Search Results (96)

Background: Despite therapeutic advances, morbidity and mortality remain high in patients with rheumatoid arthritis (RA) and psoriatic arthritis (PsA), primarily due to increased cardiovascular risk. Objectives: Our study aimed to evaluate the cardiovascular risk profile and biomarker dynamics in patients with RA and PsA treated with Janus kinase inhibitors (JAKis). To our knowledge, this is the first study assessing Lp(a) levels in this context. Methods: This prospective, observational study assessed 48 adult patients. The follow-up period was 12 months. Traditional cardiovascular risk factors and biological markers, including lipid profile, lipoprotein(a) [Lp(a)], and uric acid (UA), were assessed at baseline and follow-up. Correlations between JAKi therapy, lipid profile changes, and cardiovascular risk factors were investigated. Cox regression analysis was used to identify predictors of non-major cardiovascular events. Results: A strong positive correlation was observed between baseline and 12-month Lp(a) levels (r = 0.926), despite minor statistical shifts. No major cardiovascular events occurred during follow-up; however, 47.9% of patients experienced non-major cardiovascular events (e.g., uncontrolled arterial hypertension, exertional angina, and new-onset arrhythmias). Active smoking [hazard ratio (HR) 9.853, p = 0.005], obesity (HR 3.7460, p = 0.050), and arterial hypertension (HR 1.219, p = 0.021) were independent predictors of these events. UA (HR 1.515, p = 0.040) and total cholesterol (TC) (HR 1.019, p = 0.034) were significant biochemical predictors as well. Elevated baseline Lp(a) combined with these factors was associated with an increased event rate, particularly after age 60. Conclusions: Traditional cardiovascular risk factors remain highly prevalent and predictive, underscoring the need for comprehensive cardiovascular risk management. Lp(a) remained stable and may serve as a complementary biomarker for risk stratification in JAKi-treated patients. Full article

Background/Objectives: Elevated serum uric acid levels are associated with the occurrence, development, and adverse events of coronary heart disease (CHD) and CHD risk factors. However, the extent of any pathogenic effect of the serum uric acid on CHD and whether CHD risk factors play a confounding or mediating role are still unclear. Methods: The potential causal associations of serum uric acid with CHD were evaluated via cross-trait linkage disequilibrium score regression analysis and Mendelian randomization. The pleiotropy of genetic tools was analyzed via a Bayesian colocalization approach. Moreover, we utilized two-step MR to identify risk factors mediating the relationship between uric acid and CHD. Results: Mendelian randomization results derived from two genetic instrument selection strategies support that serum uric acid levels have a significant causal relationship with coronary artery disease, stable angina pectoris, and myocardial infarction. This causal relationship was partially mediated by diastolic blood pressure, mean arterial pressure, and serum triglycerides. Transcriptomic analysis revealed that serum uric acid may directly contribute to the development of atherosclerosis by inducing transcriptomic changes in macrophages. Conclusions: Our findings highlight that the control of serum urate concentration in the long-term management of CHD patients may be necessary. Well-designed clinical trials and foundational research are presently required to furnish conclusive proof regarding the specific clinical scenarios in which adequate reduction in urate concentrations can confer cardiovascular advantages. Full article

