Atrial fibrillation in athletes presents a complex clinical challenge rooted in structural cardiac remodeling. Intense, prolonged endurance training induces physical enlargement and structural changes in the atria, creating scar tissue that persistently disrupts electrical signals. This explains why atrial fibrillation frequently recurs in athletes even after successful ablation procedures. Multiple mechanisms contribute to this recurrence: atrial remodeling creates an arrhythmogenic substrate, athletes typically maintain the same intense training regimen that originally triggered the condition, enhanced vagal tone from athletic conditioning alters electrical stability, thicker myocardial tissue complicates complete isolation of deeper electrical pathways during ablation, and post-ablation inflammation accelerates scar formation in already-stressed cardiac tissue. These interconnected factors—ongoing hemodynamic stress, autonomic nervous system effects, and incomplete elimination of triggering mechanisms—underlie the persistent nature of atrial fibrillation in the athletic population. Understanding this multifactorial pathophysiology is crucial for developing more effective treatment strategies and patient counseling in sports cardiology.

Percutaneous coronary intervention with stent placement, or PCI, is a minimally invasive catheter-based procedure that restores blood flow to narrowed or blocked coronary arteries without open-heart surgery. One of the most commonly performed cardiac procedures in the United States, PCI typically requires only a small puncture in the wrist or groin, enabling same-day or overnight discharge. The procedure addresses cholesterol plaque buildup that restricts blood flow, causing chest pressure, shortness of breath, and fatigue. During PCI, a thin catheter advances to the blockage site where a balloon inflates to compress plaque and widen the artery. A metal mesh stent is then deployed to maintain arterial patency. PCI is indicated for acute heart attacks, unstable or stable angina limiting daily activities, abnormal stress tests, and confirmed significant blockages. However, not all narrowings require intervention; pressure-wire measurements and intravascular imaging during catheterization help determine which lesions warrant treatment versus medication management. Performed in a cardiac catheterization laboratory under conscious sedation, the procedure is typically painless and offers substantial advantages over traditional open-heart surgery.

This systematic review and meta-analysis, following PRISMA 2020 guidelines, evaluated drug-coated balloons (DCBs) against drug-eluting stents (DES) for acute myocardial infarction treatment. Analyzing 34 studies encompassing 19,642 participants and 2,313 major adverse cardiovascular events, researchers found that DCBs—which deliver antiproliferative therapy via paclitaxel or sirolimus without permanent scaffold implantation—demonstrated a 15% relative reduction in MACE compared with DES. Late stent thrombosis occurred significantly less frequently with DCBs. Rates of myocardial infarction, target lesion revascularization, and cardiovascular mortality remained comparable between groups. While paclitaxel-coated balloons dominated the evidence base, sirolimus-coated DCB data, though directionally consistent, remained limited. The findings suggest DCBs offer a viable stent-free percutaneous coronary intervention strategy with comparable safety and efficacy to DES while reducing late thrombosis risk, potentially addressing long-term DES complications such as extended dual antiplatelet therapy requirements. However, larger randomized trials, particularly for sirolimus-coated variants, are needed to confirm these results.

The A-CLOSE trial, presented at ESC Congress 2026 and published in the New England Journal of Medicine, evaluated optimal antiplatelet therapy duration in high-risk patients one year after drug-eluting stent implantation. Conducted across 19 South Korean centers, the randomized trial enrolled 3,203 patients (mean age 63 years) with high ischemic risk features including acute coronary syndrome, diabetes, chronic kidney disease, or complex coronary lesions. Participants received either clopidogrel monotherapy or extended dual antiplatelet therapy (DAPT) through 24 months. The study found that while monotherapy reduced bleeding complications, extended DAPT provided superior cardiovascular event protection in this high-risk population. These findings address a critical clinical gap, as the optimal DAPT duration beyond the standard 6-12 months remains uncertain for patients at elevated ischemic risk. The results help clinicians balance ischemic protection against bleeding risk when determining post-stent antiplatelet strategies, informing treatment decisions for complex coronary disease management.

