Ischaemic heart disease shows important differences between men and women, requiring an understanding of sex and gender dissimilarities to improve outcomes. This Scientific Statement provides an updated review of the current knowledge from risk factors to prognosis. It discusses the unequal impact of certain traditional risk factors between men and women, along with additional factors, such as hormonal changes and treatments (including those for transgender people and cancer), pregnancy-related complications, and autoimmune diseases, which contribute to the sex-specific risk profiles. Moreover, it outlines functional and structural sex differences in the pathophysiology (e.g. coronary atheroma plaques and burden, coronary dissection, vasospasm, and microvascular disease) with women being more prone to microvascular disease and endothelial dysfunction, while paradoxically experiencing less severe myocardial ischaemia at similar levels of coronary stenosis. The document further addresses the evaluation of diagnostic tools, which often have a male-centric bias, resulting in underdiagnosis in women who also tend to receive less guideline-recommended treatment. Additionally, women can have different responses and side effects to various preventive and therapeutic treatments, potentially contributing to the worse prognosis documented in acute coronary syndromes with obstructive coronary artery disease, particularly at a young age. Considering all these sex and gender differences and the low enrolment of women in randomized controlled trials, questions arise regarding the optimal treatment for women. Addressing sex differences requires conducting sex-specific research to close the knowledge gap. Overall, the Scientific Statement highlights all relevant sex- and gender-specific dissimilarities to advance clinical practice and identify directions for future research to improve guideline recommendations for equitable care.

BACKGROUND:Patients are at increased risk for recurrent ischemic events after an acute coronary syndrome event. Milvexian, an oral factor XIa inhibitor, may reduce the risk of major adverse clinical events with minimal bleeding risk. METHODS:In this phase 3, randomized, placebo-controlled trial, we evaluated the efficacy and safety of milvexian when added to standard antiplatelet therapy within 7 days after an acute coronary syndrome event. Patients were assigned in a 1:1 ratio to receive oral milvexian (25 mg twice daily) or matched placebo. The primary efficacy outcome was a composite of cardiovascular death, myocardial infarction, or ischemic stroke as evaluated in a time-to-event analysis. The principal safety outcome was Bleeding Academic Research Consortium (BARC) type 3c or 5 bleeding (intracranial or intraocular bleeding that compromises vision or fatal bleeding). RESULTS:After a planned interim analysis that was based on 556 adjudicated efficacy end points, the trial was terminated for futility. A total of 14,194 patients had been enrolled, with 7094 assigned to receive milvexian and 7100 to receive placebo. After a median follow-up of 12.2 months, a primary efficacy outcome event had occurred in 384 patients (5.4%) in the milvexian group and in 365 patients (5.1%) in the placebo group (hazard ratio, 1.05; 95% confidence interval, 0.91 to 1.21; P = 0.50). BARC type 3c or 5 bleeding occurred in 23 patients (0.3%) in the milvexian group and in 22 patients (0.3%) in the placebo group (P = 0.88). CONCLUSIONS:Among patients with a recent acute coronary syndrome event, milvexian did not decrease the risk of cardiovascular death, myocardial infarction, or ischemic stroke but did not increase the risk of intracranial or fatal bleeding, as compared with placebo. (Funded by Janssen Research and Development and Bristol Myers Squibb; LIBREXIA ACS ClinicalTrials.gov number, NCT05754957.).

Optical coherence tomography (OCT) enables high-resolution in vivo assessment of coronary atherosclerosis, identifying vulnerable plaque features linked to progression and adverse cardiovascular events across stable and acute coronary syndromes. OCT-defined high-risk morphology may add information beyond physiology, particularly in diabetes, multivessel disease, and post-ACS residual lesions. However, these findings remain risk markers, not standalone treatment indications. Advances in automation, AI, and hybrid imaging may support clinical translation.