Aim: The frontal QRS-T (fQRS-T) angle serves as an electrocardiography indicator that visually represents the disparity between the frontal QRS axis and the T axis. The heterogeneity between cardiac depolarization and repolarization rises with an increase in the fQRS-T angle. Prior research has demonstrated a relationship between the fQRS-T angle and the extent of atherosclerosis, along with the risk of cardiovascular mortality. The non-alcoholic fatty liver disease fibrosis score (NFS) is a non-invasive scoring tool used to quantify the degree of liver fibrosis in individuals with non-alcoholic fatty liver disease (NAFLD). Non-alcoholic fatty liver disease increases the risk of atherosclerotic cardiovascular disease, which can be predicted using the NFS. The objective of this study is to examine the potential correlation between the fQRS-T angle and NFS in patients with stable angina pectoris. Materials and Methods: This cross-sectional study included 177 (48 women) non-alcoholic patients who underwent coronary angiography due to stable angina pectoris. Individual NFS values were calculated using clinical and laboratory data. Patients were categorized into two groups based on a NFS threshold value of 0.67. Following a minimum fasting period of 12 h, biochemical laboratory parameters were acquired using a peripheral venous sample, and electrocardiographic data were recorded. Results: The univariate logistic regression analysis revealed significant associations between hypertension (p = 0.018), coronary artery disease (p = 0.014), neutrophil (p = 0.024), hemoglobin (p = 0.038), and low-density lipoprotein (LDL, p = 0.007) with the NFS. The electrocardiographic variables related to the score included the QRS duration (p = 0.015), Pmax (p = 0.026), QTC interval (p = 0.02), and fQRS-T angle (p < 0.001). In the multivariate logistic regression analysis, NFS was independently associated with LDL (OR: 0.984, 95% CI: 0.970–0.998, p = 0.024) and fQRS-T angle (OR: 3.472, 95% CI: 1.886–6.395, p < 0.001). Conclusions: The FQRS-T angle may exhibit a distinct correlation with NAFLD. Extensive investigations should validate this link, since the fibrosis score can serve as an effective tool for monitoring patients prior to the onset of clinical symptoms associated with liver fibrosis. Full article

Objectives: Contrast-induced acute kidney injury (CI-AKI) remains a frequent and serious complication after cardiac catheterization. Sirtuin-1 (SIRT1), a NAD+-dependent deacetylase, plays a central role in renal protection against ischemia-reperfusion injury, inflammation, and vascular dysfunction. We aimed to investigate whether serum SIRT1 levels could serve as an early diagnostic biomarker for CI-AKI. Methods: This prospective case-control study included 50 patients undergoing elective percutaneous coronary intervention (PCI) for stable angina. Serum SIRT1 levels were measured at baseline, 24 h, and 72 h post-PCI. The occurrence of CI-AKI was defined by a standard rise in serum creatinine, and patients were stratified accordingly. Results: Although SIRT1 levels tended to be lower in patients who developed CI-AKI (n = 17) compared to those without (n = 33), the differences were not statistically significant at any time point (p > 0.05). However, a significant between-group difference was observed in the 72-h change in SIRT1 levels (Δ0–72 h, p = 0.037), with a greater decline in the CI-AKI group. Multivariable logistic regression also revealed a trend-level inverse association between 72-h SIRT1 levels and CI-AKI (β = −0.536, p = 0.099). Conclusions: While SIRT1 is biologically plausible as a renal protective factor, our findings suggest that serial SIRT1 measurement may offer added value as a dynamic biomarker rather than a static diagnostic tool. Confirmatory trials incorporating serial SIRT1 measurements may help translate this molecular signal into clinically actionable tools for early detection of CI-AKI. Full article

Background: Inflammation plays a critical role in the progression of coronary heart disease (CHD). Low-dose colchicine has shown promise in reducing cardiovascular events, and green Brazilian propolis extract (EPP-AF® (standardized Brazilian green propolis extract) was provided by Apis Flora Indl. Coml. Ltda, Ribeirão Preto, SP, Brazil), known for its anti-inflammatory properties, may offer additional therapeutic benefits. This pilot study aimed to evaluate whether six weeks of EPP-AF^® supplementation improves functional capacity assessed by treadmill exercise testing. Methods: This was a randomized, double-blind, placebo-controlled pilot study conducted at a coronary disease clinic in Brazil. Patients aged ≥ 18 years with stable CHD receiving optimized medical therapy were randomized in a 2:1 ratio to receive either 200 mg of EPP-AF^® or placebo twice daily for six weeks. The primary outcome was the change in treadmill exercise duration (in seconds). Secondary outcomes included total exercise time, functional capacity (measured in metabolic equivalents of task [METs]), high-sensitivity C-reactive protein (hs-CRP) levels, the Seattle Angina Questionnaire (SAQ), and the Canadian Cardiovascular Society (CCS) angina classification. Statistical analysis was performed on an intention-to-treat basis. Results: A total of 59 patients were randomized, with a median follow-up of 6.5 weeks. There was no significant difference in the primary endpoint between groups: the median change in treadmill test time was 39 s in the EPP-AF^® group versus 30 s in the placebo group (p = 0.83). No improvements were observed in METs, hs-CRP levels, SAQ scores, or CCS class in the EPP-AF^® group. No major adverse cardiovascular events occurred during the study. Conclusions: EPP-AF^® did not improve functional capacity, inflammatory markers, or angina symptoms in patients with stable CHD compared to placebo. Full article

