Search Results (452)

This review introduces a novel integrative framework linking gut dysbiosis, systemic inflammation, and cardiovascular risk in patients with inflammatory bowel disease (IBD). We highlight emerging biomarkers, including short-chain fatty acids (SCFAs), calprotectin, and zonulin, that reflect alterations in the gut microbiome and increased intestinal permeability, which contribute to cardiovascular pathology. Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide, and recent evidence identifies IBD, encompassing ulcerative colitis (UC) and Crohn’s disease (CD), as a significant non-traditional risk factor for CVD. This review synthesizes current knowledge on how dysbiosis-driven inflammation in IBD patients exacerbates endothelial dysfunction, hypercoagulability, and atherosclerosis, even in the absence of traditional risk factors. Additionally, we discuss how commonly used IBD therapies may modulate cardiovascular risk. Understanding these multifactorial mechanisms and validating reliable biomarkers are essential for improving cardiovascular risk stratification and guiding targeted prevention strategies in this vulnerable population. Full article

Background: This study presents an innovative approach to cardiovascular disease (CVD) risk prediction based on a comprehensive analysis of clinical, immunological and biochemical markers using mathematical modelling and machine learning methods. Baseline data include indices of humoral and cellular immunity (CD59, CD16, IL-10, CD14, CD19, CD8, CD4, etc.), cytokines and markers of cardiovascular disease, inflammatory markers (TNF, GM-CSF, CRP), growth and angiogenesis factors (VEGF, PGF), proteins involved in apoptosis and cytotoxicity (perforin, CD95), as well as indices of liver function, kidney function, oxidative stress and heart failure (albumin, cystatin C, N-terminal pro B-type natriuretic peptide (NT-proBNP), superoxide dismutase (SOD), C-reactive protein (CRP), cholinesterase (ChE), cholesterol, and glomerular filtration rate (GFR)). Clinical and behavioural risk factors were also considered: arterial hypertension (AH), previous myocardial infarction (PICS), aortocoronary bypass surgery (CABG) and/or stenting, coronary heart disease (CHD), atrial fibrillation (AF), atrioventricular block (AB block), and diabetes mellitus (DM), as well as lifestyle (smoking, alcohol consumption, physical activity level), education, and body mass index (BMI). Methods: The study included 52 patients aged 65 years and older. Based on the clinical, biochemical and immunological data obtained, a model for predicting the risk of premature cardiovascular aging was developed using mathematical modelling and machine learning methods. The aim of the study was to develop a predictive model allowing for the early detection of predisposition to the development of CVDs and their complications. Numerical methods of mathematical modelling, including Runge–Kutta, Adams–Bashforth and backward-directed Euler methods, were used to solve the prediction problem, which made it possible to describe the dynamics of changes in biomarkers and patients’ condition over time with high accuracy. Results: HLA-DR (50%), CD14 (41%) and CD16 (38%) showed the highest association with aging processes. BMI was correlated with placental growth factor (37%). The glomerular filtration rate was positively associated with physical activity (47%), whereas SOD activity was negatively correlated with it (48%), reflecting a decline in antioxidant defence. Conclusions: The obtained results allow for improving the accuracy of cardiovascular risk prediction, and form personalised recommendations for the prevention and correction of its development. Full article

Metabolic syndrome (MetS) is a cluster of conditions, including obesity, insulin resistance (IR), dyslipidemia, and hypertension, that increase the risk of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). While studied often in adults, the increasing prevalence of MetS in children and adolescents underscores the need for its early detection and intervention. Among various biomarkers, sex hormone-binding globulin (SHBG) has gained substantial attention due to its associations with metabolic health and disease. This review provides a comprehensive overview of SHBG and its association with MetS, with a focus on the pediatric and adolescent population. The interplay between SHBG, puberty, and metabolic risk factors is explored, including racial and ethnic variations. SHBG plays a crucial role in transporting sex hormones and regulating their bioavailability and has been found to correlate inversely with obesity and IR, two key components of MetS. Puberty represents a critical period during which hormonal changes and metabolic shifts may further influence SHBG levels and metabolic health. Understanding SHBG’s role in early metabolic risk detection could provide novel insights into the prevention and management of MetS. Full article