Although prompt primary percutaneous coronary intervention (PCI) reduces mortality in patients with ST-elevation myocardial infarction (STEMI), the burden of post-infarction heart failure remains considerable and is expected to increase. A major contributory factor is suboptimal myocardial reperfusion, which persists in up to 60% of cases even with timely revascularization. This is largely driven by microvascular obstruction and ischaemia-reperfusion injury, culminating in the no-reflow phenomenon, a critical prognostic factor associated with impaired infarct healing, adverse left ventricular remodelling, and increased risk of heart failure and death. No-reflow is a complex and heterogeneous phenomenon, identifiable through different invasive and noninvasive technologies. When observed post-PCI, after excluding residual epicardial stenosis, it indicates poor microvascular perfusion and necessitates urgent management. Identifying patients at high risk and implementing early targeted interventions are essential to improving outcomes. Pharmacological therapies, including intracoronary adenosine and nitroprusside, have shown unclear benefit in improving microvascular flow. Non-pharmacological strategies, such as ischaemic postconditioning, intracoronary supersaturated oxygen therapy, stent-retriever thrombectomy, and mechanical left ventricular unloading, have demonstrated promise but require further validation in large-scale clinical trials. This clinical consensus statement summarizes current strategies for the prevention and treatment of no-reflow and underscores the need for improved risk stratification and novel microvasculature-targeted therapies. Addressing this persistent and significant unmet clinical need is crucial for improving care for STEMI patients and for mitigating its long-term complications, including heart failure and mortality.

Background: Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9is) have emerged as a promising class of medications, primarily recognized for inducing potent cholesterol-lowering effects. In addition to the established role of these inhibitors in reducing low-density lipoprotein cholesterol levels, recent studies suggest that PCSK9is may also modify coronary atherosclerotic plaques. Therefore, this meta-analysis aimed to comprehensively synthesize data from relevant clinical studies and trials investigating the effects of PCSK9is on coronary atherosclerotic plaque characteristics. Methods: We performed a literature search for studies assessing the evolution of coronary atherosclerotic plaques after treatment with a PCSK9i compared with a control group. We excluded reviews, editorials, case reports/case series, and studies that did not use PCSK9is or lacked a control group. The main outcomes of interest were changes in percent atheroma volume (PAV), total atheroma volume (TAV), minimal fibrous cap thickness (FCT), lipid arc, and the number of patients with improved PAVs at follow-up. Effect sizes are presented as a standardized mean difference (SMD) or risk ratio (RR) alongside the corresponding 95% confidence intervals (CIs) and were pooled based on a random-effects model. Publication bias was assessed by funnel plot inspection and Egger's regression test. Results: The literature search yielded 142 results. After applying the exclusion criteria, nine studies were selected for data extraction and inclusion in the meta-analysis. Concerning the intravascular ultrasound findings, PCSK9is significantly reduced the TAV (MD –7.09 mm3, 95% CI –11.36 to –2.81; p = 0.01) and induced non-significant reductions in the PAV (MD –1.91%, 95% CI –5.08 to 1.25; p = 0.17); meanwhile, a greater proportion of patients treated with PCSK9 inhibitors exhibited an improvement in the PAV (RR 1.30, 95% CI 1.19 to 1.42; p < 0.001). For optical coherence tomography parameters, patients treated with PCSK9 inhibitors showed an increase in minimal FCT (MD 36.25 μm, 95% CI 0.75 to 71.75; p = 0.047) and a non-significant decrease in lipid arc (MD –17.64°, 95% CI –49.73 to 14.44; p = 0.14). Conclusions: This meta-analysis suggests that PCSK9i therapy may be associated with modest favorable changes in selected intravascular imaging markers of coronary atherosclerotic plaque burden and stability.

