Search Results (1,556)

Background and Objectives: Cardiac Syndrome X (CSX), a clinical entity within the Ischaemia with Non-Obstructive Coronary Arteries (INOCA) spectrum, is increasingly recognised as an inflammatory and systemic vascular disorder. Remnant cholesterol (RC) and inflammation are emerging contributors to residual cardiovascular risk; however, their combined role in microvascular angina remains unclear. This study aimed to evaluate the association between the remnant cholesterol inflammation index (RCII), integrating RC and high-sensitivity C-reactive protein (hs-CRP), and the clinical presence of CSX. Methods: This single-centre, retrospective observational study included 392 individuals who underwent coronary angiography between January 2023 and January 2025. The study population comprised 197 patients diagnosed with CSX and 195 control subjects with normal coronary anatomy and no objective evidence of myocardial ischaemia. RC was calculated as total cholesterol minus the sum of LDL-C and HDL-C, and RCII was derived as RC × hs-CRP. Importantly, invasive microvascular testing (e.g., CFR or IMR) was not performed. Logistic regression analyses were performed to identify independent predictors of CSX, and receiver operating characteristic (ROC) curve analysis was used to evaluate diagnostic performance. Results: Patients with CSX exhibited significantly higher levels of hs-CRP, SII, and RCII compared with controls (all p < 0.001). In the multivariable logistic regression analysis, RCII demonstrated an independent association with CSX (odds ratio 1.095, 95% confidence interval 1.060–1.131; p < 0.001). ROC curve analysis showed that RCII provided moderate but significant discrimination for CSX (area under the curve [AUC] 0.765, 95% CI 0.695–0.795). Pairwise comparisons confirmed that RCII had a significantly higher AUC than RC, hs-CRP, or SII individually. Conclusions: Higher RCII levels appear to be significantly associated with the clinical diagnosis of CSX. By integrating atherogenic remnant cholesterol burden and systemic inflammation, RCII may serve as a valuable composite biomarker for identifying residual inflammatory lipid risk. Rather than acting as a definitive diagnostic tool, these findings warrant further validation in large-scale prospective cohort studies. Full article

Open-heart surgery with cardiopulmonary bypass (CPB) is a high-risk procedure with significant morbidity and mortality. CPB, tissue injury, blood loss, endotoxemia and ischemia–reperfusion injury induce a pronounced systemic inflammatory response, leading to endothelial glycocalyx (EG) damage and vascular endothelial dysfunction. Consequently, immune cells, reactive oxygen species, and enzymes gain free access to vascular endothelial cells, resulting in their dysfunction and enhancing inflammation, vascular permeability, and microvascular impairment. EG degradation is most commonly assessed by measuring the circulating levels of its degradation products. Additionally, CPB triggers an early inflammatory response that is characterized by the secretion of interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor alpha, and IL-18, which play roles in initiating the process of EG injury. EG damage is further propagated by the sustained release of cytokines, inhibiting the regeneration of the glycocalyx layer. Heparanase and matrix metalloproteinases are enzymatic pathways involved in cytokine-mediated EG degradation after cardiac surgery, and the balance between the pro- and anti-inflammatory cytokines determines the magnitude and duration of the inflammatory response and EG impairment, which correlates with adverse clinical outcomes, including myocardial dysfunction, acute lung and kidney injury, neurological complications, and prolonged need for intensive care. Thus, identifying patients with an exaggerated cytokine response could potentially provide more personalized therapy based on the circulating biomarkers of EG shedding, and cytokine-directed preservation of EG represents a promising therapeutic strategy in vascular dysfunction prevention during and after open-heart surgery. In this review, we summarize the current knowledge on cytokine-mediated EG impairment following open-heart surgery with CPB. Full article