This review highlights recent findings on the potent anti-angiogenic serpin protein, pigment epithelium-derived factor (PEDF) as it relates to metabolic disease, diabetes, angiogenesis and cardiovascular disease (CVD), listing a majority of all the publicly available studies reported to date. PEDF is involved in various physiological roles in the body, and when awry, it triggers various disease states clinically. Biomarkers such as insulin, AMP-activated protein kinase alpha (AMPK-α), and peroxisome proliferator-activated receptor gamma (PPAR-γ) are involved in PEDF effects on metabolism. Wnt, insulin receptor substate (IRS), Akt, extracellular signal-regulated kinase (ERK), and mitogen-activated protein kinase (MAPK) are implicated in diabetes effects displayed by PEDF. For CVD, oxidised LDL, Wnt/β-catenin, and reactive oxygen species (ROS) are players intertwined with PEDF activity. The review also presents an outlook on where efforts could be devoted to bring this serpin closer to clinical trials for these diseases and others in general. Full article

C-reactive protein (CRP) has long been recognized as a biomarker of systemic inflammation and cardiovascular disease (CVD) risk. However, emerging evidence highlights the distinct and potent pro-inflammatory role of its monomeric form (mCRP), which is predominantly tissue-bound and directly implicated in vascular injury and plaque destabilization. This narrative review explores the interactions and overlapping pathways that converge within and modulate CRP, mCRP, the associated pathophysiology of diabetes mellitus, and cardiovascular disease. We examine how mCRP promotes endothelial dysfunction, leukocyte recruitment, platelet activation, and macrophage polarization, thereby contributing to the formation of unstable atherosclerotic plaques. Furthermore, we discuss the critical influence of diabetes in amplifying mCRP’s pathogenic effects through metabolic dysregulation, chronic hyperglycemia, and enhanced formation of advanced glycation end products (AGEs). The synergistic interaction of mCRP with the AGE-receptor for AGE (RAGE) axis exacerbates oxidative stress and vascular inflammation, accelerating atherosclerosis progression and increasing cardiovascular risk in diabetic patients. Understanding these mechanistic pathways implicates mCRP as both a biomarker and therapeutic target, particularly in the context of diabetes-associated CVD. This review highlights the need for further research into targeted interventions that disrupt the mCRP-[AGE-RAGE] inflammatory cycle to reduce plaque instability and improve cardiovascular outcomes in high-risk populations. Full article

Despite notable advancements in clinical care, cardiovascular disease (CVD) remains a leading global cause of mortality. Encompassing a wide range of heart and blood vessel disorders, CVD requires targeted prevention and treatment strategies to mitigate its public health impact. In recent years, extracellular vesicles (EVs) have emerged as crucial mediators of intercellular communication, influencing key processes such as vascular remodeling, inflammation, and immune responses in CVDs. EVs, including exosomes and microvesicles, carry bioactive molecules such as miRNAs, proteins, and lipids that contribute to disease progression. They are released by various cell types, including platelets, erythrocytes, leukocytes, endothelial cells, and cardiomyocytes, each playing distinct roles in cardiovascular homeostasis and pathology. Given their presence in circulating blood and other body fluids, EVs are increasingly recognized as promising non-invasive biomarkers for CVD diagnosis and prognosis. Furthermore, EV-based therapeutic strategies, including engineered EVs for targeted drug delivery, are being explored for treating atherosclerosis, myocardial infarction, heart failure, and hypertension. However, challenges remain regarding the standardization of EV isolation and characterization techniques, which are critical for their clinical implementation. This review highlights the diverse roles of EVs in CVD pathophysiology, their potential as diagnostic and prognostic biomarkers, and emerging therapeutic applications, clearing the way for their integration into cardiovascular precision medicine. Full article