Background:There is a lack of robust comparative data between limus drug-coated balloons (DCBs) versus paclitaxel-coated balloons (PCBs) on their efficacy and safety in treating in-stent restenosis (ISR). Aims:The objective of this systematic review and meta-analysis was to compare the efficacy and safety of limus DCBs versus PCBs in terms of clinical and angiographic outcomes during a 12-month follow-up. Methods:Following PRISMA guidelines, we systematically explored PubMed, Scopus, and Cochrane databases up to 20 February 2025 for studies comparing limus DCBs versus PCBs in terms of safety, efficacy, and angiographic outcomes in treating ISR. The primary outcomes were the incidence of clinically driven target lesion revascularisation (TLR) and failure (TLF). Secondary endpoints were major adverse cardiovascular events (MACE) and angiographic findings during follow-up. Results:Data from six randomised controlled trials (RCTs), including a total of 639 patients treated with limus DCBs and 569 with PCBs for ISR, were analysed with a mean follow-up of 12 months. In this analysis, all six RCTs reported on TLR (limus DCB 14% vs PCB 11.4%) and TLF (limus DCB 15% vs PCB 14%) incidence, showing no significant difference between the limus DCB and PCB groups. No significant differences were observed in MACE (16.4% vs 13.5%), all-cause mortality (1.8% vs 1.4%), cardiac death (1.4% vs 1.0%) or target vessel myocardial infarction (0.9% vs 1.0%), for limus DCBs versus PCBs, respectively. Angiographic outcomes showed no significant differences in post-intervention minimal lumen diameter (standardised mean difference [SMD] +0.06, 95% confidence interval [CI]: -0.07 to 0.18; I2=0%) or binary restenosis (limus DCB 19.5% vs PCB 12.9%) at follow-up between the groups. The risk of late lumen loss was also comparable between limus DCBs and PCBs for both in-segment (SMD +0.02, 95% CI: -0.18 to 0.23; I2=32%) and in-lesion (SMD -0.03, 95% CI: -0.31 to 0.24; I2=27%) analyses. Low heterogeneity was observed across the studies. Conclusions:Our findings suggest that limus DCBs are equally as effective and safe as PCBs for treating ISR, demonstrating non-inferiority in both clinical and angiographic outcomes at 12 months post-intervention.

AIMS:The identification of reliable biomarkers for atrial fibrillation (AF) recurrence post-catheter ablation remains a clinical challenge. This study aimed to identify circulating microRNAs (miRNAs) associated with post-ablation AF recurrence and examine their underlying molecular pathways using an integrative translational approach. METHODS AND RESULTS:This two-phase study included a discovery case-control phase (n = 29) followed by a prospective validation cohort (n = 126). In the discovery phase, 84 miRNAs were quantified via real-time PCR, and candidates were selected using differential expression analysis and machine learning. In the validation phase, five candidate miRNAs (hsa-miR-342-3p, hsa-miR-424-5p, hsa-miR-486-5p, hsa-miR-10b-5p, and hsa-let-7d-5p) were further evaluated to assess their prognostic performance. Pathway enrichment analysis was performed for the most predictive miRNA. Differential expression analysis identified 14 miRNAs to be significantly associated with AF recurrence. In the validation cohort, hsa-miR-10b-5p showed the highest discriminative performance (AUC = 0.96, P < 0.001). Multivariable logistic regression confirmed that lower expression of hsa-miR-10b-5p was an independent predictor of recurrence (OR = 0.06, P < 0.001), significantly improving the baseline clinical model (ΔR = 63.3%). Pathway analysis linked hsa-miR-10b-5p to FOXO signalling, p53 signalling, circadian rhythm and cellular senescence, pathophysiologic mechanisms that are critical to atrial remodelling, and fibrotic persistence. CONCLUSION:Down-regulation of circulating hsa-miR-10b-5p was independently associated with AF recurrence after catheter ablation and improved risk discrimination beyond clinical variables. These findings support its potential role as a prognostic biomarker, although further multicentre validation is required before clinical application.