Background: Diabetic cardiomyopathy (DCM), a common cardiovascular complication associated with diabetes mellitus, has the potential to progress to heart failure. Apocynum venetum L. leaves extract (AVLE) possesses known cardioprotective activity, but its effect on DCM remains unclear. This study explored the protective effects of AVLE against myocardial injury in type 2 diabetes and the underlying mechanisms. Methods: DCM was established in vivo using db/db mice and in vitro using high-glucose, high-fat (HGHF)-stimulated H9c2 cardiomyocytes. We evaluated metabolic profiles, cardiac function, histopathology, oxidative stress, inflammation, and ferroptosis. Results: In vivo, following 12 weeks of AVLE treatment, cardiac function and structural integrity were significantly improved, serum cardiac injury markers and dyslipidemia were reduced, and pathological myocardial remodeling was attenuated in db/db mice; in vitro, AVLE enhanced cell viability and attenuated cellular damage under HGHF conditions. Mechanistically, AVLE alleviated oxidative stress and inflammation, restored mitochondrial function, and inhibited ferroptosis by regulating key pathway proteins; it upregulated GPX4 and SLC7A11, while downregulating TfR1 and ACSL4. Conclusions: AVLE exerts cardioprotective effects against diabetic cardiomyopathy by reducing oxidative stress and inflammation, mitigating lipid peroxidation and mitochondrial damage, ultimately inhibiting ferroptosis through regulation of the Xc⁻/GSH/GPX4 axis. Full article

Heart failure (HF) is a heterogeneous condition with a prevalence of about 1–3% in the population worldwide (percentage expected to rise), related to a significant clinical and economic burden. However, despite medical advancements in HF management, difficulties in facing this condition still persist, as the etiology and phenotype largely differ between patients. Thus, the identification of further key biomarkers remains attractive. One area of interest in recent years has focused on the role of lipids in HF pathophysiology and its clinical manifestations. In this context, ceramides, complex bioactive lipids with activity in key pathways related to stress response, cellular growth, proliferation, differentiation, apoptosis, oxidative stress, inflammation, and energy production, may be important in the HF scenario, primarily for the development and application of new therapeutic strategies targeting ceramide species. Accordingly, this review aims to discuss the role of ceramides in HF pathophysiology and clinical progression in view of available evidence, focusing on the possibility of therapeutic tools for improving cardiac function and outcomes in HF by modulating ceramide signaling and metabolism. Full article

Kalanchoe daigremontiana, a succulent herbaceous plant in the Crassulaceae family from Madagascar, has gained global popularity as an ornamental and medicinal species. This review examines the traditional uses, phytochemical composition, biological properties, toxicological aspects, and regulatory challenges of K. daigremontiana. The traditional medicinal uses of its leaves and roots include treating burns, rheumatic disorders, hypertension, diabetes, kidney pain, diarrhea, cough, fever, gastric issues, anxiety, inflammation, and cancer. Chemical compounds identified include phenolic acids, flavonoids, tannins, alkaloids, glycosides, saponins, sterols, terpenes, and fatty acids, with phenolic compounds and bufadienolides being predominant. In vitro studies of the crude extracts, bufadienolide-rich fractions, and isolated compounds have shown antioxidant, antibacterial, antifungal, antiviral, antiparasitic, anthelmintic, anti-inflammatory, anticoagulant, anti-aging, cytotoxic, antitumoral, and antiproliferative properties. In vivo studies have demonstrated hepatoprotective, skincare, and cardiac-glycoside-like effects. While crude extracts and bufadienolide-rich fractions have shown toxic effects in 2-week-old chicks, guinea pigs, and Artemia salina, no toxicity has been reported in goats, broiler chickens, laying hens, or human erythrocytes. Although K. daigremontiana-based products are commercially available as dietary supplements with various health claims, these lack scientific validation. Despite the potential pharmaceutical applications of K. daigremontiana, further research is needed to determine its effects, dosage, mechanisms, long-term safety, and side effects, with clinical studies essential to validate its therapeutic potential. Full article