The intensified strategy failed to improve ischemic outcomes. At 6 weeks, the primary efficacy endpoint—a hierarchical composite including death, stent thrombosis, myocardial infarction (MI), ischemic stroke, systemic thromboembolism and urgent revascularization—showed a win-loss ratio of 1.19 (95% CI 0.61–2.32; P=0.61), with no significant reduction in individual ischemic endpoints.  More importantly, potent P2Y12 inhibition produced a consistent excess of bleeding. The primary hierarchical safety endpoint favored standard therapy numerically (win-loss ratio 0.66, 95% CI 0.39–1.11), and conventional analyses demonstrated increased BARC bleeding with ticagrelor/prasugrel. The bleeding signal was sufficiently concerning that the independent DSMB recommended premature termination of the trial. Interestingly, BARC ≥2 bleeding was itself associated with a subsequent increase in ischemic complications (HR 2.18, 95% CI 1.16–4.11).

Platelets contract forcefully after their activation, contributing to the strength and stability of platelet aggregates and fibrin clots during blood coagulation. Viscoelastic approaches can be used to assess platelet-induced clot strengthening, but they require thrombin and fibrin generation and are unable to measure platelet forces directly. Here, we report a rapid, microfluidic approach for measuring the contractile force of platelet aggregates for the detection of platelet dysfunction. We find that platelet forces are significantly reduced when blood samples are treated with inhibitors of myosin, GPIb-IX-V, integrin αIIbβ3, P2Y12, or thromboxane generation. Clinically, we find that platelet forces are measurably lower in cardiology patients taking aspirin. We also find that measuring platelet forces can identify Emergency Department trauma patients who subsequently require blood transfusions. Together, these findings indicate that microfluidic quantification of platelet forces may be a rapid and useful approach for monitoring both antiplatelet therapy and traumatic bleeding risk.

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.

The outcomes of patients with acute coronary syndrome events have been improving as percutaneous coronary intervention and its accompanying medical therapy have evolved. Newer, more potent antiplatelet agents are preferred over clopidogrel when possible. Two earlier studies showed no advantage of extended dual antiplatelet therapy over the standard 12-month duration, but the recent Dual Antiplatelet Therapy trial did. The protection against ischemia afforded by dual anti-platelet therapy comes at the price of increased risk of bleeding.

Platelets are essential anucleate blood cells that play pivotal roles in hemostasis, tissue repair, and immune modulation. Originating from megakaryocytes in the bone marrow, platelets are small in size but possess a highly specialized structure that enables them to execute a wide range of physiological functions. The platelet cytoplasm is enriched with functional proteins, organelles, and granules that facilitate their activation and participation in tissue repair processes. Platelet membranes are densely populated with a variety of receptors, which, upon activation, initiate complex intracellular signaling cascades. These signaling pathways govern platelet activation, aggregation, and the release of bioactive molecules, including growth factors, cytokines, and chemokines. Through these mechanisms, platelets are integral to critical physiological processes such as thrombosis, wound healing, and immune surveillance.

In spite of treatment with the current standard of care antiplatelet regimens including dual antiplatelet therapy, recurrence rates of ischemic events remain elevated for high-risk patients with atherosclerotic disease. This may be in part attributed to the fact that other key platelet activation pathways remain uninhibited and can thus continue to trigger platelet activation and lead to thrombotic complications. Thrombin is a powerful inducer of platelet activation and mediates its effects directly on platelets through protease activator receptors (PARs), particularly the PAR-1 subtype, making PAR-1 inhibition an attractive approach for reducing atherothrombotic events. These observations have led to the development of several PAR-1 antagonists. Vorapaxar is a direct inhibitor of PAR-1 and the only agent of this class approved for the prevention of recurrent ischemic events in patients with prior myocardial infarction or peripheral artery disease. In the present manuscript, we present a review of the pathophysiologic role of thrombin on thrombotic complications, the impact of vorapaxar on outcomes, including the most recent updates deriving from clinical trials, as well as future perspectives in the field.

The platelet, once thought to be solely involved in clot formation, is now known to be a key mediator in various others processes such as inflammation, thrombosis, and atherosclerosis. Supported by the wealth of evidence from clinical trials demonstrating their benefits in patient outcomes, antiplatelet agents have become paramount in the prevention and management of various diseases involving the cardiovascular, cerebrovascular, and peripheral arterial systems. Despite being among the most widely used and studied classes of medical therapies, new discoveries regarding important clinical aspects and properties of these agents continue to be made. As our understanding of platelet biology expands, more effective and safer novel therapies continue to be developed. The use of more refined agents in conjunction with a better understanding of their effects will further the ability to provide more optimized care on an individual basis.