Background: Chronic liver disease (CLD) and cirrhosis contribute to approximately 2 million deaths annually, with primary causes including alcohol-related liver disease (ALD), metabolic dysfunction-associated steatotic liver disease (MASLD), and chronic hepatitis B and C infections. Among these, MASLD has emerged as a significant global health concern, closely linked to metabolic disorders and a leading cause of liver failure and transplantation. Objective: This review aims to highlight the interplay between cirrhosis and cardiac dysfunction, emphasizing the pathophysiology, diagnostic criteria, and management of cirrhotic cardiomyopathy (CCM). Methods: A comprehensive literature review was conducted to evaluate the hemodynamic and structural cardiac alterations in cirrhosis. Results: Cirrhosis leads to portal hypertension and systemic inflammation, contributing to CCM, which manifests as subclinical cardiac dysfunction, impaired contractility, and electrophysiological abnormalities. Structural changes, such as increased left ventricular mass, myocardial fibrosis, and ion channel dysfunction, further impair cardiac function. Vasodilation in the splanchnic circulation reduces peripheral resistance, triggering compensatory tachycardia, while the activation of the renin–angiotensin–aldosterone system (RAAS) promotes fluid retention and increases cardiac preload. Chronic inflammation and endotoxemia exacerbate myocardial dysfunction. The 2005 World Congress of Gastroenterology (WCG) and the 2019 Cirrhotic Cardiomyopathy Consortium (CCC) criteria provide updated diagnostic frameworks that incorporate global longitudinal strain (GLS) and tissue Doppler imaging (TDI). Prolonged QT intervals and arrhythmias are frequently observed. Managing heart failure in cirrhotic patients remains complex due to intolerance to afterload-reducing agents, and beta-blockers require careful use due to potential systemic hypotension. The interaction between CCM and major interventions, such as transjugular intrahepatic portosystemic shunt (TIPS) and orthotopic liver transplantation (OLT), highlights the critical need for thorough preoperative cardiac evaluation and vigilant postoperative monitoring. Conclusions: CCM is a frequently underdiagnosed yet significant complication of cirrhosis, impacting prognosis, particularly post-liver transplantation. Early identification using echocardiography and thorough evaluations of arrhythmia risk in cirrhotic patients are critical for optimizing management strategies. Future research should focus on targeted therapeutic approaches to mitigate the cardiac burden in cirrhotic patients and improve clinical outcomes.

Hypertension, characterized by elevated blood pressure levels, remains a global health concern due to its association with cardiovascular complications, notably thrombosis. Thrombosis, the formation of blood clots within blood vessels, poses a significant risk for myocardial infarction, stroke, and limb ischemia, leading to adverse patient outcomes. Understanding the pathophysiological mechanisms underlying thrombosis in hypertension is crucial for developing effective preventive and therapeutic strategies. Hypertension induces structural and functional alterations in the vasculature, endothelium, and platelets, creating a prothrombotic milieu. Endothelial dysfunction, increased platelet activation, and alterations in coagulation factors contribute to the heightened thrombotic risk observed in hypertensive individuals. Biomarkers associated with thrombotic events, such as mean platelet volume, D-Dimer, and fibrinogen offer valuable insights into the pathogenesis of thrombosis and may serve as prognostic indicators for cardiovascular events in hypertensive populations. Investigating the impact of antihypertensive treatment on thrombotic risk is essential, as these medications exert pleiotropic effects on the vasculature and hemostatic system. By elucidating the intricate interplay between hypertension and thrombosis, this review aims to enhance our understanding of cardiovascular risk in hypertensive individuals and identify novel therapeutic targets for preventing thrombotic complications.