Objectives: Early identification of myocardial ischemia is critical for the management of patients with stable angina pectoris (SAP). The Naples Prognostic Score (NPS) and the Systemic Immune-Inflammation (SII) index are emerging biomarkers that may improve risk stratification prior to myocardial perfusion scintigraphy (MPS) Methods: We retrospectively analyzed 615 patients with SAP who underwent MPS to assess the predictive value of the NPS and SII index for myocardial ischemia. Clinical, laboratory, and imaging data were collected. The associations between the NPS, SII, and ischemia detected on MPS were evaluated through univariate and multivariate logistic regression analyses. Results: A higher NPS was strongly associated with the presence of myocardial ischemia (p < 0.001). Male sex, elevated SII, and increased C-reactive protein (CRP) and neutrophile-to-lymphocyte ratio (NLR) values were also significantly related to ischemia. In multivariate analysis, NPS (p < 0.001), SII (p = 0.023), CRP (0.005), and NLR (0.037) values remained independent predictors of ischemia. Albumin levels were significant in univariate analysis but lost independent significance after adjustment. The incorporation of the NPS and SII index provided additional value in identifying patients at high risk of ischemia. Conclusions: The NPS and the SII index are inexpensive, very simple, non-invasive, and valuable markers of myocardial ischemia in patients with SAP. Their integration into clinical practice may enhance risk stratification and optimize diagnostic pathways, minimizing unnecessary invasive procedures. Full article