Cardiovascular emergencies most frequently arise from the sudden destabilization of atherosclerotic plaques. Conventional diagnostic strategies predominantly focus on luminal stenosis, despite the fact that most acute coronary events originate from non-obstructive lesions with high inflammatory activity. Recent advances in cardiac computed tomography (CCT) enable visualization of plaque morphology and surrounding perivascular fat, offering a unique window into coronary inflammation. The fat attenuation index (FAI), derived from pericoronary adipose tissue (PCAT) radiodensity, has emerged as a dynamic imaging biomarker capable of detecting vascular inflammation before clinical events occur. This review summarizes current evidence on the role of PCAT inflammation in plaque vulnerability, its implications for acute cardiovascular presentations, and recent technological innovations—including AI-enhanced analysis and photon-counting CT—that advance risk prediction. Inflammation-based imaging derived from CCT, including PCAT-FAI, has emerged as a promising research tool that may enhance risk stratification in patients presenting with chest pain. These developments signify a shift from purely anatomical assessment toward biological characterization of CAD, potentially transforming prevention and acute care. Full article

Background: Thrombosis in light chain amyloidosis (LCA) occurs in the context of multiple organ dysfunction and inflammation. Conventional coagulation tests (screening) may not sufficiently capture the procoagulant substrate in the inflammatory/therapeutic dynamics. Methods: A total of 61 consecutive patients with LCA were prospectively included in the study. Clinical data, including organ involvement, time of diagnosis, treatment phase, DOAC exposure and thrombosis history were systematically recorded and subjected to screening. Specialized hemostasis tests such as APTT/PT, fibrinogen, D-dimer, TEG and TGT were performed and conventional times were analyzed in the subgroup without DOAC. Results: The prevalence of documented thrombosis was 32.8%, and thrombosis status was associated with TEG positivity and more strongly with TGT positivity. Hypercoagulability was identified in 50.8% by TEG and 41.0% by TGT, regardless of whether APTT/PT were within the reference values. APTT/PT did not predict thrombosis recurrence (p > 0.05), which was predicted by TEG (p = 0.0027) and TGT (p = 0.0006). An inflammation/fibrin turnover panel (CRP, fibrinogen, D-dimer) predicted TEG positivity (p < 0.0001), but not TGT, and was correlated with assessment at diagnosis, daratumumab-based therapy, and cardiac involvement. Conclusions: Global tests (TEG/TGT) promptly correlate with thrombosis recurrence in our cohort and provide crucial information in addition to clotting times for thrombotic phenotyping. Inflammation can influence TEG, so the decision to recommend the tests and the timing of their performance should be adapted to the clinical, biological, and therapeutic context. Full article

Background: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by immune dysregulation and systemic inflammation, with the cardiovascular (CV) system representing a major yet frequently under-recognized target. Cardiac involvement spans from subclinical myocardial inflammation to overt pericardial disease, myocarditis, valvular abnormalities, coronary microvascular dysfunction, and accelerated atherosclerosis. Given that CV disease remains a leading cause of morbidity and mortality in SLE, early detection of silent cardiac injury is crucial. Aim: This review aims to provide a comprehensive and clinically oriented overview of CV involvement in SLE, focusing on the role of multimodal cardiac imaging in the detection, characterization, and risk stratification of cardiac abnormalities, as well as its potential implications for clinical management and preventive strategies. Methods: This narrative review is based on a structured, non-systematic search of PubMed (2013–2026), combining the term “systemic lupus erythematosus” with imaging-related keywords including “transthoracic echocardiography,” “cardiac magnetic resonance,” and “cardiac computed tomography.” English-language studies in adult populations were screened and selected according to clinical relevance, methodological robustness, and contribution to understanding SLE-related cardiac involvement. Discussion: Multimodal cardiac imaging plays a central role in the evaluation of SLE-related cardiac disease. Transthoracic echocardiography (TTE) represents the first-line modality for the assessment of ventricular function, pericardial disease, and valvular abnormalities, while deformation imaging enables the detection of subtle myocardial dysfunction. Cardiac magnetic resonance (CMR) provides comprehensive tissue characterization, allowing differentiation between active inflammation and chronic fibrosis. Cardiac computed tomography (cCT) identifies subclinical coronary atherosclerosis and high-risk plaque features, whereas nuclear imaging techniques offer insight into inflammatory activity and microvascular dysfunction. Conclusions: An integrated, imaging-based approach enables early diagnosis, refined CV risk stratification, longitudinal monitoring, and personalized therapeutic strategies. Multimodal imaging thus represents a key pillar of precision medicine in lupus-associated CV disease. Full article

