Optimisation of individual cardiovascular risk assessment in a German coronary artery disease cohort using a commercial test for genetic polymorphisms - a pilot study.

Background And Aims: Assessment of cardiovascular risk using established risk scores such as ESC SCORE2 or PROCAM insufficiently emphasise the role of genetic factors. We hypothesise that commercially available genetic assays may provide additional information on hereditary cardiovascular risk in a timely and cost-efficient manner.

Methods: In a cohort of 51 patients treated for coronary artery disease (CAD) at University Hospital Heidelberg, Germany, a subgroup of patients with "unstable" CAD (i.

Identification of Specific Coronary Artery Disease Phenotypes Implicating Differential Pathophysiologies.

Background And Aims: The roles of multiple risk factors of coronary artery disease (CAD) are well established. Commonly, CAD is considered as a single disease entity. We wish to examine whether coronary angiography allows to identify distinct CAD phenotypes associated with major risk factors and differences in prognosis.

Apolipoprotein E derived from CD11c cells ameliorates atherosclerosis.

Atherosclerosis is studied in models with dysfunctional lipid homeostasis-predominantly the ApoE mouse. The role of antigen-presenting cells (APCs) for lipid homeostasis is not clear. Using a LacZ reporter mouse, we showed that CD11c cells were enriched in aortae of ApoE mice.

Functional association of a CD40 gene single-nucleotide polymorphism with the pathogenesis of coronary heart disease.

Aims: Endothelial dysfunction is a major contributor to the pathogenesis of atherosclerosis. CD40-CD40 ligand interactions confer a pro-inflammatory phenotype to endothelial cells (ECs). Recently, a thymine to cytosine transition (-1T>C) in the Kozak sequence of the CD40 gene (rs1883832) has been associated with coronary heart disease (CHD) in an Asian population.

15-Deoxy-Δ12,14-Prostaglandin J Reinforces the Anti-Inflammatory Capacity of Endothelial Cells With a Genetically Determined NO Deficit.

Rationale: Fluid shear stress (FSS) maintains NOS-3 (endothelial NO synthase) expression. Homozygosity for the C variant of the T-786C single-nucleotide polymorphism of the NOS3 gene, which solely exists in humans, renders the gene less sensitive to FSS, resulting in a reduced endothelial cell (EC) capacity to generate NO. Decreased bioavailability of NO in the arterial vessel wall facilitates atherosclerosis.

Procedural advantages of a novel coronary stent design with ultra-thin struts and bioabsorbable abluminal polymer coating in an all-comers registry.

Introduction: The implications of novel drug-eluting stent (DES) design modifications including ultra-thin struts and new concepts of polymer coating for procedural efficacy are still unknown.

Aim: To evaluate procedural efficacy and short-term safety of a novel DES design.

Material And Methods: In this all-comers registry, 407 consecutive patients were enrolled upon undergoing percutaneous coronary interventions (PCI) with the thin-strut bioabsorbable abluminal polymer-coated SYNERGY stent.

Systematic RNA-interference in primary human monocyte-derived macrophages: A high-throughput platform to study foam cell formation.

Macrophage-derived foam cells are key regulators of atherogenesis. They accumulate in atherosclerotic plaques and support inflammatory processes by producing cytokines and chemokines. Identifying factors that regulate macrophage lipid uptake may reveal therapeutic targets for coronary artery disease (CAD).

To change or not to change - That is the question: A qualitative study of lifestyle changes following acute myocardial infarction.

Objective The purpose of this study was to investigate key factors related to lifestyle changes following acute myocardial infarction (AMI) by eliciting survivors' subjective needs for, attitudes towards and experiences with behaviour changes in their everyday life to improve future interventions promoting lifestyle changes. Methods Semi-structured interviews were conducted with 21 individuals who had recently experienced an AMI. The interviews were audio-recorded and transcribed verbatim.

Adventitial tertiary lymphoid organ classification in human atherosclerosis.