Atrial fibrillation (Afib) is a common arrhythmia with significant public health implications, affecting millions of individuals worldwide. Catheter ablation (CA) is an established treatment for drug-resistant Afib, yet recurrence remains a major concern, impacting quality of life in a significant portion of patients. Inflammation plays a critical role in the recurrence of Afib after ablation, with systemic inflammatory markers such as C-reactive protein being linked to higher recurrence rates. In this editorial, we discuss the study by Wang et al, published in the latest issue, which investigates the predictive role of the systemic immune inflammation index (SII) in Afib recurrence following radiofrequency CA. Elevated pre-ablation SII levels are identified as an independent predictor of recurrence, significantly enhancing the predictive power of the APPLE score. Integration of SII improved the APPLE score's predictive performance, as shown by enhanced area under the curve, net reclassification improvement, and integrated discrimination improvement. This combined model highlights the importance of both structural and inflammatory factors in Afib recurrence, offering a more personalized approach to patient management. Additionally, the affordability and accessibility of SII enhance its practicality in clinical workflows. The study by Wang et al underscores the potential of integrating SII with existing scoring systems to refine risk stratification and optimize treatment strategies. Future research should validate these findings across diverse populations, explore limitations such as the potential influence of comorbidities on SII reliability, and investigate additional biomarkers to enhance predictive accuracy.

Background: Endothelial dysfunction and inflammation are associated with the progression of coronary artery disease (CAD) and the pathophysiology of acute coronary syndrome (ACS). We examined the prognostic role of endothelial function and pro-inflammatory cytokines in patients admitted with ACS. Methods: The study population consisted of 864 subjects. From 663 subjects who presented with chest pain, ACS was diagnosed in 460. We additionally recruited 201 consecutive patients with stable CAD. Endothelial function was assessed using flow-mediated dilatation (FMD). Tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) levels were measured via ELISA. Subjects with ACS were followed up for major adverse cardiovascular events (MACE), defined as cardiovascular death, cardiac arrest, myocardial infarction, stroke, nonfatal stroke, other arterial thrombotic events, and hospitalization due to cardiovascular conditions. Results: There was a stepwise impairment in FMD, logTNF-α, and logIL-6 in patients with chest pain of non-epicardial CAD etiology compared to patients with stable CAD and those with ACS (p < 0.001 for all). Moreover, patients who presented with chest pain had increased odds of ACS in accordance with the increasing levels of TNF-α, IL-6, and impaired FMD (p < 0.05 for all). Interestingly, from all these markers, in patients with ACS, we found that only TNF-α levels above 5.19 pg/mL had a 2.5-times-increased risk of MACE compared to patients with TNF-α levels below 5.19 pg/mL, independently of other confounders. Conclusions: In the current study, we found that patients who presented with ACS had impaired endothelial function and increased levels of IL-6 and TNF-α.

Background: HER2-positive breast cancer patients receiving chemotherapy and targeted therapy (including anthracyclines and trastuzumab) face an elevated risk of cardiotoxicity, which can lead to long-term cardiovascular complications. Identifying predictive biomarkers is essential for early intervention. Circulating microRNAs (miRNAs), known regulators of gene expression and cardiovascular function, have emerged as potential indicators of cardiotoxicity. This study aims to evaluate the differential expression of circulating miRNAs in HER2-positive breast cancer patients undergoing chemotherapy and to assess their prognostic ability for therapy-induced cardiotoxicity using machine learning models. Methods: Forty-seven patients were assessed for cardiac toxicity at baseline and every 3 months, up to 15 months. Blood samples were collected at baseline. MiRNA expression profiling for 84 microRNAs was performed using the miRCURY LNA miRNA PCR Panel. Differential expression was calculated via the 2−∆∆Ct method. The five most upregulated and five most downregulated miRNAs were further assessed using univariate logistic regression and receiver operating characteristic (ROC) analysis. Five machine learning models (Decision Tree, Random Forest (RF), Support Vector Machine (SVM), Gradient Boosting Machine (GBM), k-Nearest Neighbors (KNN)) were developed to classify cardiotoxicity based on miRNA expression. Results: Forty-five miRNAs showed significant differential expression between cardiac toxic and non-toxic groups. ROC analysis identified hsa-miR-155-5p (AUC 0.76, p = 0.006) and hsa-miR-124-3p (AUC 0.75, p = 0.007) as the strongest predictors. kNN, SVM, and RF models demonstrated high prognostic accuracy. The decision tree model identified hsa-miR-17-5p and hsa-miR-185-5p as key classifiers. SVM and RF highlighted additional miRNAs associated with cardiotoxicity (SVM: hsa-miR-143-3p, hsa-miR-133b, hsa-miR-145-5p, hsa-miR-185-5p, hsa-miR-199a-5p, RF: hsa-miR-185-5p, hsa-miR-145-5p, hsa-miR-17-5p, hsa-miR-144-3p, and hsa-miR-133a-3p). Performance metrics revealed that SVM, kNN, and RF models outperformed the decision tree in overall prognostic accuracy. Pathway enrichment analysis of top-ranked miRNAs demonstrated significant involvement in apoptosis, p53, MAPK, and focal adhesion pathways, all known to be implicated in chemotherapy-induced cardiac stress and remodeling. Conclusions: Circulating miRNAs show promise as biomarkers for predicting cardiotoxicity in breast cancer patients. Machine learning approaches may enhance miRNA-based risk stratification, enabling personalized monitoring and early cardioprotective interventions.

