Association between admission ECG changes and long-term mortality in patients with an incidental myocardial infarction: Results from the KORA myocardial infarction registry.

Background: The aim of this study was to examine the predictive value of specific changes in admission ECG on long-term outcome in acute myocardial infarction (AMI).

Methods: From 2000 until 2017 all AMI cases (n = 9,689) in the study area of Augsburg, Germany, were prospectively recorded. For this study, all patients with a first-time AMI, who survived the first 28 days, were considered.

Subendothelial matrix components influence endothelial cell apoptosis in vitro.

The programmed form of cell death (apoptosis) is essential for normal development of multicellular organisms. Dysregulation of apoptosis has been linked with embryonal death and is involved in the pathophysiology of various diseases. Specifically, endothelial apoptosis plays pivotal roles in atherosclerosis whereas prevention of endothelial apoptosis is a prerequisite for neovascularization in tumors and metastasis.

CD34 circulating cells display signs of immune activation in patients with acute coronary syndrome.

Bone marrow-derived endothelial progenitor cells (EPC) are released into the peripheral blood in situations of vascular repair/angiogenesis. Regulation of vascular repair and angiogenesis by EPC depends not only on the number of circulating EPC but also on their functionality. As endothelial cells can act as antigen-presenting cells in coronary artery disease (CAD), we postulated that EPC can be immune activated here as well.

Glucocorticoid-remediable aldosteronism in a young adult with a family history of Conn's syndrome.

Glucocorticoid-remediable aldosteronism is a hereditary form of primary hyperaldosteronism and the most common monogenic cause of hypertension. We present the case of a 24-year-old man with a family history of Conn's syndrome. Yet, in the index patient, classical characteristics of mineralocorticoid excess could be reversed by exogenous glucocorticoids.

3D matrix-embedding inhibits cycloheximide-mediated sensitization to TNF-alpha-induced apoptosis of human endothelial cells.

The programmed form of cell death (apoptosis) is essential for normal development of multicellular organisms. Dysregulation of apoptosis has been linked with embryonal death and is involved in the pathophysiology of various diseases. Others and we previously demonstrated endothelial biology being intertwined with biochemical and structural composition of the subendothelial basement membrane.

Influence of polyphenol-rich diet on exercise-induced immunomodulation in male endurance athletes.

Stress is associated with increased susceptibility to infection. We investigated if the mechanism involves immunomodulation of dendritic cells and whether this can be inhibited by a polyphenol-rich diet. Blood samples were taken from a total of 100 male endurance athletes at 5 time points around a marathon run: 4 weeks before; 1 week before; and immediately, 24 h, and 72 h after.

Influence of High Polyphenol Beverage on Stress-Induced Platelet Activation.

Objectives: Platelets are playing a crucial role in acute cardiovascular events. We investigated if physical stress activates platelets and whether this activation can be inhibited by a polyphenol-enriched diet.

Methods: Blood samples were taken from a total of 103 athletes three weeks before, one day before, immediately as well as 24 hours and 72 hours after a marathon run.

Cell matrix contact modifies endothelial major histocompatibility complex class II expression in high-glucose environment.

Atherosclerosis is a chronic inflammatory disease. Cardiovascular risk factors such as hyperglycemia, hyperlipidemia, and arterial hypertension induce endothelial dysfunction with alterations in endothelial biosecretion and immune behavior. The aim of this study is to elucidate whether glucose-induced modifications of endothelial biosecretory and immune functions are regulated by interactions of endothelial cells (ECs) with their extracellular matrix [ECs plated on polystyrene-coated tissue culture plates (TC-EC) vs.

The effect of substrate modulus on the growth and function of matrix-embedded endothelial cells.

Endothelial cells (EC) are potent bioregulatory cells, modulating thrombosis, inflammation and control over mural smooth muscle cells and vascular health. The biochemical roles of EC are retained when cells are embedded within three-dimensional (3D) denatured collagen matrices. Though substrate mechanics have long been known to affect cellular morphology and function and 3D-EC systems are increasingly used as therapeutic modalities little is known about the effect of substrate mechanics on EC in these 3D systems.

Relation of matrix metalloproteinase-9/tissue inhibitor of metalloproteinase-1 ratio in peripheral circulating CD14+ monocytes to progression of coronary artery disease.

Atherosclerosis is an inflammatory disease in which systemic inflammation correlates with disease activity. Matrix metalloproteinases (MMPs) contribute to collagen breakdown in atherosclerotic plaques. In the present study, we investigated whether the ratio of MMP-9 and its endogenous inhibitor, tissue inhibitor of metalloproteinase (TIMP)-1, in circulating monocytes correlates with the clinical stages of coronary artery disease.

T-helper 2 cells are essential for modulation of vascular repair by allogeneic endothelial cells.