Background: Atherosclerosis is a chronic inflammatory disease of the arterial wall. Adjacent to lamina intima lesion progression, a cellular compound develops in the lamina adventitia, defined as tertiary lymphoid organs (TLO) in mice. But in human system, it remains unknown whether these adventitial cellular accumulations represent these highly organized immunological structures.

CXCL4-induced macrophages in human atherosclerosis.

Atherosclerosis is considered an inflammatory disease of the arterial wall. Monocytes and monocyte-derived cells (most often termed macrophages) play an essential role in the formation of atherosclerotic lesions, as they take up lipids leading to subsequent foam cell formation accompanied by release of pro-inflammatory cytokines. Similarly, platelets have been discovered to represent an important cell type mediating inflammatory and immune processes in atherogenesis, mainly by secreting chemokines, which are stored in the platelets' alpha granules, upon platelet activation.

Galectin-3 binding protein, coronary artery disease and cardiovascular mortality: Insights from the LURIC study.

Background And Aims: Galectin-3 binding protein (Gal-3BP) has been associated with inflammation and cancer, however, its role in coronary artery disease (CAD) and cardiovascular outcome remains unclear.

Methods: Gal-3BP plasma levels were measured by ELISA in 2922 individuals from the LURIC study (62.7 ± 10.

The influence of surgical technique on early posttransplant atrial fibrillation - comparison of biatrial, bicaval, and total orthotopic heart transplantation.

Purpose: Early posttransplant atrial fibrillation (AF) has been associated with worse clinical outcomes after heart transplantation (HTX). The type of surgical technique may constitute a relevant risk factor for AF.

Patients And Methods: This retrospective single-center study included 530 adult patients.

The Two Faces of Interleukin-17A in Atherosclerosis.

A complex network of different cytokines and chemokines modulates atherosclerosis, a chronic inflammatory disease. Interleukin-17A (IL-17A) is expressed by different leukocyte subsets such as CD4+IL-17+ T cells (Th17), γδ T cells, natural killer cells, natural killer T cells, and neutrophils. IL-17A plays an important role in host defense and is involved in the pathology of different autoimmune and inflammatory diseases.

Histopathological assessment of calcification and inflammation of calcific aortic valves from patients with and without diabetes mellitus.

Background: Calcific aortic valve disease (CAVD) is the most common valvular heart disease and likely evolves from inflammatory pre-conditions in the valve. Type II diabetes mellitus (DMII) has been associated with pathogenesis of CAVD, however, the mechanism initiating CAVD in DMII is not well understood and the human valve pathology in DMII has not been described. We therefore performed quantitative histological analyses of aortic valves of CAVD patients with and without DMII.

Galectin-3 binding protein plasma levels are associated with long-term mortality in coronary artery disease independent of plaque morphology.

Background And Aims: Galectin-3 binding protein (Gal-3BP) is a secreted protein associated with inflammation and carotid atherosclerosis. We hypothesized that high Gal-3BP levels may indicate unfavorable plaque morphology and outcome in coronary artery disease (CAD).

Methods: Gal-3BP plasma levels were measured by ELISA in 233 patients (63 ± 10 years, 50.

Translational atherosclerosis research: From experimental models to coronary artery disease in humans.

Atherosclerosis is the leading cause of death worldwide. Research on the pathophysiological mechanisms of atherogenesis has made tremendous progress over the past two decades. However, despite great advances there is still a lack of therapies that reduce adverse cardiovascular events to an acceptable degree.

Myocardial Perfusion Reserve and Strain-Encoded CMR for Evaluation of Cardiac Allograft Microvasculopathy.

Objectives: This study sought to evaluate myocardial perfusion reserve index (MPRI) and diastolic strain rate, both assessed by cardiac magnetic resonance (CMR) as a noninvasive tool for the detection of microvasculopathy.

Background: Long-term survival of cardiac allograft recipients is limited primarily by cancer and cardiac allograft vasculopathy (CAV). Besides epicardial CAV, diagnosed by coronary angiography, stenotic microvasculopathy was found to be an additional independent risk factor for survival after heart transplantation.

