Ultrathin DES were associated with reduced DOCE, TLR and TVR risks in diffuse ISR compared to DEBs.

Suboptimal stent implantation affects the local hemodynamic forces and can lead to unfavorable clinical outcomes. Regions of low ESS after PCI are colocated with neointima and neoatherosclerosis formation. High shear gradients and flow disturbances have been shown to increase the risk of thrombosis. Therefore, effort should be made to optimize stent deployment and stent/scaffold designs to ensure an optimal hemodynamic profile and reduce the risk of complications after PCI.

Second-generation drug-eluting stents (DES) are considered standard of care for revascularization of patients undergoing percutaneous coronary intervention. Besides the polymer and antiproliferative drug used, the metallic backbone of DES is an attractive target for further development. Ultrathin-strut DES (≤70 µm strut thickness) are more flexible, have an improved trackability and crossability compared to conventional second-generation DES. Importantly, ultrathin-strut DES reduce the risk of in-stent restenosis, thereby decreasing the risk of angiographic and clinical restenosis. In this narrative review, we will discuss the clinical outcomes of the commercially available ultrathin-strut DES.

Emerging evidence has brought platelet adhesion molecules back into the spotlight as targets for the development of novel anti-thrombotic agents. These potential antiplatelet targets mainly include the platelet receptors glycoprotein (GP) Ib-IX-V complex, β3 integrins (αIIb subunit and PSI domain of β3 subunit) and GPVI. Numerous efforts have been made aiming to balance the efficacy of inhibiting thrombosis without compromising hemostasis. This mini-review will update the mechanisms of thrombosis and the current state of antiplatelet therapies, and will focus on platelet adhesion molecules and the novel anti-thrombotic therapies that target them.

Endothelial injury at implantation worsens the endothelial dysfunction as a result of rejection after heart transplantation and compounds the intimal thickening leading to cardic allograft vasculopathy. All efforts should be deployed to maintain a morphologically intact and functional endothelium at the time of graft implantation.

The endothelium is the monolayer of endothelial cells lining the lumen of all blood vessels. These cells function as a protective biocompatible barrier between all tissues and the circulating blood. Endothelial cells also function as a selective sieve to facilitate bidirectional passage of macromolecules and blood gases to and from tissues and blood. The strategic location of the endothelium allows it to “sense” changes in hemodynamic forces and blood-borne signals and “respond” by releasing a number of autocrine and paracrine substances. A balanced release of these bioactive factors facilitates vascular homeostasis. Endothelial cell dysfunction disrupts this balance, thereby predisposing the vessel wall to vasoconstriction, leukocyte adherence, platelet activation, mitogenesis, pro-oxidation, thrombosis, impaired coagulation, vascular inflammation, and atherosclerosis.1 Our understanding of these endothelial cell responses has led to the development of tests that are believed to reflect endothelial cell dysfunction or integrity in vivo.

The issue of stent biocompatibility remains unsolved. At present, there is no stent that can successfully bio-integrate into the vasculature with low enough throm-bogenicity as to not require prolonged DAPT. There is also no platform that can simultaneously promote a rapid reinstitution of a functional vascular endothelium while controlling the reactive smooth muscle response. The constant juggling act between the three cornerstones of stent biocompatibility healing, restenosis and thrombogenicity is complex and inter connected.

Device-related problems of drug-eluting stents, including stent thrombosis related to antiproliferative drugs and polymers, can cause adverse events such as inflammation and neointimal hyperplasia. Stent surface modification, wherein the drug and polymer are not required, may overcome these problems. We developed hydrophilic polyethylene glycol (PEG)-coating and hydrophobic octadecylthiol (ODT)-coating stents without a drug and polymer and evaluated their histopathologic response in a porcine coronary restenosis model.

Anti-inflammation and anti-coagulation are the primary requirements for cardiovascular stents and also the widely accepted trajectory for multi-functional modification. In this work, we proposed an extracellular matrix (ECM)-mimetic coating for cardiovascular stents with the amplified functionalization of recombinant humanized collagen type III (rhCOL III), where the biomimetics were driven by structure mimicry and component/function mimicry.

For patients with severely calcified coronary lesions, routine treatment with orbital atherectomy prior to drug-eluting stent implantation does not yield greater minimal stent area or reduce the rate of target vessel failure compared with conventional balloon angioplasty, according to a study presented at the annual Transcatheter Cardiovascular Therapeutics conference, held from Oct. 27 to 30 in Washington, D.C.

Generally, we can conclude that, by the evaluation of coronary thrombi, delicate, constant structural changes are observed during their age evolution. The appearance of FXIII closely follows the structure and amount of fibrin, while the amount of α2-PI is lower and it rather shows a discrete and consistent association to fibrin. Since both FXIII and α2-PI are pivotal factors in thrombus stabilization and fibrinolysis, it seems to be beneficial to test them as therapeutic targets in coronary atherosclerosis for the prevention and treatment of STEMI. PC/APC has a high amount in all stages of coronary thrombi and the close association with the elements of NET suggests its function in histone degradation. The protective role of APC in thrombo-inflammatory processes makes it a potential therapeutic agent in acute cardiovascular complications.

