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Siemens Healthineers has developed vFFR (vessel Fractional Flow Reserve), a software solution that derives coronary physiology assessments directly from angiographic image data to evaluate hemodynamic significance of coronary lesions. This non-invasive technique eliminates the need for invasive pressure-wire based hyperemic FFR measurements, which currently serve as the gold standard. The technology has undergone rigorous clinical validation through the FAST study series, culminating in the FAST III trial—a multicenter European study of 2,235 patients across 37 sites conducted in partnership with the European Cardiovascular Research Institute and Pie Medical Imaging under Dr. Joost Daemen's leadership. The trial compared vFFR-guided percutaneous coronary intervention against traditional FFR guidance in patients with stable coronary artery disease or non-ST elevation acute coronary syndrome requiring physiological assessment of intermediate lesions. Recently presented results at the American College of Cardiology conference confirmed vFFR's non-inferiority to wire-based FFR while offering significant advantages: reduced invasiveness, faster assessment, and lower procedural costs. vFFR is now integrated into Siemens' ARTIS icono and pheno platforms as QuantWeb vFFR and available as a standalone CAAS vFFR application, with table-side operation capabilities via ARTIS Touch UI.

The AIR-STEMI trial, presented at ESC Congress 2026 and published in the NEJM, investigates optimal strategies for treating multivessel disease following ST-segment myocardial infarction. While complete revascularization within 45 days is guideline-recommended, determining which non-culprit lesions require intervention remains challenging. Traditional wire-based physiology proves cumbersome in acute settings, whereas functional coronary angiography offers a wire-free alternative, deriving fractional flow reserve estimates and physiological pullback data directly from angiographic images without pharmacological hyperaemia. This investigator-initiated, multicenter randomized trial enrolled 1,823 patients across 21 centers in Italy and Pakistan. Patients with successful culprit-lesion PCI and at least one non-culprit lesion with 50-99% diameter stenosis were randomly assigned to complete revascularization guided by either functional coronary angiography or conventional angiography. The trial evaluates physiology as an integrated strategy incorporating physiological pullback to guide PCI planning, rather than a simple binary tool. This approach promises to reduce overtreatment while optimizing outcomes in acute coronary syndromes with multivessel involvement.

Researchers from Fuwai Yunnan Hospital conducted a prospective randomized controlled trial comparing two interventional strategies for treating small coronary vessel disease. The study evaluated the non-inferiority of paclitaxel-coated balloons against rapamycin-eluting metal stents in patients with de novo non-complex lesions. Paclitaxel-coated balloons represent an emerging alternative to traditional drug-eluting stents, utilizing drug-delivery technology through balloon coating rather than permanent metal implants. The trial addresses growing clinical interest in drug-coated balloon angioplasty as a potentially effective treatment option for small-vessel coronary disease, where stent placement carries specific challenges. Published in Advances in Interventional Cardiology, this research contributes to the expanding body of evidence supporting drug-coated balloons as viable alternatives to conventional stent therapy, potentially offering patients reduced long-term complications from metallic implants while maintaining therapeutic efficacy in treating coronary artery narrowing.

The Journal of Clinical Medicine's special issue on advances in antithrombotic therapy addresses the evolving landscape of cardiovascular treatment. Antithrombotic agents—antiplatelet and anticoagulant medications—have significantly reduced ischemic events across acute coronary syndromes, atrial fibrillation, and peripheral artery disease. However, clinicians face the ongoing challenge of balancing ischemic protection against bleeding risk. The field is shifting from standardized treatment approaches toward personalized medicine, employing escalation and de-escalation strategies for antiplatelet therapy intensity tailored to individual patient profiles. Novel agents under clinical investigation, including factor XI inhibitors and subcutaneous P2Y12 receptor inhibitors, show promise in optimizing the ischemia-bleeding trade-off. The special issue, edited by Dr. Daniele Giacoppo and Dr. Antonio Greco, encompasses key topics including antiplatelet therapy in coronary artery disease, antithrombotic strategies in high-risk complex percutaneous coronary intervention, emerging pharmacological agents targeting thrombosis and coagulation, bleeding complication management, perioperative antithrombotic strategies, and guideline implementation. This comprehensive collection reflects the field's commitment to advancing patient outcomes through evidence-based, precision medicine approaches.

Across studies, pooled AUCs were 0.84 for RF, 0.74 for LR, 0.73 for DNN/MLP, and 0.59 for SVM; RF heterogeneity was extreme. Exploratory RF subgroup analysis showed an AUC of 0.91 in DES-only cohorts versus 0.72 in mixed BMS/DES cohorts. Age and lipid-related variables were most frequently reported, followed by sex and diabetes, supporting external validation.