Cardiac sarcoidosis (CS) is a critical and frequently underdiagnosed phenotype of sarcoidosis, characterized by non-caseating granulomatous infiltration of the myocardium. This review synthesizes current knowledge regarding the pathogenesis, diagnosis, and management of CS. The disease manifests with a heterogeneous clinical spectrum ranging from asymptomatic conduction abnormalities to life-threatening ventricular arrhythmias and heart failure. Diagnosis remains challenging due to the patchy distribution of granulomas, which limits the sensitivity of endomyocardial biopsy. Consequently, a multimodal diagnostic approach is essential, integrating advanced imaging modalities such as cardiac magnetic resonance (CMR) with late gadolinium enhancement (LGE) and ¹⁸F-fluorodeoxyglucose positron emission tomography (FDG-PET). These tools not only facilitate detection but also enable the differentiation of active inflammation from chronic fibrosis. Histopathological assessment, supported by specific immunophenotyping and electron microscopy, remains the gold standard for confirming diagnosis and excluding mimics like giant cell myocarditis or infectious granulomatous diseases. Management requires a multidisciplinary strategy combining immunosuppressive therapy, primarily corticosteroids and steroid-sparing agents, with guideline-directed cardiac care, including implantable cardioverter-defibrillators for arrhythmia risk stratification. Emerging biomarkers and artificial intelligence-driven imaging analysis promise to further refine risk stratification and therapeutic monitoring, advancing precision medicine in this complex disorder. Full article

Heart failure (HF) is a systemic syndrome in which cardiac dysfunction is closely linked to multiorgan involvement, including the gastrointestinal tract. Increasing evidence highlights the relevance of the gut–heart axis in HF pathophysiology, whereby intestinal hypoperfusion, congestion, and barrier dysfunction promote gut microbiota dysbiosis, systemic inflammation, and adverse cardiovascular outcomes. In parallel, the advent of novel HF therapies, particularly sodium–glucose cotransporter 2 inhibitors (SGLT2i) and the angiotensin receptor–neprilysin inhibitor sacubitril/valsartan, has markedly improved clinical outcomes across HF phenotypes. Beyond their established cardiovascular benefits, these therapies may exert pleiotropic effects that extend to the intestinal environment and the gut microbiota. Through integrated actions on hemodynamics, neurohormonal activation, metabolic pathways, and inflammatory processes, recent data suggest that novel HF drugs may indirectly influence the gut-microbial composition and function. Conversely, the gut microbiota may modulate drug efficacy and result in interindividual variability in therapeutic responses, suggesting a bidirectional interaction between pharmacological treatment and the gut ecosystem. This narrative review summarizes current evidence of gut microbiota alterations in HF and critically examines emerging data on interactions between the gut microbiota and novel HF therapies, focusing on SGLT2 inhibitors and sacubitril/valsartan. Understanding this crosstalk may support the development of microbiota-informed, personalized therapeutic strategies in heart failure. Full article