The results of 15 studies describing 16 case reports indicate a correlation between the cessation of direct oral anticoagulant therapy and the development of hypercoagulability state. The findings of this study suggest that the discontinuation of DOACs therapy may be associated with an increased risk of thrombotic incidents. Further clinical trials or meta-analyses are required to ascertain whether DOACs treatment cessation can be linked to rebound phenomena associated with thromboembolic events. This will provide the data needed to determine the incidence and risk of this phenomenon.

PTX and SRL exhibit different pharmacodynamic properties, which translate into different clinical performance sand safety profiles. The divergent effects of PTX and SRL observed in preclinical models and varying conditions underscore the complexity of drug selection in clinical settings. While PTX has demonstrated potent cytotoxicity and antirestenotic effects, concerns about its safety in certain environments persist. Conversely, SRL’s mechanism of action, particularly its inhibition of the mTOR pathway, offers an alternative approach, but raises questions about effective drug distribution in the vessel wall and permanence. So far, we have sufficient information on when to use the more potent cytotoxic effect of paclitaxel, aiming at observing a higher lumen enlargement, or the more anti-inflammatory effect of sirolimus, with both devices aiming to optimize DCB use in clinical practice.

Inflammation is a major component of the pathogenesis of atherosclerosis and the formation of in-stent restenosis (ISR). A novel flavonoid, DHIF, attenuates reactive oxygen species and nf-κB signaling and has potential to limit ISR via antioxidant action. While current drug eluting stents (DESs) perform well in clinical practice, new therapies to prevent ISR without dependance on cytotoxic drugs are warranted. Our objective was to test whether DHIF reduces ISR in a hyperlipidemic rabbit aorta model of ISR via attenuated inflammatory responses. WHHL rabbit aortas (n = 24) were denuded. Six weeks after injury, stents were implanted into the denuded aortas. DHIF was dissolved in carboxymethyl cellulose (CMC) and administered orally with two doses. CMC served as a control.

That knowledge is invaluable when it comes to heart health and the procedures doctors use in diagnosing, treating—and preventing—a host of cardiovascular issues. The two most popularly discussed procedures are angiography and Angioplasty, both of which are often named together but have entirely different purposes. Every component has a place within the broader framework of coronary artery disease management and understanding how they interact with one another is critical during stenting.

Lp(a) is considered a major risk factor for atherosclerotic CVD, with several studies confirming an association between elevated Lp(a) levels and incident CAD in the general population. Additionally, observational data suggest that Lp(a) is associated with increased adverse events in patients with established CAD and with aortic stenosis. Imaging data suggest that the mechanism of Lp(a) and worse CV outcomes may be due to the adverse effect of high Lp(a) levels on plaque vulnerability. Promising pharmacotherapy interventions show reductions in serum Lp(a) levels, but trial data of cardiovascular risk reduction are awaited.

“As physicians treat more patients with complex lesions, it is important to have a device that helps to maintain durable patency while preserving future treatment options,” said David Kandzari (Piedmont Heart Institute and Cardiovascular Services, Atlanta, USA), co-principal investigator of the Prevail Global Study. “Drug-coated balloons provide clinicians with an anti-restenosis solution, without the need of a permanent stent. This groundbreaking trial will include the first head-to-head randomised trial of two drug coated balloons in the USA and will provide important additional evidence for this growing therapy.”

SirPlux Duo DCB is the only therapy designed to deliver sirolimus and paclitaxel simultaneously to inhibit cell growth at a higher potency and efficient dose, according to Advanced NanoTherapies. The novel nanoparticle drug encapsulation and delivery platform is designed to provide the two drugs with safe, reliable, and sustained long-term in-tissue bioavailability with no stent burden.

Platelets are essential for haemostasis and thrombosis; however, platelets also have multifaceted roles in regulating immune responses and contributing to the pathogenesis of inflammatory diseases Thrombocytosis is usually reported in Kawasaki disease, a systemic paediatric vasculitis, and has been associated with increased risk of developing coronary artery aneurysms Levels of monocyte–platelet aggregates (MPAs) and neutrophil–platelet aggregates (NPAs) increase during Kawasaki disease; these leukocyte–platelet aggregates (LPAs) might amplify Kawasaki disease pathogenesis through their pro-inflammatory and thrombotic functions and have been related to the development of coronary artery aneurysms in Kawasaki disease Although aspirin therapy does not reduce MPA formation, studies suggest that targeting the P-selectin–PSGL1 axis or inhibiting the P2Y12 receptor might attenuate platelet-induced monocyte activation Platelets are active participants and mediators of cardiovascular inflammation during Kawasaki disease vasculitis, not innocent bystanders. Hence, platelets might be promising therapeutic targets for Kawasaki disease vasculitis.

Expected results and conclusions: OVER-TIME is the first randomized controlled trial to assess different antithrombotic strategies in patients with CAE and acute coronary syndrome, and its results will offer preliminary data for the prevention of major cardiovascular events and bleeding events in this group of patients.