Cardiovascular complications are a hallmark of Post-Acute Sequelae of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection (PASC), yet the mechanisms driving persistent cardiac dysfunction remain poorly understood. Emerging evidence implicates mitochondrial dysfunction in immune cells as a key contributor. This study investigated whether CD14⁺⁺ monocytes from long COVID patients exhibit bioenergetic impairment, mitochondrial DNA (mtDNA) damage, and defective oxidative stress adaptation, which may underlie cardiovascular symptoms in PASC. CD14⁺⁺ monocytes were isolated from 14 long COVID patients with cardiovascular symptoms (e.g., dyspnea, angina) and 10 age-matched controls with similar cardiovascular risk profiles. Mitochondrial function was assessed using a Seahorse Agilent Analyzer under basal conditions and after oxidative stress induction with buthionine sulfoximine (BSO). Mitochondrial membrane potential was measured via Tetramethylrhodamine Ethyl Ester (TMRE) assay, mtDNA integrity via qPCR, and reactive oxygen species (ROS) dynamics via Fluorescence-Activated Cell Sorting (FACS). Parallel experiments exposed healthy monocytes to SARS-CoV-2 spike protein to evaluate direct viral effects. CD14⁺⁺ monocytes from long COVID patients with cardiovascular symptoms (n = 14) exhibited profound mitochondrial dysfunction compared to age-matched controls (n = 10). Under oxidative stress induced by buthionine sulfoximine (BSO), long COVID monocytes failed to upregulate basal respiration (9.5 vs. 30.4 pmol/min in controls, p = 0.0043), showed a 65% reduction in maximal respiration (p = 0.4035, ns) and demonstrated a 70% loss of spare respiratory capacity (p = 0.4143, ns) with significantly impaired adaptation to BSO challenge (long COVID + BSO: 9.9 vs. control + BSO: 54 pmol/min, p = 0.0091). Proton leak, a protective mechanism against ROS overproduction, was blunted in long COVID monocytes (3-fold vs. 13-fold elevation in controls, p = 0.0294). Paradoxically, long COVID monocytes showed reduced ROS accumulation after BSO treatment (6% decrease vs. 1.2-fold increase in controls, p = 0.0015) and elevated mitochondrial membrane potential (157 vs. 113.7 TMRE fluorescence, p = 0.0179), which remained stable under oxidative stress. mtDNA analysis revealed severe depletion (80% reduction, p < 0.001) and region-specific damage, with 75% and 70% reductions in amplification efficiency for regions C and D (p < 0.05), respectively. In contrast, exposure of healthy monocytes to SARS-CoV-2 spike protein did not recapitulate these defects, with preserved basal respiration, ATP production, and spare respiratory capacity, though coupling efficiency under oxidative stress was reduced (p < 0.05). These findings suggest that mitochondrial dysfunction in long COVID syndrome arises from maladaptive host responses rather than direct viral toxicity, characterized by bioenergetic failure, impaired stress adaptation, and mitochondrial genomic instability. This study identifies persistent mitochondrial dysfunction in long COVID monocytes as a critical driver of cardiovascular complications in PASC. Key defects—bioenergetic failure, impaired stress adaptation and mtDNA damage—correlate with clinical symptoms like heart failure and exercise intolerance. The stable elevation of mitochondrial membrane potential and resistance to ROS induction suggest maladaptive remodeling of mitochondrial physiology. These findings position mitochondrial resilience as a therapeutic target, with potential strategies including antioxidants, mtDNA repair agents or metabolic modulators. The dissociation between spike protein exposure and mitochondrial dysfunction highlights the need to explore host-directed mechanisms in PASC pathophysiology. This work advances our understanding of long COVID cardiovascular sequelae and provides a foundation for biomarker development and targeted interventions to mitigate long-term morbidity. Full article

Objectives: This study compared the efficacy of continuous insulin infusion therapy (CIT) versus standard bolus insulin therapy in maintaining optimal perioperative glycemic control in patients with type 2 diabetes mellitus (T2DM) undergoing coronary artery bypass grafting (CABG), focusing on postoperative outcomes. Methods: In this single-center, open comparative study, 214 T2DM patients were selected from 1372 CABG cases (2016–2018) and divided into CIT (n = 28) and bolus therapy (n = 186) groups. Both groups were matched for sex, age, smoking status, body mass index, functional class of angina or heart failure, surgical characteristics and preoperative HbA1c. The target glucose range was 7.8–10 mmol/L (140–180 mg/dL), consistent with current guidelines. Glycemic control was assessed through frequent postoperative measurements, with particular attention to glucose variability and hypoglycemic events. Results: The CIT group demonstrated superior glycemic control, with significantly lower median glucose levels at 7, 8, 10, 12, and 13 h post-CABG (p < 0.05). Glycemic variability was reduced by 32% in the CIT group (p = 0.012), and the incidence of hypoglycemia (<3.9 mmol/L) was 3.6% versus 8.1% in the bolus group. While overall complication rates were similar, the CIT group had 0 cases of stroke, myocardial infarction, or wound infections versus 2.7%, 3.2%, and 5.9%, respectively, in the bolus group. Logistic regression confirmed that each 1 mmol/L increase in first-day glucose levels independently predicted both significant (OR 1.20, 95% CI 1.06–1.36) and serious complications (OR 1.16, 95% CI 1.03–1.30). Conclusions: CIT provided more stable postoperative glycemic control with reduced variability and hypoglycemia risk in T2DM patients after CABG. Although underpowered to detect differences in rare complications, our findings suggest CIT may improve outcomes. These results warrant validation in larger randomized trials. Full article