Ticagrelor monotherapy after abbreviated DAPT lowers bleeding without increasing ischemic events, providing a favorable net clinical benefit in high-risk PCI patients and supporting guideline trends toward shorter DAPT.

Coronary artery disease remains the leading cause of global morbidity and mortality, traditionally managed through percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG). However, this review examines the critical importance of concurrent optimal medical therapy (OMT) alongside revascularization procedures. OMT encompasses antiplatelet agents, lipid-lowering drugs for all patients, beta-blockers and ACE inhibitors or angiotensin receptor blockers for most patients, complemented by cardiac risk factor management and lifestyle modifications. For stable angina patients, OMT represents the recommended initial treatment, with revascularization indicated only when symptoms persist despite optimal medical management or when prognosis improvement is expected. Following acute coronary syndromes or revascularization procedures, long-term OMT significantly improves clinical outcomes and patient prognosis. While revascularization techniques have revolutionized CAD treatment, the concomitant use of evidence-based OMT remains vital for maximizing therapeutic benefits and ensuring optimal patient outcomes in contemporary practice.

Recent studies of platelet endothelial cell adhesion molecule-1 (PECAM-1 [CD31])-deficient mice have revealed that this molecule plays an important role in controlling the activation and survival of cells on which it is expressed. In this review, we focus on the complex cytoplasmic domain of PECAM-1 and describe what is presently known about its structure, posttranslational modifications, and binding partners. In addition, we summarize findings that implicate PECAM-1 as an inhibitor of cellular activation via protein tyrosine kinase–dependent signaling pathways, an activator of integrins, and a suppressor of cell death via pathways that depend on damage to the mitochondria. The challenge of future research will be to bridge our understanding of the functional and biochemical properties of PECAM-1 by establishing mechanistic links between signals transduced by the PECAM-1 cytoplasmic domain and discrete cellular responses.

The role of platelets in hemostasis and thrombosis is dependent on a complex balance of activatory and inhibitory signaling pathways. Inhibitory signals released from the healthy vasculature suppress platelet activation in the absence of platelet receptor agonists. Activatory signals present at a site of injury initiate platelet activation and thrombus formation; subsequently, endogenous negative signaling regulators dampen activatory signals to control thrombus growth. Understanding the complex interplay between activatory and inhibitory signaling networks is an emerging challenge in the study of platelet biology, and necessitates a systematic approach to utilize experimental data effectively. In this review, we will explore the key points of platelet regulation and signaling that maintain platelets in a resting state, mediate activation to elicit thrombus formation, or provide negative feedback. Platelet signaling will be described in terms of key signaling molecules that are common to the pathways activated by platelet agonists and can be described as regulatory nodes for both positive and negative regulators.

While current oral antiplatelet therapies benefit many patients, they deregulate the hemostatic balance leaving patients at risk of systemic side-effects such as hemorrhage. Dual antiplatelet treatment is the standard approach, combining aspirin with P2Y12 blockers. These therapies mainly target autocrine activation mechanisms (TxA2, ADP) and, more recently, the use of thrombin or thrombin receptor antagonists have been added to the available approaches. Recent efforts to develop new classes of anti-platelet drugs have begun to focus on primary platelet activation pathways such as through the immunoreceptor tyrosine-based activation motif (ITAM)-containing collagen receptor GPVI/FcRγ-chain complex. There are already encouraging results from targeting GPVI, with reduced aggregation and smaller arterial thrombi, without major bleeding complications, likely due to overlapping activation signaling pathways with other receptors such as the GPIb–V–IX complex. An alternative approach to reduce platelet activation could be to inhibit this signaling pathway by targeting the inhibitory pathways intrinsic to platelets. Stimulation of endogenous negative modulators could provide more specific inhibition of platelet function, but is this feasible? In this review, we explore the potential of the two major platelet immunoreceptor tyrosine-based inhibitory motif (ITIM)-containing inhibitory receptors, G6b-B and PECAM-1, as antithrombotic targets.

Platelets are not only crucial for hemostasis but also play a vital role in a wide range of physiological and pathological processes. The continuous expansion of knowledge in platelet biology holds significant therapeutic implications, offering new avenues for treating various diseases. Sustained research and innovation in platelet-targeted therapies, coupled with a deeper understanding of their molecular mechanisms, will pave the way for novel and more effective treatment approaches, ultimately improving patient outcomes and advancing medical science.

