significant link with the severity of CAD, but they were significantly correlated with triglyceride and total cholesterol levels[487]. Furthermore, a study on patients with hypothyroidism showed that ANGPTL3 is an independent predictor of endothelial and cardiac function[488].
The CASP3 gene encodes caspase-3, a caspase protein that interacts with CASP8 and CASP9. Many mammals with complete genome data have been shown to have orthologs of CASP3, along with birds, lizards, lissamphibians, and te
A study involving 27 participants showed that following PCI, the peak p17 peptide (a fragment of CASP) level was observed, and it exhibited a positive correlation with the peak levels of cTnI (r = 0.48, P = 0.011) and CK-MB (r = 0.56, P = 0.002, Spearman for all). The initial application of this unique assay creates the framework for further research into this vital balance. The fluctuating levels of p17 peptide and their association with peak cTnI and CK-MB indicate that the damaged myocardium is most likely the source of serum p17[490]. Another study suggested that before and after cardioplegia, peripheral venous (PV) levels of p17 segment of CASP3 were substantially higher than those of the control group. PV levels rose with cardioplegia. Coronary sinus levels were higher at both time points than PV levels. The peripheral levels were influenced by the heart-derived indicators, which implies that cardiac preservation may be assessed by measuring PV biomarker concentrations[491].
The human MDK gene encodes the protein known as midkine. With a molecular weight of just 46%, it is a basic heparin-binding growth factor that is part of the neurite growth-promoting factor-1 family, which also contains pleiotrophin. This protein has two domains joined by disulfide links and is not glycosylated. As suggested by its name, MDK is extremely responsive to retinoic acid and is expressed significantly during mid-gestation, when development is at its most critical. During normal circumstances, it is mainly located in particular tissues in adults; but, during conditions such as oncogenesis, inflammation, and tissue repair, its expression greatly rises. Multifunctional in nature, MDK affects various biological processes, including angiogenesis, migration, proliferation of cells, and fibrinolysis. It engages in interactions with a molecular complex that includes syndecans, LDL receptor-related protein 1, anaplastic leukemia kinase, and receptor-type tyrosine phosphatase zeta[492,493].
In one study, serum MDK levels were first measured at the time of admission in 216 patients who had been admitted for HF and 60 control subjects. After that, these patients were monitored for an average of 653 +/- 375 days, with an emphasis on outcomes including cardiac death and worsening HF that necessitated hospitalization again. According to the study, patients with HF MDK concentrations were noticeably higher than those of the controls. MDK levels were significantly higher in patients with HF who had cardiac episodes than in those who did not. A strong link was shown by Kaplan-Meier analysis: The incidence of CEs increased directly to MDK levels. Moreover, MDK was an independent predictor of CEs in a multivariate analysis that controlled for age, sex, and comorbidities[494]. In another study, the levels of MDK were almost found to be four times more than those of a group of 100 healthy controls. The use of non-fractionated heparin contributed to the average tenfold increase in MDK levels during dialysis (correlation coefficient r2 = 0.17). Variations in each person's MDK response were consistent between assessments. A lower-than-average rise in MDK levels was observed in hypervolemic individuals during dialysis (P < 0.02); this effect was particularly prominent in patients with diabetes and longer intervals between dialysis sessions (P < 0.001). An independent sample of patients on dialysis (n = 88) confirmed this finding. While other markers (NT-proANP, Gal, and tenascin-C) were less predictive, Kaplan-Meier survival analysis showed that lesser fluctuations in MDK levels (delta MDK) corresponded with increased rates of CV and total mortality, similar to heightened uPAR levels. MDK levels rose (P < 0.002) in patients with hypervo
HSPs are proteins that are produced by cells in reaction to a variety of stressful situations. Although they were initially identified for their role in responding to heat shock, HSPs are now known to react to cold exposure, ultraviolet light, wound healing, and tissue remodeling processes. These proteins frequently function as molecular chaperones, helping nascent proteins fold correctly and helping stressed out proteins fold again. The considerable rise in their expression during the heat shock response is mostly attributed to the heat shock factor, whose transcriptional regulation is carefully controlled. HSPs are present in virtually all living organisms, including bacteria and humans. HSP names, such as HSP60, HSP70, and HSP90, are based on their molecular weight and correspond to protein families that are roughly 60 kDa, 70 kDa, and 90 kDa in size, respectively. HSPs are similar to ubiquitin, a tiny 8-kDa protein that is involved in protein disintegration. Furthermore, small HSPs include an alpha crystallin-like conserved protein binding domain that consists of about 80 amino acids[496].
HSPs may play a role in the regulation of CVDs, including hypertension, atherosclerosis, AF, cardiomyopathy, and HF, according to a growing body of research. Higher levels of circulating HSP antibodies have been linked to CVDs, according to studies, and some of these antibodies may even act as indicators for these diseases. The variety of functions that HSPs play in cellular signaling emphasizes the importance of comprehending their relationships to the pathophy
In a study by Giannessi et al[498], the following parameters were measured in serum: LVEF levels: ≥ 50% (n = 22), 35% to < 50% (n = 32), and < 35% (n = 28)[498]. The patients were divided into 44 healthy individuals and 82 patients with angiographically normal coronary arteries. The researchers also measured serum levels of IL-6, HSP72, HSP60, anti-HSP60 antibodies, and CRP. Higher levels of circulating HSP60, auto-antibodies to HSP60, HSP72, and CRP were seen in patients with more severe illness, which was defined by lower myocardial blood flow during rest and dipyridamole, indicative of coronary microvascular impairment. With the severity of LV failure, IL-6 levels gradually rose. There was a strong correlation found between BNP levels and LV end-diastolic dimensions and anti-HSP60 antibodies, HSP72, and IL-6 levels. In individuals with more advanced illness, in particular, IL-6 tended to correlate with HSP72 (r = 0.45, P = 0.021). In patients with angiographically normal coronary arteries, activation of HSP60 and HSP72 as well as increased inflammatory markers corresponded with the degree of cardiac and microvascular dysfunction. These results imply that even in the absence of obvious CAD, infectious-metabolic insults, and inflammatory responses may be pathogenic in the development of vascular and myocardial damage in patients with HF[498].