Improved antiretroviral therapy (ART) has significantly increased the life expectancy of people living with HIV (PLWH). At the same time, other complications like metabolic syndrome (MetS) are coming up as new challenges to handle. This review aims to explore the emerging evidence of gut microbiome and virome alterations in human immunodeficiency virus-1 (HIV-1) infection and associated metabolic disorders, such as type-2 diabetes (T2DM) and cardiovascular disease (CVD), with a focus on their interplay, contribution to immune dysfunction, and potential as therapeutic targets. We conducted a comprehensive review of the current literature on gut bacteriome and virome changes in HIV-1-infected individuals and those with metabolic comorbidities emphasizing their complex interplay and potential as biomarkers or therapeutic targets. HIV-1 infection disrupts gut microbial homeostasis, promoting bacterial translocation, systemic inflammation, and metabolic dysregulation. Similarly, metabolic disorders are marked by reduced beneficial short-chain fatty acid-producing bacteria and an increase in pro-inflammatory taxa. Alterations in the gut virome, particularly involving bacteriophages, may exacerbate bacterial dysbiosis and immune dysfunction. Conversely, some viral populations have been associated with immune restoration post-ART. These findings point toward a dynamic and bidirectional relationship between the gut virome, bacteriome, and host immunity. Targeted interventions such as microbiome modulation and fecal virome transplantation (FVT) offer promising avenues for restoring gut homeostasis and improving long-term outcomes in PLWH. Full article

Cardiovascular disease (CVD), particularly atherosclerotic cardiovascular disease (ASCVD), is the leading cause of death worldwide, driven by factors like oxidative stress, inflammation, and lipid metabolism disorders. Although phenolic compounds such as Tyrosol (Tyr) and Hydroxytyrosol (HTyr) found in extra virgin olive oil (EVOO) have shown promising antioxidant and anti-inflammatory effects, their specific roles in modulating oxidative stress biomarkers and high-density lipoprotein (HDL) functionality in elderly populations, especially in those with prior myocardial infarction, are not fully understood. This study aimed to investigate the effects of EVOO phenolic compounds on oxidative stress biomarkers and HDL functionality, and related metabolic outcomes in both healthy and post-myocardial infarction (post-MI) elderly individuals. This pilot randomized clinical trial study included healthy and post-MI participants aged 65–85 years. Participants in each group were randomly assigned to consume 25 mL per day of one of three types of olive oils: high phenolic (HTyr/Tyr) extra virgin olive oil (HP-EVOO), extra virgin olive oil (EVOO), or refined olive oil (ROO) for a period of 26 weeks. Blood samples were collected at baseline and post-intervention to assess key biomarkers. Plasma levels of (poly)phenols, malondialdehyde (MDA), total antioxidant capacity (FRAP), lecithin-cholesterol acyltransferase activity (LCAT), and serum paraoxonase-1 (PON-1) activity were measured. A total of 34 individuals completed the study (mean age: 74 years). Baseline characteristics, including sex, age, body mass index (BMI), weight, blood pressure, and inflammatory markers like C-reactive protein (CRP) levels, did not differ significantly between the two groups. A significant increase in both FRAP levels and PON-1 activity was observed in post-MI participants following HP-EVOO consumption compared to baseline (p = 0.014). No significant changes were observed in MDA levels, LCAT activity, or plasma (poly)phenols. These results indicate that HP-EVOO may enhance antioxidant capacity, particularly FRAP and PON-1 activity, in elderly post-MI individuals. The observed differences between groups suggest that underlying cardiometabolic status may influence the response to olive oil phenolic compounds. Further studies are needed to explore the long-term cardiovascular effects. Full article