Mechanical complications following acute myocardial infarction (MI) represent some of the most challenging conditions in contemporary cardiology, often leading to rapid clinical deterioration and high mortality despite advances in reperfusion therapy. These complications span a spectrum of presentations, from early-phase structural disruptions such as ventricular septal rupture, papillary muscle rupture with acute mitral regurgitation (MR), and left ventricular free wall rupture (LVFWR), to later-stage manifestations, including true ventricular aneurysms and pseudoaneurysms. While surgical intervention has traditionally been considered the standard of care, surgical intervention is often associated with prohibitive risk in hemodynamically unstable or frail patients. In this context, transcatheter approaches have gained traction as viable, less invasive alternatives, offering the potential for hemodynamic stabilization, symptom relief, and improved short-term outcomes in selected patients. Nonetheless, data from observational studies and registry-based analyses remain limited, underscoring the need for further research. This review synthesizes the current evidence base and clinical experience related to transcatheter management of mechanical complications after MI, emphasizing patient selection, procedural strategies, device selection, and reported outcomes.

Hypertension is a modifiable cardiovascular risk factor and displays a rapidly growing incidence due to aging and the acquisition of an unhealthy lifestyle. Hypertension is linked to the development of target organ damage in several vascular beds such as coronary arteries, peripheral, cerebral, and renal arteries. Besides, along with the presence of other cardiovascular risk factors, it aggravates vascular dysfunction due to the aging process. The mechanisms of vascular dysfunction in hypertension are complex and involve excessive salt intake and water retention, activation of neurohormonal systems, induction of endothelial dysfunction of large arteries and microcirculation, development of arterial stiffness, and complex interactions with cellular pathways of inflammation, oxidative stress, and thrombosis. The extent of vascular dysfunction in patients with hypertension can be assessed by evaluating endothelial function, measuring arterial stiffness, and testing the levels of circulating biomarkers of oxidative stress, pro-inflammatory cytokines, and thrombosis. Assessing these markers in subjects with and without hypertension could aid in identifying those at risk of vascular damage and improving risk prediction for future cardiovascular events. While several lifestyle and pharmacological therapies have shown promise in addressing vascular dysfunction in hypertension, none of these biomarkers have been established as an independent risk factor or treatment target. Therefore, in this article, we review the literature on the evidence that exists regarding the role of vascular dysfunction in the pathophysiology, diagnosis, progression, and treatment of hypertension, highlighting the lack of conclusive evidence in this field.