The results of the PREMIUM trial demonstrate that the omission of upfront aspirin in STEMI patients undergoing PPCI is not noninferior to standard DAPT with respect to the primary composite endpoint of all-cause death, stroke or MI. The trial failed to meet its primary endpoint therefore, the secondary endpoint of reduced bleeding events with prasugrel monotherapy can only be considered hypothesis generating. The separation of the curves occurred shortly after PCI, and the prespecified landmark analysis demonstrated that the majority of both the ischaemic and major bleeding events occurred within the first 30 days post PCI.

Angiography-derived FFR-guided revascularization was noninferior to pressure wire–based FFR-guided strategy for determining revascularization in patients with stable coronary artery disease. This finding suggests that angiography-derived FFR may serve as a practical, wire-free alternative for physiologic guidance of coronary revascularization, warranting confirmation in larger outcome-driven trials. (PROVISION; UMIN000049230)

Low-dose aspirin has long been an unquestioned therapy option as the default single antiplatelet therapy for patients with coronary artery disease. This was built on decades of clinical practice, low cost, easy availability, and historical evidence showing that low-dose aspirin could reduce recurrent thrombotic events after myocardial infarction, later reinforced by collaborative meta-analyses.1,2 For patients undergoing percutaneous coronary intervention with coronary stents, dual antiplatelet therapy (DAPT) with aspirin and P2Y12 inhibitors was established as a cornerstone for the prevention of stent-related thrombosis. Even in such cases, aspirin was the drug continued at baseline; the duration of DAPT was determined by adding a P2Y12 inhibitor for a certain period and then discontinuing it, and it was common practice to continue lifelong aspirin monotherapy after discontinuing DAPT. However, just as the optimal duration of DAPT following the implantation of drug-eluting stents has been a major clinical question, so too has the choice of which drug to use as monotherapy after discontinuing DAPT.

DCB angioplasty shows comparable short-term safety and efficacy to modern DES for de novo coronary disease. Long-term follow-up is necessary to confirm whether avoidance of permanent implants translates into clinical benefit.

The outcomes of patients with acute coronary syndrome events have been improving as percutaneous coronary intervention and its accompanying medical therapy have evolved. Newer, more potent antiplatelet agents are preferred over clopidogrel when possible. Two earlier studies showed no advantage of extended dual antiplatelet therapy over the standard 12-month duration, but the recent Dual Antiplatelet Therapy trial did. The protection against ischemia afforded by dual anti-platelet therapy comes at the price of increased risk of bleeding.

Sirolimus-coated balloons (SCB) have been recently introduced for percutaneous coronary intervention (PCI). Nonetheless, evidence on the comparison of different SCB is scant. We aim to compare clinical outcomes after percutaneous coronary intervention with 2 different SCB. SIROMILANO is an observational, retrospective, investigator-driven cohort study conducted at 2 Italian centers, and enrolling between May 2021 and December 2023, consecutive all-comer patients treated with biodegradable polymer microsphere SELUTION SLR SCB (SLR SCB [Cordis, Miami, FL]) or phospholipid nanocarrier Magic Touch SCB (MT SCB [Concept Medical, Surat, India]) for de novo lesions or in-stent restenosis.

A ShedWise device inspired by the snake's molting process for simultaneous cardiovascular repair and reendothelialization. Innovative self-sacrificing coating integrates ROS scavenging with endothelial cell recruitment for vascular repair. Efficacy in reducing restenosis and enhancing tissue repair in a rat vascular injury model.

In ACS patients treated with PCI, early discontinuation of aspirin while maintaining P2Y12 inhibitor monotherapy appears to reduce adverse clinical events compared with standard 12-month DAPT. These findings show net benefit of following early aspirin discontinuation strategy due to reduction in major bleeding events without jeopardizing ischemic outcomes.

Dual antiplatelet therapy (DAPT) is the combined use of aspirin and an oral P2Y12 receptor inhibitor. It is central to the prevention of platelet-mediated coronary thrombosis after acute coronary syndrome (ACS) and percutaneous coronary intervention (PCI). The clinical rationale for DAPT is particularly strong after ACS and coronary stent implantation. ACS is associated with a high risk of platelet-driven atherothrombosis, while interruption of antiplatelet therapy after recent stenting is associated with increased risk of major adverse cardiovascular events (MACE) and stent thrombosis. Premature DAPT interruption is described as the strongest predictor of stent thrombosis in this setting.