Postprandial dysmetabolism, which refers to the impaired regulation of glucose and lipid levels after meals, is recognized as an independent risk factor for cardiovascular diseases (CVDs). Diets rich in polyphenols have demonstrated potential in improving postprandial hyperglycemia and hyperlipidemia. This study investigates the effects of olive leaf polyphenols on postprandial metabolic outcomes following a high-fat and high-carbohydrate meal. A total of 36 healthy adults participated in a three-arm randomized crossover trial. They ingested either a biscuit made from olive leaf powder (OLB), olive leaf tea (OLT), or a placebo meal (CTRL) to assess the impact of olive leaf polyphenols on postprandial glycemia, lipid levels, platelet aggregation factor (PAF), and plasma antioxidant status (TAC). Although no statistically significant differences were observed in the primary biomarkers, including glucose and lipid profiles, a delayed insulin response was noted in the interventions involving olive leaf. These findings suggest that while acute olive leaf supplementation did not significantly alter postprandial glycemia or lipidemia, it may subtly influence insulin kinetics. Further research is needed to explore the long-term effects of olive leaf polyphenols on metabolic health, especially in populations at risk for CVDs. Full article

Background: Coronary artery disease (CAD) is a leading global cause of mortality. The role of calcium (Ca), a key metabolic and structural element, in atherosclerosis and inflammation remains unclear. Ca influences immune cell function and is a component of atherosclerotic plaques. Hair analysis reflects long-term mineral exposure and may serve as a non-invasive biomarker. Objectives: This pilot study aimed to investigate the association between hair Ca levels and acute coronary syndrome (ACS), and to evaluate correlations with the Systemic Inflammatory Index (SII), Systemic Inflammatory Response Index (SIRI), and selected CAD risk factors. Methods: Ca levels were measured in hair samples from patients undergoing coronary angiography for suspected myocardial infarction. Associations with ACS diagnosis, Syntax score, SII, SIRI, and CVD risk factors were analyzed. Results: Serum calcium levels were not significantly associated with the presence of acute coronary syndrome (ACS) (p = 0.392) or with its clinical subtypes, including ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), and unstable angina (UA) (p = 0.225). Diagnosis of ACS was linked to higher SII (p = 0.028) but not SIRI (p = 0.779). Ca levels correlated negatively with Syntax score (R = −0.19, p = 0.035) and SII (R = −0.22, p = 0.021) and positively with HDL-C (R = 0.18, p = 0.046). Conclusions: Hair calcium content may reflect subclinical inflammation and CAD severity. Although no direct link to ACS was observed, the associations with SII, HDL-C, and Syntax score suggest a potential diagnostic role which should be further explored in larger, well-controlled studies. Full article

Periodontal disease is a chronic inflammatory condition that extends beyond the oral cavity and is increasingly recognized as a significant contributor to cardiovascular disease, the leading cause of global mortality. Systemic inflammation serves as the key link between the two, with elevated biomarkers such as C-reactive protein and interleukin-6 observed in individuals with PD, driving endothelial dysfunction and atherogenesis. Epidemiological and mechanistic studies consistently demonstrate that PD not only heightens the risk of major adverse cardiovascular events but is also independently associated with increased all-cause and cardiovascular mortality. In parallel, emerging research underscores the protective role of regular physical activity and improved cardiorespiratory fitness, which attenuate systemic inflammation and may reduce the burden of both PD and CVD. This review integrates current evidence on the shared inflammatory mechanisms linking PD and CVD, highlights the systemic impact of poor oral health, and advocates for incorporating exercise-based interventions and oral health assessments into comprehensive cardiovascular risk management. A multidisciplinary approach—bridging cardiology, dentistry, and preventive medicine—may offer a novel strategy to reduce inflammation-driven morbidity and mortality. Full article