Several studies evaluated the association between adipokines, including leptin, in patients with acute coronary syndrome (ACS). Nevertheless, the results have been inconclusive and conflicting. Therefore, we assessed the pertinent published studies and evaluated the association between leptin levels and ACS. In January 2023, we conducted a comprehensive systematic search using Web of Science, PubMed, Scopus, and Embase. Using the Newcastle–Ottawa Scale, we evaluated the quality of all the articles we included. The principal summary outcome was the mean difference (MD) in leptin levels. We included 16 studies in our systematic review, 10 of which were included in meta-analysis. The MD in leptin levels was then evaluated in each subgroup: the patients with ACS versus the controls, the patients with ACS versus the patients with stable angina pectoris (SAP), and the patients with type 2 diabetes mellitus (T2DM) and ACS versus the patients without diabetes, but with ACS. Respectively, the following MDs were obtained: 10.508 (95% CI 3.670–17.346); 2.408 (95% CI −0.150–4.966); and 17.089 (95% CI 5.565–28.612). The leptin levels were significantly higher in the patients with ACS compared to the healthy controls, as well as in the patients with ACS and T2DM compared to those without T2DM. However, no statistically significant increase in leptin levels was observed when comparing the patients with ACS to those with SAP. Full article

Background: Lower socioeconomic status (SES) has been associated with increased mortality from coronary heart disease. This excess risk, relative to affluent patients, may be due to a combination of more adverse cardiovascular-risk factors, inequalities in access to cardiac investigations, longer waiting times for cardiac revascularisation and lower use of secondary prevention drugs. We sought to investigate whether socio-economic status influenced long-term all-cause mortality after PCI in a large metropolitan city (London), which serves a population of 11 million people with a mixed social background over a 10-year period. Methods: We conducted an observational cohort study of 123,780 consecutive PCI procedures from the Pan-London (United Kingdom) PCI registry. This data set is collected prospectively and includes all patients treated between January 2005 and December 2015. The database includes PCI performed for stable angina and ACS (ST-elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina). Patient socio-economic status was defined by the English Index of Multiple Deprivation (IMD) score, according to residential postcode. Patients were analysed by quintile of IMD score (Q1, least deprived; Q5, most deprived). Median follow-up was 3.7 (IQR: 2.0–5.1) years and the primary outcome was all-cause mortality. Results: The mean age of the patients was 64.3 ± 12.1 years and 25.2% were female. A total of 22.4% of patients were diabetic and 27.3% had a history of previous myocardial infarction. The rates of long-term all-cause mortality increased progressively across quintiles of IMD score, with patients in Q5 showing significantly higher long-term mortality rates compared with patients in Q1 (p = 0.0044). This persisted following the inclusion of a propensity score in the proportional hazard model as a covariate (HR for Q5 compared to Q1: 1.15 [95% CI: 1.10–1.42]). Conclusions: This study has demonstrated that low SES is an independent predictor of adverse clinical outcomes following PCI in the large, diverse metropolitan city of London. There clearly are inequalities in cardio-vascular risk factors, time to access to medical treatment/PCI, access to complex imaging and devices during PCI, access to secondary prevention after PCI, and even race differences. Hence, attention to reducing the burden of cardiovascular risk factors and improving primary prevention, particularly in patients with lower SES, is required. Full article

Background: Invasive coronary angiography is the gold standard for assessing in-stent restenosis (ISR) in patients with coronary artery disease. However, the predictive value of non-invasive Tissue Doppler Imaging (TDI) to evaluate patients with ISR has not been studied extensively. Methods: A total of 41 patients (19 with acute myocardial infarction and 22 with stable angina pectoris) who received percutaneous coronary intervention (PCI) were enrolled in the study. Time-to-peak velocities (TpV) of 12 non-apical segments of the left ventricle, by pulse wave TDI echocardiography, were obtained within two days prior to the PCI and six months later. Results: A 12-segmental mean TpV ≥ 279.6 ms at six months after PCI was able to detect ISR (odds ratio: 2.09, 95% CI 1.004–4.352, p = 0.049). Moreover, a significant decrease in the standard deviation of TpV was demonstrated in patients without ISR (85.8 ± 44.8 vs. 60.3 ± 31.7 ms, p = 0.001), but not in patients with ISR (97.7 ± 53.3 vs. 91.2 ± 52.6 ms, p = 0.57). Conclusions: Pulse-wave TDI echocardiography is a promising tool in the detection of ISR six months after PCI in patients with coronary artery disease. Full article