The circulation contains soluble receptors for AGEs, which can competitively inhibit RAGE activity by binding to ligands without initiating intracellular signaling due to the absence of the receptor's intramembrane and intracellular domains. There are two primary methods for producing soluble RAGE: Endogenous secretory RAGE (esRAGE), a splice variant derived from a shortened RAGE mRNA, and the cleavage of full-length RAGE on the cell membrane by metalloproteinases[499,500]. Current measures of soluble RAGE typically assess either esRAGE or the total amount of sRAGE, with esRAGE comprising approximately 20% of the total sRAGE. Although the distinct roles of secreted and cleaved sRAGE remain unclear, the upregulation of RAGE in response to ligand stimulation, which coincides with increased secretion of sRAGE, suggests that circulating sRAGE levels may reflect heightened activity within the RAGE system. This feature underscores the potential utility of sRAGE as a biomarker[499].
In a study by Wannamethee et al[501], sRAGE demonstrated a strong positive correlation with renal dysfunction in men, irrespective of diabetic status. Even after adjusting for CVD risk factors, metabolic markers, renal function, and inflammation, sRAGE remained significantly and positively associated with NT-proBNP, as well as augmentation pressure and augmentation index, in both diabetic and non-diabetic men. However, no significant association was found between sRAGE and central aortic blood pressure, carotid intima-media thickness, or arterial stiffness measured by pulse wave velocity in either group. Another study, conducted by Wang et al[502] demonstrated that elevated plasma sRAGE and S100A12 levels were found to be significantly associated with ACS severity and inflammation, suggesting their potential as predictors for severe CAD.
Hcy, a homolog of cysteine, is a non-proteinogenic α-amino acid characterized by an additional methylene bridge
Higher Hcy levels have also been associated with an increased risk of CHF in individuals without a history of MI. Research has shown that experimentally induced hyperhomocysteinemia increases BNP expression and causes both diastolic and systolic dysfunction in animals[505]. Furthermore, animals with hyperhomocysteinemia exhibit adverse cardiac remodeling, characterized by the accumulation of perivascular and interstitial collagen. The exact mechanisms by which high Hcy levels contribute to adverse cardiac remodeling and reduced pump function remain unclear. Current research suggests that Hcy may exert direct effects on the heart and have NO-independent vascular effects. Preliminary results from short intervention trials indicate that micronutrients may help improve clinical and laboratory indicators of CHF by lowering Hcy levels. However, further research is needed to elucidate the precise pathomechanisms by which hyperhomocysteinemia may contribute to CHF.
In a study involving 101 normal control individuals and 54 patients with coronary slow flow syndrome (CSFS), diag
Adiponectin (APN), also known as GBP-28, apM1, AdipoQ, and Acrp30, is a protein hormone and adipokine involved in the breakdown of FAs and regulation of blood glucose levels. Predominantly produced in adipose tissue, APN is also present in muscle and brain tissues in humans, and it is encoded by the ADIPOQ gene[507]. In a study using data from up to 25050 person examinations involving 8,469 participants from the Whitehall II cohort, researchers assessed the relationships between APN and subsequent changes in HR and HR variability (HRV) among individuals with and without diabetes[508]. Assessments of cardiac autonomic neuropathy included various HRV markers and HRs. The study found that the relationships among APN, HR, and HRV differed based on the presence of diabetes. Higher APN levels were linked to more significant reductions in HR and increases in three HRV parameters indicating both vagal and sympathetic activity in people with type 2 diabetes. These results suggest that increased APN levels are associated with more favorable CV autonomic function development in people with type 2 diabetes, independent of other confounding factors.
Another study investigated the role of APN in high-fat diet-induced cardiomyopathy in adult C57BL/6 wild-type and APN knockout mice fed a high-fat diet for 22 weeks[509]. The study found that APN deficiency exacerbated cardiac hypertrophy and contractile dysfunction. High-fat diet-induced cardiac and intracellular calcium disturbances were more pronounced in the absence of APN. Additionally, APN deficiency intensified the reduction in AMPK phosphorylation and the upregulation of the autophagy adaptor p62, both induced by the high-fat diet. Remarkably, treatment with rapamycin mitigated the high-fat diet and APN deficiency-induced cardiac hypertrophy and contractile dysfunction. These findings suggest that APN deficiency may exacerbate high-fat diet-induced cardiomyopathy, potentially through impairments in related pathways.
Natriuretic peptides (e.g., BNP, NT-proBNP) and cTns are well-established in clinical practice for diagnosing HF and AMI. While many novel biomarkers show promise for risk stratification and prognosis, widespread adoption is limited by cost, regulatory approval, and validation challenges. Guidelines from European Society of Cardiology (ESC), Ameri
The integration of novel cardiac biomarkers and the adoption of a multiple-marker approach represent a significant evolution in the field of cardiology. This review has elucidated the potential of biomarkers such as GGT, miRNAs, EMPs, PlGF, TMAO, and RBP4 in enhancing the early detection, risk stratification, and management of CVDs. These biomarkers provide a more comprehensive understanding of the underlying pathophysiological mechanisms, offering improved diagnostic precision and prognostic capabilities. As research continues to validate the clinical utility of these biomarkers, their incorporation into routine clinical practice is expected to facilitate early disease detection, enable personalized the
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