Background: Endothelial cells (ECs) embedded within 3-dimensional matrices (MEEC) control lumenal inflammation and intimal hyperplasia when placed in the vascular adventitia. Matrix embedding alters endothelial immunogenicity in vitro. T-helper (Th) cell-driven host immunity is an impediment of allogeneic grafts.

NF-kappaB activity in endothelial cells is modulated by cell substratum interactions and influences chemokine-mediated adhesion of natural killer cells.

Because changes in subendothelial matrix composition are associated with alterations of the endothelial immune phenotype, we sought to understand if cytokine-induced NF-kappaB activity and downstream effects depend on substrate adherence of endothelial cells (EC). We compared the upstream phosphorylation cascade, activation of NF-kappaB, and expression/secretion of downstream effects of EC grown on tissue culture polystyrene plates (TCPS) with EC embedded within collagen-based matrices (MEEC). Adhesion of natural killer (NK) cells was quantified in vitro and in vivo.

Function and mode of regulation of endothelial major histocompatibility complex class II.

Tissue engineering is a promising approach to implement endothelial cells as a cellular delivery therapy for vascular disease. We and others previously demonstrated that endothelial cells embedded in three-dimensional collagen-based matrices retain their full biosecretory spectrum, enabling them to serve as powerful regulators of vascular diseases. Fascinatingly, matrix embedding of endothelial cells not only allows for their implantation but also seems to provide protection from allo- and xenogeneic-triggered host immune responses.

Torsades de Pointes: a rare complication of an extra-adrenal pheochromocytoma.

Pheochromocytoma is an infrequent secondary cause of arterial hypertension, often associated with paroxysmal headache, sweating, weight loss, and palpitations. Cardiovascular complications of pheochromocytoma include sudden death, heart failure due to toxic cardiomyopathy, and hypertensive encephalopathy. Here we report the case of a female with an acquired long-QT-syndrome as a rare complication of an extra-adrenal pheochromocytoma.

The effect of three-dimensional matrix-embedding of endothelial cells on the humoral and cellular immune response.

The endothelium is a unique immunologic target. The first host-donor reaction in any cell, tissue or organ transplant occurs at the blood-tissue interface, the endothelium. When endothelial cells are themselves the primary component of the implant a second set of immunologic reactions arises.

Endothelial immunogenicity--a matter of matrix microarchitecture.

The endothelium is a highly specialized active interface between blood and the underlying tissues, maintaining vascular tone, thrombo-resistance and selective permeability to cells and proteins. It is also an important regulator of inflammatory diseases, and endothelial-leukocyte interactions often herald complex diseases with an inflammatory component. Yet, the exact mechanisms promoting immune activation of endothelial cells (EC) are incompletely understood.

Endothelial cell-matrix interactions determine maturation of dendritic cells.

The fate of allo- and xenogeneic endothelial cell (EC) implants is regulated by EC-matrix interactions. While free EC are destroyed by a vigorous immune reaction, EC embedded within 3D collagen cells are well tolerated. Given the critical role DC serve in immune reactivity, we hypothesized that EC-driven DC maturation depends on EC-matrix contact.

Matrix adherence of endothelial cells attenuates immune reactivity: induction of hyporesponsiveness in allo- and xenogeneic models.

Endothelial integrity regulates vascular tone, luminal patency, and the immune reactivity to tissue grafts. Endothelial dysfunction is the first marker and site of disease initiation and severity. It has long been known that endothelial biochemical function is density dependent, and we have recently shown that endothelial immunobiology is anchorage dependent.

Vascular bed origin dictates flow pattern regulation of endothelial adhesion molecule expression.

Endothelial cell phenotypes markedly differ, depending upon function and vascular bed of origin. Differences might account for specific susceptibility to pathological conditions. As leukocyte adhesion to activated endothelium is the initiating event in a range of diseases, we compared the influence of vascular bed-specific flow patterns on adhesion molecule expression in human saphenous vein (HSVEC) and coronary artery endothelial cells (HCAEC).

Tissue engineering of endothelial cells and the immune response.

Background: While tissue engineering offers promise for organ and tissue transplantation, it can also be used to examine transplant and immune biology. Endothelial cells engrafted within 3-dimensional matrices create stable units that produce all of the factors of a functional quiescent endothelium. Perivascular implantation of tissue engineered endothelial cell constructs provides long-term control of vascular repair after injury.

Cell-matrix contact prevents recognition and damage of endothelial cells in states of heightened immunity.

Background: Autoimmunity may exacerbate vascular disease, particularly in the form of anti-endothelial cell (EC) antibodies. The increased morbidity of cardiovascular diseases in concert with diabetes mellitus, hypertension, and other systemic illnesses may reflect the increase presence and potency of these antibodies. Matrix-embedded ECs act as powerful regulators of vascular repair accompanied by significant reduction in expected systemic and local inflammation.