Background: Cardiac amyloidosis (CA) is an increasingly recognized cause of heart failure with preserved ejection fraction, resulting from myocardial deposition of misfolded amyloid fibrils derived predominantly from transthyretin (ATTR wild-type [ATTRwt] or variant [ATTRv]) or immunoglobulin light chains (AL). Despite advances in noninvasive imaging and disease-modifying therapies, delayed diagnosis remains common, and clinically actionable molecular biomarkers for early detection, phenotypic discrimination, and therapeutic monitoring are limited. MicroRNAs (miRNAs), small noncoding regulators of post-transcriptional gene expression, have emerged as key modulators of cardiovascular remodeling and systemic amyloid biology. Methods: We performed a comprehensive review of experimental, translational, and clinical studies to evaluate the role of miRNAs in transthyretin and light-chain cardiac amyloidosis, incorporating data from myocardial tissue analyses, circulating miRNA profiling, and mechanistic studies in cellular and animal models. Results: Dysregulated miRNA networks contribute to amyloid-induced cardiac injury by modulating mitochondrial energetics, oxidative stress, inflammation, fibrosis, proteostasis, and neurocardiac signaling. Specific miRNAs, including members of the miR-21, miR-29, and miR-30 families, as well as miR-150-5p and miR-339, have been associated with amyloid burden, adverse myocardial remodeling, plasma cell biology, and disease severity. Distinct circulating and tissue miRNA signatures differentiate transthyretin from light-chain cardiac amyloidosis and correlate with functional status, heart failure biomarkers, and clinical outcomes. Conclusions: MiRNAs represent promising diagnostic and prognostic biomarkers in cardiac amyloidosis and offer mechanistic insights into disease pathogenesis. Integration of miRNA profiling with multimodality imaging and emerging RNA-based therapeutics may enable earlier diagnosis and support precision management of amyloid-related heart failure. Full article

Risk assessment for immediate mortality is a vital component of the preoperative assessment in elective cardiac surgeries of the adult population. It is generally used to inform consent and plan postoperative care, but can also help identify patients who need preoperative optimization. Risk assessment for open cardiac interventions remains difficult, as an absolute risk assessment tool is still lacking. In this narrative review, we examine recent data on the predictive performance of commonly used risk assessment tools in cardiac surgery and explore missed opportunities to improve predictive performance, including overlooked independent predictors and alternative calculation strategies, such as machine learning. The literature shows that the most popular risk assessment tools are the Parsonnet score, EuroSCORE II, STS-PROM, and ACEF. These have reasonable discriminative capabilities across most populations but occasionally suffer from poor calibration and over- or underprediction. Preoperative inflammation, functional status, physical performance, nutrition, and frailty are potentially relevant clinical factors that could improve mortality prediction modeling using traditional approaches. By far, the largest advancement comes from artificial intelligence-based models that demonstrate superior predictive capabilities utilizing the same predictors. These models are still in development, have not received external validation, are not yet trusted by physicians, and may not be accessible to all institutions due to computing limitations, and thus are not ready for global rollout. Further research in identifying novel predictors of mortality is required, and efforts are needed to validate machine learning models in external cohorts. Full article

Myocardial infarction is a major cardiovascular event that leads to heart failure and death. Although current vascular regeneration and pharmacological therapies can salvage some myocardial tissue, they cannot effectively reverse established necrosis, fibrosis, or adverse ventricular remodeling, thus necessitating novel repair strategies. Silk fibroin (SF), a natural biomaterial, has emerged as an ideal substrate for cardiac tissue engineering owing to its excellent biocompatibility, tunable mechanical properties, and controllable biodegradability. This paper systematically reviews SF-based myocardial repair strategies: SF cardiac patches can be directly applied to infarct areas, providing mechanical support and delivering bioactive substances, while injectable SF hydrogels can be formed in situ via minimally invasive methods, serving as three-dimensional delivery vehicles for cells or drugs. These approaches synergistically promote cardiac repair through multiple mechanisms, including active regulation of inflammation, promotion of angiogenesis, and inhibition of fibrosis. Future development of SF-based therapies will focus on creating smart responsive materials, constructing biomimetic structures via advanced biomanufacturing techniques, and accelerating clinical translation, thereby providing comprehensive solutions for myocardial infarction repair. Full article

