Impact of Access Site on Periprocedural Bleeding and Cerebral and Coronary Events in High-Bleeding-Risk Percutaneous Coronary Intervention: Findings from the RIVA-PCI Trial.

Introduction: The preference for using transradial access (TRA) over transfemoral access (TFA) in patients requiring percutaneous coronary intervention (PCI) is based on evidence suggesting that TRA is associated with less bleeding and fewer vascular complications, shorter hospital stays, improved quality of life, and a potential beneficial effect on mortality. We have limited study data comparing the two access routes in a patient population with atrial fibrillation (AF) undergoing PCI, who have a particular increased risk of bleeding, while AF itself is associated with an increased risk of thromboembolism.

Methods: Using data from the RIVA-PCI registry, which includes patients with AF undergoing PCI, we analyzed a high-bleeding-risk (HBR) cohort.

Rivaroxaban in Patients With Atrial Fibrillation Who Underwent Percutaneous Coronary Intervention in Clinical Practice.

Little is known about the efficacy and safety of rivaroxaban in patients with atrial fibrillation (AF) who underwent percutaneous coronary intervention (PCI) in clinical practice. We therefore conducted a prospective observational study to determine the rate of ischemic, embolic, and bleeding events in patients with AF and PCI treated with rivaroxaban in a real-world experience. The RIVA-PCI ("rivaroxaban in patients with AF who underwent PCI") (clinicaltrials.

Current status of antithrombotic therapy and in-hospital outcomes in patients with atrial fibrillation undergoing percutaneous coronary intervention in Germany.

Background: Little is known about current patterns of antithrombotic therapy in patients with atrial fibrillation (AF) undergoing percutaneous coronary intervention (PCI) in clinical practice in Germany.

Methods: The RIVA-PCI is a prospective, non-interventional, multicenter study with follow-up until hospital discharge including consecutive patients with AF undergoing PCI.

Results: Between January 2018 and March 2020, 1636 patients (elective in 52.

Immunomodulation by interleukin-4 suppresses matrix metalloproteinases and improves cardiac function in murine myocarditis.

Immune response is critically involved in determining the course of viral myocarditis and immunomodulation. Different cytokines may have either deleterious or protective effects. Following acute Coxsackievirus B3 infection, intramyocardial inflammation is associated with altered myocardial matrix metalloproteinase (MMP) expression and left ventricular dysfunction.

Adventitial VEGF165 gene transfer prevents lumen loss through induction of positive arterial remodeling after PTCA in porcine coronary arteries.

Negative arterial remodeling still plays an important role in the pathogenesis of coronary restenosis even in the era of interventional stenting (e.g. arterial narrowing occurs proximal and distal of a stented segment).

Abciximab therapy is associated with increased platelet activation and decreased heparin dosage in patients with acute myocardial infarction.

The inhibition of the glycoprotein (GP) IIb/IIIa receptor for reducing periprocedural ischemic events in patients undergoing coronary intervention is known to influence platelet reactivity. Suboptimal doses of GP IIb/IIIa antagonists have been suggested to be prothrombotic and proinflammatory. This study was performed to observe platelet activation markers, whole blood aggregation and the dosage of unfractionated heparin (UFH) in the presence or absence of the GP IIb/IIIa inhibitor abciximab.

ADP induced platelet degranulation in healthy individuals is reduced by clopidogrel after pretreatment with atorvastatin.

Statins inhibit platelet reactivity and reduce blood thrombogenicity. The effectiveness of clopidogrel in inhibiting platelet reactivity was suggested to be reduced in the presence of atorvastatin due to shared enzymes in metabolism. Healthy individuals, 17 pretreated with atorvastatin (20 mg/d for 3 days) and 17 without pretreatment, as well as 15 patients with stable coronary artery disease (CAD) and concurrent atorvastatin therapy were started on clopidogrel (loading dose 300 mg, then 75 mg/d).

Hemodynamic characterization of left ventricular function in experimental coxsackieviral myocarditis: effects of carvedilol and metoprolol.

Background: Carvedilol, a vasodilating nonselective beta-adrenoceptor antagonist, but not metoprolol, a selective beta1-adrenoceptor antagonist, has been shown to increase the production of cardiac antiinflammatory cytokines in experimental myocarditis. However, the hemodynamic consequences of these differences had not been investigated until today. Therefore, we determined the effects of carvedilol and metoprolol on left ventricular function in a murine model of coxsackievirus B3 (CVB3)-induced myocarditis.

Leukocyte CD15 expression and platelet activation in the coronary sinus after coronary intervention.

Markers associated with coronary restenosis must be identified to develop therapeutic strategies for improving the clinical outcome. We studied whether adhesion proteins on leukocytes and platelets from coronary sinus blood were associated with restenosis after coronary intervention in patients with stable coronary artery disease. Adhesion proteins on platelets and leukocytes were measured by flow cytometry.

sICAM-1 correlates with myocardial ICAM-1 expression in dilated cardiomyopathy.

Background: Dilated cardiomyopathy (DCM) is etiopathogenically linked to intramyocardial inflammation, which is reflected by ICAM-1 abundance. We investigated whether soluble ICAM-1 (sICAM-1) levels in the sera of DCM patients are associated with intramyocardial ICAM-1 expression.

Methods: Immunohistochemically detected ICAM-1 expression was quantified semiquantitatively in endomyocardial biopsies from DCM patients (n=45; n=17 females; age: 48+/-15 years) and from n=12 donor hearts (controls) by a human observer (baseline vs.

Interferon-beta treatment eliminates cardiotropic viruses and improves left ventricular function in patients with myocardial persistence of viral genomes and left ventricular dysfunction.

Background: Viral infections are important causes of myocarditis and may induce cardiac dysfunction and finally lead to dilated cardiomyopathy. We investigated whether interferon (IFN)-beta therapy is safe and may achieve virus clearance and prevent deterioration of left ventricular (LV) function in patients with myocardial virus persistence.

Methods And Results: In this phase II study, 22 consecutive patients with persistence of LV dysfunction (history of symptoms, 44+/-27 months) and polymerase chain reaction-proven enteroviral or adenoviral genomes were treated with 18x10(6) IU/week IFN-beta (Beneferon) subcutaneously for 24 weeks.

[Mechanisms of extracellular matrix remodeling in dilated cardiomyopathy].

Background: The mechanisms underlying myocardial remodeling during heart failure have historically been attributed as the consequence of intrinsic changes in cardiac myocytes. Nevertheless, over the last several years, it has become increasingly evident that disruption of extracellular matrix (ECM) homeostasis is also a deciding factor for the progression of myocardial failure.

Pathogenetic Mechanisms: Collagens, the chief components of extracellular matrix, are a tightly regulated family of proteins that determine the structural and functional integrity of heart.

Collagen degradation in a murine myocarditis model: relevance of matrix metalloproteinase in association with inflammatory induction.

Objective: Myocardial collagen degradation is regulated by matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinase (TIMPs). The possible relevance of MMPs in association with the inflammatory induction was investigated in a murine coxsackievirus B3 myocarditis model.

Methods: Hearts from viral infected and sham-infected BALB/c mice were analyzed by semi-quantitative RT-PCR, picrosirius red staining, Western blot analysis, and immunohistochemistry.