Background: A considerable number of patients with angina undergo invasive coronary angiography, which might reveal non-obstructive coronary arteries (ANOCA). In this setting, they might have coronary microvascular disease (CMD). Its prevalence significantly varies in the literature. This systematic review aims to document the prevalence of CMD over time according to the diagnostic modalities. Methods: A systematic literature review was conducted using PubMed, the Cochrane Library, and Embase, covering publications from inception to 1 May 2024. Among 1471 identified articles, 297 full-text articles were assessed for eligibility. All studies reporting the prevalence of CMD in ANOCA patients based on invasive coronary artery (ICA), positron emission tomography–computed tomography (PET-CT), transthoracic echocardiography (TTE), or cardiac magnetic resonance (CMR) were included. Results: The review included 53 studies (published between 1998 and 2024), encompassing a total of 16,602 patients. Of these studies, 23 used ICA, 15 used PET-CT, 8 used TTE, and 7 used CMR. A statistically significant increase in CMD prevalence over time was observed across all diagnostic modalities (p < 0.05), except for PET-CT, which showed a consistent and stable prevalence over time. Notably, the prevalence rates from all of the diagnostic methods converged towards the 50% prevalence detected by PET-CT. Conclusions: The prevalence of CMD in patients with ANOCA is subject to debate. However, the current data suggest that regardless of the diagnostic method used, the most recent studies tend to converge towards a prevalence value of 50%, which has been consistently reported by PET-CT from the beginning. Full article

Background/Objectives: Vitamin K2 analogs are associated with decreased vascular calcification, which may provide protective benefits for individuals with coronary artery disease (CAD) by stimulating anti-calcific proteins like matrix Gla protein and adjusting innate immune responses. This study addresses a significant gap in understanding the association between serum levels of vitamin K2 analogs in different CAD types and examines their correlations with clinical risk parameters in CAD patients. Methods: This case–control study enrolled CAD patients and healthy controls to assess and compare serum concentrations of two vitamin K2 analogs including menaquinone-4 (MK-4) and menaquinone-7 (MK-7) via ultra-performance liquid chromatography with tandem mass spectrometry (UPLC-MS/MS). CAD risk factors were evaluated and related to serum levels of vitamin K2 analogs. The CAD group was further subdivided into stable angina, STEMI, NSTEMI, and unstable angina groups to investigate potential differences in vitamin K2 analog levels. Results: Patients experiencing acute coronary syndrome exhibited notably reduced serum levels of MK-4 and MK-7 (1.61 ± 0.66, and 1.64 ± 0.59 ng/mL, respectively) in comparison to the control group (2.29 ± 0.54, and 2.16 ± 0.46 ng/mL, respectively), with MK-4 and MK-7 displaying stronger associations with CAD risk indicators. Notable variations in vitamin K2 analog levels were found between CAD patients and control groups (p < 0.001). Unstable angina patients showed the lowest serum levels of MK-4 and MK-7. Conclusions: The present study demonstrated a higher prevalence rate of vitamin K2 deficiency among patients with CAD. The most pronounced decrease in MK-4 and MK-7 was observed in unstable angina patients. Moreover, these outcomes indicate the imperative requirement for an integrative approach that incorporates metabolic, lipid, and vitamin K2-related pathways in the risk stratification and management of CAD. Full article