Diabetes Mellitus (DM) is among the most common non-infectious causes of death globally, with Type 2 DM (T2DM) representing the majority of cases. T2DM is primarily characterized by insulin resistance, leading to hyperglycemia and compensatory hyperinsulinemia. Rapid changes in lifestyle, technological advancement, and societal evolution have fueled a global rise in T2DM, making it a major public health concern. The condition is associated with numerous complications—both macrovascular and microvascular—including coronary artery disease, heart failure, chronic kidney disease, and diabetic retinopathy, all of which contribute to increased morbidity and early mortality. Chronic tissue inflammation is now recognized as a key factor in the development of T2DM, with elevated inflammatory markers serving as predictors of the disease. In particular, the NLRP3 inflammasome complex has emerged as a central player in this inflammatory process. NLRP3 acts as an intracellular sensor for danger signals and tissue injury, triggering inflammatory responses and contributing to endothelial dysfunction and T2DM pathogenesis. Its role in linking metabolic stress to inflammation has positioned it as a promising therapeutic target. This review focuses on the mechanisms underlying NLRP3 inflammasome activation and its role in T2DM and related vascular complications. Additionally, it highlights emerging therapies that target NLRP3, offering new potential strategies for the prevention and treatment of T2DM.

Infective endocarditis (IE) is an increasingly prevalent condition with relatively high mortality, whose epidemiology has become more complex with an aging population, an increased number of comorbidities, and an increasing incidence of health-care associated IE. Epidemiological data on the causative microorganisms of IE, prevalence of involvement of the different cardiac valves, and IE-associated mortality are clinically relevant. Eligible studies were identified through a systematic search of PubMed/MEDLINE database from 2010 to 2020, and a random effects model meta-analysis was conducted. 133 studies comprising 132,584 patients from six continents were included in this systematic review. The most common causative agents were Staphylococci species in 36% of cases, followed by Streptococci species (26%) and Enterococci species (10%). Out of studies that provided further speciation, the predominant species was Staphylococcus aureus with an incidence of 29%, followed by Viridans group Streptococcus (12%). The short-term mortality rate (defined as in-hospital or 30-day mortality) was 17%. The highest mortality was reported in studies from Latin America with a mean mortality rate of 33% and the lowest mortality was reported in studies from Oceania at 13%. The aortic valve was the most commonly affected valve (46%), followed closely by the mitral valve (43%). The prevalence of tricuspid valve IE was 7% and multivalvular IE occurred in 14% of cases. Our study highlights a shift in epidemiological profile of IE over the last decade with S. aureus identified as the most common causative microorganism of IE. PROTOCOL REGISTRATION: PROSPERO CRD42024602342.

INTRODUCTION:Coronary atherosclerosis, marked by lipid deposition and inflammation, drives cardiovascular morbidity. Traditional treatments focus on lipid reduction, yet newer therapies target plaque composition, aiming to enhance stability and prevent coronary events. AREAS COVERED:A comprehensive literature search was conducted across PubMed, Embase, and Scopus till January 2025 to identify studies on coronary plaque modification. This review highlights current and emerging therapies for coronary plaque modification. Key pharmacologic agents include Proprotein convertase subtilisin/kexin type 9 inhibitors for lipid management, colchicine for inflammation control, and Glucagon-like peptide-1 receptor agonists, and Sodium-glucose cotransporter-2 inhibitors for metabolic benefits. Clinical trials indicate these agents' roles in reducing plaque volume and vulnerability. Advances in imaging and biomarkers, such as lipoprotein(a) and inflammatory markers, enable refined monitoring of plaque changes over time. EXPERT OPINION:Future management of atherosclerosis may involve personalized strategies, integrating AI-driven predictive tools and biomarkers to assess individual plaque characteristics and optimize therapy. Continued exploration of targeted anti-inflammatory therapies and novel biomarkers like Lp(a) could enhance outcomes, offering a more precise approach to reducing cardiovascular risk and stabilizing high-risk plaques.