Long-term use of amiodarone before heart transplantation significantly reduces early post-transplant atrial fibrillation and is not associated with increased mortality after heart transplantation.

Background: Amiodarone is a frequently used antiarrhythmic drug in patients with end-stage heart failure. Given its long half-life, pre-transplant use of amiodarone has been controversially discussed, with divergent results regarding morbidity and mortality after heart transplantation (HTX).

Aim: The aim of this study was to investigate the effects of long-term use of amiodarone before HTX on early post-transplant atrial fibrillation (AF) and mortality after HTX.

Differential regulation of aldose reductase expression during macrophage polarization depends on hyperglycemia.

Aldose reductase (AR; gene AKR1B1) is the rate-limiting enzyme of the polyol pathway and has been associated with diabetes and atherosclerosis. Here, we sought to identify the mechanisms underlying differential AR expression in human atherosclerotic plaque macrophages. In vitro, M1-polarized human monocyte-derived macrophages expressed significantly higher levels of AKR1B1 mRNA and AR protein compared with M2-polarized macrophages.

CXCL4 Plasma Levels Are Not Associated with the Extent of Coronary Artery Disease or with Coronary Plaque Morphology.

Background: CXCL4 is a platelet chemokine released at micromolar concentrations upon platelet activation. CXCL4 has been shown to promote atherogenesis by various mechanisms. However, data on CXCL4 plasma levels in patients with coronary artery disease are largely inconclusive.

Prevalence of M4 macrophages within human coronary atherosclerotic plaques is associated with features of plaque instability.

Background: The platelet chemokine CXCL4 induces monocyte differentiation resulting in a macrophage phenotype called "M4", which co-expresses CD68, MMP7, and S100A8. We hypothesized that M4 macrophages are associated with plaque destabilization.

Methods: Atherosclerotic arteries were obtained from explanted hearts of patients with severe coronary artery disease (CAD, n = 32) and of patients with dilated cardiomyopathy and no or mild CAD (controls, n = 19).

Advantageous effects of immunosuppression with tacrolimus in comparison with cyclosporine A regarding renal function in patients after heart transplantation.

Background: Nephrotoxicity is a serious adverse effect of calcineurin inhibitor therapy in patients after heart transplantation (HTX).

Aim: In this retrospective registry study, renal function within the first 2 years after HTX in patients receiving de novo calcineurin inhibitor treatment, that is, cyclosporine A (CSA) or tacrolimus (TAC), was analyzed. In a consecutive subgroup analysis, renal function in patients receiving conventional tacrolimus (CTAC) was compared with that of patients receiving extended-release tacrolimus (ETAC).

Analysis of malignancies in patients after heart transplantation with subsequent immunosuppressive therapy.

Objective: The aim of this study was to analyze the distribution of malignancies in patients after heart transplantation (HTX) and to evaluate the risk factors including immunosuppressive therapy with regard to the development of malignancies and survival. Special emphasis was placed on the effects of a mammalian target of rapamycin (mTOR) containing immunosuppressive regimen.

Methods: A total of 381 patients (age ≥18 years) receiving HTX were included in the present analysis.

Inflammatory therapeutic targets in coronary atherosclerosis-from molecular biology to clinical application.

Atherosclerosis is the leading cause of death worldwide. Over the past two decades, it has been clearly recognized that atherosclerosis is an inflammatory disease of the arterial wall. Accumulating data from animal experiments have supported this hypothesis, however, clinical applications making use of this knowledge remain scarce.

CCL19 and CCL21 modulate the inflammatory milieu in atherosclerotic lesions.

Despite advances in the pharmacologic and interventional treatment of coronary artery disease, atherosclerosis remains the leading cause of death worldwide. Atherosclerosis is a chronic inflammatory disease, and elevated expression of CCL19 and CCL21 has been observed in ruptured lesions of coronary arteries of patients with myocardial infarction and carotid plaques of patients with ischemic symptoms, as well as in plasma of coronary artery disease patients. However, the exact role of CCL19 and CCL21 in atherosclerosis remains unknown.