Von Willebrand factor (VWF) and VWF propeptide (VWFpp) are stored in eccentric nanodomains within platelet alpha-granules. VWF and VWFpp can undergo differential secretion following Weibel-Palade body exocytosis in endothelial cells; however, it is unclear if the same process occurs during platelet alpha-granule exocytosis. Using a high-throughput 3-dimensional super-resolution imaging workflow for quantification of individual platelet alpha-granule cargo, we studied alpha-granule cargo release in response to different physiological stimuli.

The ALL-RISE trial evaluated whether FFRangio, an angiography-derived fractional flow reserve technology from Medtronic, could safely replace traditional pressure wire-based physiological assessment for guiding percutaneous coronary intervention in patients with intermediate coronary stenoses. Enrolling 1,930 patients across 59 international sites, the study randomly assigned participants to either FFRangio or pressure wire assessment, which included either FFR or nonhyperemic pressure ratio measurement. The primary endpoint of death, myocardial infarction, or unplanned revascularization at one year occurred in 6.9% of the FFRangio group and 7.1% of the pressure wire group, demonstrating noninferiority. FFRangio significantly reduced procedural burden with shorter procedure duration (39 versus 42 minutes), less fluoroscopy time (9 versus 12 minutes), and lower contrast volume (100 versus 105 milliliters). However, FFRangio identified more physiologically significant lesions and led to higher intervention rates (44.3% versus 35.4%). These findings, published alongside the similar FAST III trial results, support FFRangio as a viable wire-free alternative for guiding revascularization decisions, though they contrast with mixed evidence from QFR studies, providing clinicians with an additional option for streamlined coronary assessment.

Electrospun aligned CS/SF scaffolds loading heparin are successfully fabricated. Scaffolds exhibit oriented fibers, good mechanical properties, hydrophilicity, and controllable degradation. The scaffolds synergistically improve anticoagulant, antibacterial and endothelialization effect. Scaffolds represents a promising candidate for next-generation vascular grafts and interventional devices. The study provides experimental and theoretical basis for artificial cardiovascular implants.

Stentless PCI with DCB was frequently used in patients undergoing PCI for bypass graft lesions in Japan and was not associated with a significant difference in 1-year clinical outcomes compared with contemporary DES-based PCI strategies.

Patients preparing for coronary angioplasty are rarely handed a choice between stent types in any meaningful sense today. Yet, many still arrive at consultation having read, somewhere online, that one kind of stent is inherently superior to another. The honest answer is more interesting than a simple hierarchy, and understanding it equips a patient to ask better questions and to understand, with genuine clarity, what is actually being placed inside their artery.

In-stent restenosis of coronary arteries is the major reason for the recurrence of occlusion after successful percutaneous coronary intervention (PCI) and occurs in 20–50% of patients.1 The development of in-stent restenosis depends on complex cellular interactions within the vessel wall involving endothelial cells (ECs), smooth muscle cells (SMCs), fibroblasts, lymphocytes, and macrophages.2 Vessel injury from balloon angioplasty and stenting cause the release of soluble mediators that initiate cellular activation, migration, proliferation, extracellular matrix production and secretion via autocrine or paracrine mechanisms.

Despite significant advances in stent technology, long-term complications—such as restenosis and stent thrombosis—remain relatively common and clinically impactful due to their association with recurrent myocardial infarction and adverse outcomes. Among the causes of stent failure, neoatherosclerosis has gained recognition as a key pathological mechanism, driven by impaired vascular healing, chronic inflammation, platelet activation, and immune responses following coronary stenting. Advances in diagnostic accuracy, particularly intracoronary imaging, have provided new insights into its development. In response, emerging strategies—including refined pharmacotherapy, targeted intraprocedural interventions, novel stent designs, and alternative drug-delivery systems—are being explored. This review presents recent preclinical, diagnostic, and clinical advances in understanding and addressing neoatherosclerosis and discusses current and emerging therapeutic approaches (Graphical Abstract).

Conventional cardiology has long treated coronary artery disease like a plumbing problem, using stents or bypass surgery to physically open blocked arteries. However, landmark research is fundamentally challenging this approach. The COURAGE trial, which followed over 2,000 patients with stable heart disease, and the ISCHEMIA trial, involving 5,179 patients with moderate-to-severe ischemia, revealed surprising findings: patients receiving immediate stent placement plus medical therapy showed no significant survival advantage over those treated with medication and lifestyle changes alone, with benefits sustained over up to 15 years of follow-up. These massive studies suggest the human body functions more like a self-healing biological system than mechanical plumbing. This paradigm shift has profound implications for cardiac care, suggesting that for many patients with stable coronary artery disease, aggressive pharmaceutical interventions and lifestyle modifications—potentially including dietary changes—may be as effective as invasive procedures, potentially sparing millions from unnecessary surgery while reducing healthcare costs and associated risks.