Background and aims: Coronary obstruction following plaque rupture is a critical pathophysiological change in the progression of stable angina (SAP) to acute coronary syndrome (ACS). The accumulation of platelets and various inflammatory cells on apoptotic endothelial cells is a key factor in arterial obstruction after plaque rupture. Through single-cell sequencing analysis (scRNA-seq) of plaques from SAP and ACS patients, we identified significant changes in the annexin V and P-selectin glycoprotein ligand 1 pathways. Staphylococcal superantigen-like 5 (SSL5) is an optimal antagonist P-selectin glycoprotein ligand 1 (PSGL1), while annexin V (AnxA5) can precisely detect dead cells in vivo. We constructed the SSL5-AnxA5 fusion protein and observed its role in preventing the interaction between apoptotic endothelial cells, platelets, and inflammatory cells. Methods: The scRNA-seq data were extracted from the Gene Expression Omnibus (GEO) database. Single-cell transcriptome analysis results and cell–cell communication were analyzed to identify the ACS and SAP cell clusters and elucidate the intercellular communication differences. Then, we constructed and verified a fusion protein comprising SSL5 and AnxA5 domains via polymerase chain reaction (PCR) and Western blot. The binding capacity of the fusion protein to P-selectin and apoptotic cells was evaluated by flow cytometry and AnxA5-FITC apoptosis detection kit, respectively. Furthermore, co-incubation and immunofluorescence allowed us to describe the mediation effect of it between inflammatory cells and endothelial cells or activated platelets. Results: Our analysis of the scRNA-seq data showed that SELPLG (PSGL1 gene) and ANNEXIN had higher information flowing in ACS compared to SAP. The SELPLG signaling pathway network demonstrated a higher number of interactions in ACS, while the ANNEXIN signaling pathway network revealed stronger signaling from macrophages toward monocytes in ACS compared to SAP. Competition binding experiments with P-selectin showed that SSL5-AnxA5 induced a decrease in the affinity of PSGL1. SSL5-AnxA5 effectively inhibited the combination of endothelial cells with inflammatory cells and the interaction of activated platelets with inflammatory cells. Additionally, this fusion protein exhibited remarkable capability in binding to apoptotic cells. Conclusions: The bifunctional protein SSL5-AnxA5 exhibits promising potential as a protective agent against local inflammation in arterial tissues, making it an excellent candidate for PSGL1-related therapeutic interventions. Full article

Introduction: A Warthin tumor is a benign salivary gland neoplasm, mostly found in the parotid gland. The number of reported Warthin tumors has increased over the years due to better diagnostic modalities and health system modernization. Warthin tumor rarely transforms into a malignant tumor; in this work, we present all cases reported in the English literature of different types of lymphomas within Warthin tumors. In this case, we present a low-grade follicular lymphoma arising within a Warthin tumor. Clinical report: A 64-year-old man presented to an oral and maxillofacial surgery clinic with a growing right facial mass. The medical history was significant for stable angina pectoris, hypertension, hypercholesterolemia, obesity, and a 20-pack-year smoking history. Fine needle aspiration suggested a diagnosis of Warthin tumor. A contrast CT scan of the parotid gland demonstrated a 2.9 × 2.7 × 4.1 cm diameter mass. The patient underwent right superficial parotidectomy. Histological examination of the mass revealed a low-grade follicular lymphoma arising in a pre-existing Warthin tumor. The postoperative PET CT showed no distant disease, and bone marrow biopsy during hematologic evaluation confirmed Stage 1 low-grade follicular lymphoma. The patient received 24 Gy of VMAT radiation therapy to the right parotid gland and continued hematologic follow-up. Conclusions: Based on a literature review, this is one of the few well-documented cases reported of low-grade follicular lymphoma within a Warthin tumor. This case highlights the importance of the thorough evaluation and diagnosis of parotid masses. Furthermore, this case reopens the debate on the “wait and see” approach regarding Warthin tumors. Fine needle aspiration-based diagnosis should not be considered final, as some malignant characteristics can be missed if declining surgery. Full article