Patients with chronic kidney disease (CKD) face an increased risk of early vascular aging, progressive vascular calcification, and premature death. With increasing age, mitochondrial function and mitochondrial DNA copy number (mtDNA-cn) decline. This has been identified as an independent predictor of frailty and mortality in cardiovascular diseases (CVDs) and cancer. However, the relationship between mtDNA-cn and vascular calcification in the context of a uremic milieu remains ambiguous. We hypothesize that a lower mtDNA-cn is associated with medial calcification, as both are linked to impaired vascular health and accelerated aging. mtDNA-cn was analyzed in 211 CKD5 patients undergoing renal transplantation (RTx) and 196 healthy controls using quantitative PCR (qPCR) for three mtDNA genes (mtND1, mtND4, and mtCOX1) and single-locus nuclear gene hemoglobin beta (HbB). In 32 patients, mtDNA-cn was also quantified one year after RTx. The association between mtDNA-cn and vascular calcification scores, circulatory cell-free (ccf) mtDNA in plasma, and the surrogate marker of biological aging (skin autofluorescence) and CVD risk was assessed. mtDNA-cn was significantly lower in CKD5 patients than in controls and correlated with biological age, vascular calcification, and CVD risk. One year after RTx there was a significant recovery of mtDNA-cn in male patients compared to baseline levels. mtDNA-cn and ccf-mtDNA were inversely correlated. This prospective study provides novel insights into the link between low mtDNA-cn and vascular aging. It demonstrates that RTx restores mtDNA levels and may improve oxidative phosphorylation capacity in CKD. Further investigation is warranted to evaluate mtDNA as a biologically relevant biomarker and a potential therapeutic target for early vascular aging in the uremic environment. Full article

Rising morbidity and mortality from cardiovascular disease (CVD) have increased interest in precision and preventive management to reduce long-term sequelae. While retinal imaging has traditionally been recognized for identifying vascular changes in systemic conditions such as hypertension and type 2 diabetes mellitus, a new ophthalmologic field, cardiac-oculomics, has associated retinal biomarker changes with other cardiovascular diseases with retinal manifestations. Several imaging modalities visualize the retina, including color fundus photography (CFP), optical coherence tomography (OCT), and OCT angiography (OCTA), which visualize the retinal surface, the individual retinal layers, and the microvasculature within those layers, respectively. In these modalities, imaging-derived biomarkers can present due to CVD and have been linked to the presence, progression, or risk of developing a range of CVD, including hypertension, carotid artery disease, valvular heart disease, cerebral infarction, atrial fibrillation, and heart failure. Promising artificial intelligence (AI) models have been developed to complement existing risk-prediction tools, but standardization and clinical trials are needed for clinical adoption. Beyond risk estimation, there is growing interest in assessing real-time cardiovascular status to track vascular changes following pharmacotherapy, surgery, or acute decompensation. This review offers an up-to-date assessment of the cardiac-oculomics literature and aims to raise awareness among cardiologists and encourage interdepartmental collaboration. Full article

Cardiovascular diseases (CVDs) are among the leading causes of morbidity and mortality rates globally, presenting a severe threat to human health and life. Acute myocardial infarction (AMI) is one of the most common and extremely severe disorders within CVDs, causing an estimated 17.5 million deaths each year. Cardiac troponin I (cTnI) is considered a biomarker for myocardial infarction and a “gold standard” method for diagnosing AMI due to its high specificity and sensitivity. The ability to rapidly detect cTnI with high sensitivity is critical throughout the diagnosis and treatment process of AMI. It is a necessary precursor for doctors to quickly assess the disease and initiate subsequent therapies. This work comprehensively explores various techniques for the analysis and detection of cTnI. We systematically review current cutting-edge technologies used for cTnI detection. According to optical, electrical, and intelligent technology dimensions, this study meticulously classifies and elaborates on the research progress of related sensors. Based on current research findings and technological development trends, we further project the future research directions and application prospects of cTnI sensors. This is geared towards providing valuable references for the further development of this field. Full article

Cardiovascular diseases (CVDs) are the most prevalent cause of global mortality, highlighting the importance of understanding their molecular bases. Recently, small non-coding RNAs (miRNAS) were shown to affect messenger RNA (mRNA) stability, either by inhibiting translation or by causing degradation through base pairing with mRNAs, being negative regulators of protein translation. Moreover, miRNAs modulate many signaling pathways and cellular processes, including cell-to-cell communication. In the cardiovascular system, miRNAs control functions in cardiomyocytes, endothelial cells, smooth muscle cells, and fibroblasts. Because miRNA expression was detected in the blood of patients with various cardiovascular diseases, they are considered attractive candidates for noninvasive biomarkers. This study reviews the literature on the role played by miRNAs in heart development and diseases. The findings suggest that miRNA regulation may offer new perspectives for therapeutic interventions in heart diseases. Full article