Disruption of the intercellular interactions between endothelial cells leads to endothelial dysfunction. The role of nanoparticles in plasma membrane stability, actin cytoskeleton organization and intercellular junctions is unclear. Human umbilical vein endothelial cells were treated with zinc oxide NPs in vitro. Cell shape, adhesiveness and plasma membrane integrity were analyzed by means of optical fluorescence microscopy, scanning electron microscopy and flow cytometry methods. Additionally, lactate dehydrogenase activity assay and annexin V staining were performed. The scanning electron microscopy analysis showed changes in morphology and surface topography. The F-actin organization was typical for migrating cells. Cell membrane damage (significant increase in lactate dehydrogenase release and annexin V staining) was observed in the concentration of ZnO nanoparticles above 30 g/ml. The relationship between ZnO nanoparticles and endothelial dysfunction was clearly established and the importance of cytoskeleton reorganization and loosening of the continuous endothelial monolayer after nanoparticles exposure has been documented.

There is insufficient evidence to demonstrate benefit or harm of using anticoagulants with or without ASA versus ASA alone in people with aPL antibodies and a history of recurrent pregnancy loss and with no such history; ASA versus placebo in people with aPL antibodies; and ASA with LMWH versus placebo or IVIG, and ASA with high-dose LMWH versus ASA with low-dose LMWH or UFH, in women with aPL antibodies and a history of recurrent pregnancy loss, for the primary prevention of thrombotic events. In a mixed population of people with a history of previous pregnancy loss and without such a history treated with anticoagulant combined with ASA, the incidence of minor bleeding (nasal bleeding, menorrhagia) was increased when compared with ASA alone. Studies that are adequately powered and that focus mainly on thrombotic events are needed to draw any firm conclusions on the primary prevention of thrombotic events in people with antiphospholipid antibodies.

(Cardiol J 2019; 26, 1: 77-86)

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Introduction Diabetes mellitus (DM) is the most common metabolic disease. A WHO report from 2016 indicates that 422 million people worldwide suffer from DM or hyperglycaemia because of impaired glucose metabolism. Chronic hyperglycaemia leads to micro- and macrovessel damage, which may result in life-threatening complications. The Wnt pathway regulates cell proliferation and survival by modulating the expression of genes that control cell differentiation. Three linked Wnt pathways have been discovered thus far: a β-catenin-dependent pathway and two pathways independent of β-catenin – the planar cell polarity pathway and calcium-dependent pathway. The Wnt pathway regulates genes associated with inflammation, cell cycle, angiogenesis, fibrinolysis and other molecular processes. Areas covered This review presents the current state of knowledge regarding the contribution of the Wnt pathway to endothelial ageing under hyperglycaemic conditions and provides new insights into the molecular basis of diabetic endothelial dysfunction. Conclusion The β-catenin-dependent pathway is a potential target in the prophylaxis and treatment of early-stage diabetes-related vascular complications. However, the underlying molecular mechanisms remain largely undetermined and require further investigation.

INTRODUCTION Long and diffuse coronary lesions (LDCLs) are routinely subjected to percutaneous management, but long term clinical outcomes and complication predictors with the use of contemporary stents and techniques remain undetermined. OBJECTIVES The aim of the study was to address long term effects of percutaneous management of LDCLs, using contemporary devices and optimization techniques. PATIENTS AND METHODS Long and diffuse coronary lesion was defined as a lesion requiring an implanta tion of 30 mm or longer total stent(s) length (TSL) into one coronary artery (bail outs excluded). There were 290 LDCL interventions with the use of newer generation drug eluting stents (DESs; cobalt chro mium everolimus-or zotarolimus-eluting stents) performed between January 2013 and January 2016. RESULTS The mean (SD) TSL was 55.5 (16.8) mm. The use of intravascular ultrasound / optical coher ence tomography was 17.1%, rotablation, 6.9%, and noncompliant balloon, 88.9%. The median (range) follow up duration was 831 (390-1373) days. All cause mortality and cardiac death rates were 11.7% and 6.9%, respectively. The myocardial infarction (MI) rate was 6.6%, including target vessel MI in 4.1%. The rate of clinically driven repeat revascularization was 13.8%, and of definite or probable LDCL stent thrombosis, 7.2%. Overall patient oriented adverse event rate (any death, MI, or repeat revascularization) was 25.5%, and device oriented rate (cardiac death, target vessel MI, or target lesion restenosis), 13.4%. Adverse outcome predictors were chronic kidney disease, acute coronary syndrome as an indication for the procedure, chronic heart failure with reduced left ventricular ejection fraction, multivessel disease, and coexisting peripheral artery disease, but not lesion related factors, such as bifurcation, calcification, chronic total occlusion, or TSL. CONCLUSIONS Adverse outcomes following contemporary LDCL management using newer generation DESs in routine clinical practice are associated with clinical patient characteristics rather than lesion characteristics or TSL. We identified high risk patient cohorts that may benefit from enhanced surveillance.

Atherosclerosis remains a large health and economic burden. Even though it has been studied for more than a century, its complex pathophysiology has not been elucidated. The relatively well-established contributors include: chronic inflammation in response to oxidized cholesterol, reactive oxygen species-induced damage and apoptosis. Recently, profilin 1, a regulator of actin dynamics emerged as a potential new player in the field. Profilin is abundant in stable atherosclerotic plaques and in thrombi extracted from infarct-related arteries in patients with acute myocardial infarction. The exact role of profilin in atherosclerosis and its complications, as well as its mechanisms of action, remain unknown. Here, we summarize several pathways in which profilin may act through mitochondria in a number of processes implicated in atherosclerosis.