Background: Inflammatory bowel disease (IBD), comprising Crohn’s disease (CD) and ulcerative colitis (UC), has been associated with elevated cardiovascular risks. However, the impact of IBD on outcomes following percutaneous coronary intervention (PCI) remains underexplored. We aimed to evaluate the clinical and procedural outcomes of PCI in patients with concurrent IBD. Methods: This study utilized the National Readmission Database from 2016 to 2020 to evaluate outcomes such as all-cause mortality and post-PCI complications, including various cardiovascular and gastrointestinal (GI) complications in IBD patients undergoing PCI. Patients with concurrent IBD and PCI were compared to non-IBD controls via multivariable logistic regression. Results: On propensity-score-matching analysis, IBD patients undergoing PCI had a higher prevalence of GI complications, including acute liver failure (Odds ratio (OR) 1.48, 95% confidence interval (CI) 1.13–1.93, p = 0.004), mesenteric ischemia (OR 5.34, 95% CI 1.56–18.40, p = 0.007), and need for blood transfusion (OR 1.74, 95% CI 1.46–2.08, p < 0.001). There was also a higher rate of cardiac complications (OR 1.31, 95% CI 1.05–1.64, p = 0.017). No significant difference in all-cause mortality (OR 0.86, 95% CI 0.72–1.04, p = 0.113) was observed. Conclusions: IBD patients undergoing PCI face increased GI and cardiovascular complications without a significant mortality difference. These findings highlight the complex interplay between systemic inflammation, vascular integrity, and procedural outcomes in IBD patients. Full article

Background: Systemic inflammation is a key driver of heart failure (HF) progression across all ejection fraction (EF) phenotypes, with diet emerging as a modifiable factor influencing cardiac metabolism and inflammatory signaling. This narrative review integrates current evidence on the inflammatory mechanisms underlying HF, their links with common comorbidities and emerging anti-inflammatory therapeutic strategies, with a particular focus on the role of nutrition in supporting healthy cardiac metabolism. Methods: We searched MEDLINE/PubMed, EMBASE, Web of Science, the Cochrane Library, Scopus and reference lists of relevant publications using terms related to systemic inflammation, dietary patterns and HF prioritizing high-impact studies on nutrition–inflammation–HF interactions published from 2000 onward. Results: Major HF comorbidities sustain chronic, low-grade inflammation through elevated cytokine activity. Dietary patterns—especially those with high Dietary Inflammatory Index (DII)—substantially shape inflammatory milieu. The Mediterranean diet appears to have a favorable inflammatory profile with reduction in circulating pro-inflammatory biomarkers, especially C-reactive protein (CRP) and interleukin-6 (IL-6). Established therapies for HF with reduced ejection fraction and vagus nerve stimulation elicit anti-inflammatory efficacy through cytokine suppression. Sodium glucose cotransporter-2 (SGLT2) inhibitors demonstrate positive metabolic effects and anti-inflammatory actions through decrease in IL-6 and tumor necrosis factor-α (TNF-α). Interleukin-1 blockade has produced heterogeneous clinical outcomes, while definitive findings examining the role of IL-6 inhibitors in inflammation suppression and possible benefit on cardiac outcomes are anticipated. Preliminary data show the potential synergistic effects of dietary patterns/nutrients and pharmacological agents combination on improvement of endothelial function and attenuation of the fibrotic process, although there is a need for further research in large-scale trials. Conclusions: Systemic inflammation demonstrates a key role in HF initiation and progression, and the effect of diet on inflammatory pathways is central. Dietary patterns targeting inflammation-related mechanisms (inflammasome, gut dysbiosis) can lead to attenuation of systemic inflammatory response and restoration of cardiac metabolic flexibility. A deeper mechanistic discernment of cardiac inflammatory cascades, together with identification of HF subpopulations with excessive inflammatory activity, may facilitate the design of targeted randomized controlled trials (RCTs) aiming for novel personalized, inflammation-targeted HF therapies with potential clinical benefit. Full article