Cytokeratin 18 as a Novel Biomarker in Patients with Hypertrophic Cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is a heart muscle disease associated with an increased risk for sudden cardiac death (SCD). Cytokeratin 18-based proteins, such as M30 and M65 antigens, are known cell-death biomarkers. M30 antigen is released from cells during apoptosis, and M65 antigen is released during cell death from any cause, such as apoptosis or necrosis.

Oxygen venous saturation is associated with subclinical myocardial systolic dysfunction in patients with end-stage renal disease undergoing hemodialysis.

Introduction: The aim of this prospective study was to evaluate the impact of hemodialysis (HD) on myocardial injury, of both right and left ventricle function as well as their association with venous oxygen saturation (ScvO2) alterations.

Material And Methods: We included in the study stable consecutive patients with end-stage renal disease (ESRD) undergoing regular HD. Right and left ventricular speckle-tracking echocardiographies were performed in all patients.

CT coronary angiography in asymptomatic male patients with high atherosclerosis risk: Is it justified?

Purpose: To study the necessity of coronary artery screening with computerized tomography coronary angiography (CTCA) in asymptomatic male patients.

Material And Methods: A total of 226 asymptomatic male patients aged over 50 years were included in this prospective study, according to a clinical protocol approved by the Heraklion University Hospital's Ethics Committee. All participants had at least 3 or more known atherosclerosis risk factors.

Left dominant arrhythmogenic cardiomyopathy: a morbid association of ventricular arrhythmias and unexplained infero-lateral T-wave inversion.

Left-dominant arrhythmogenic cardiomyopathy is a subtype of arrhythmogenic right ventricular cardiomyopathy characterized by early predominant left ventricular involvement. Α 34-year-old man presented with palpitations and a history of frequent ventricular extrasystoles of both LBBB and RBBB configuration. Cardiac workup revealed repolarization abnormalities at infero-lateral leads in the absence of diagnostic structural/functional alterations or obstructive coronary artery disease.

Genetic variability of the distal promoter of the ST2 gene is associated with angiographic severity of coronary artery disease.

Genetic polymorphy of the distal promoter region of the ST2 gene influences transcriptional activity and susceptibility to atopic dermatitis and asthma. Based on the inflammatory background of atherosclerosis we hypothesized that ST2 distal promoter genetic polymorphy could also affect susceptibility to coronary artery disease (CAD). To test our hypothesis we performed direct sequencing of a 825 bp locus of the distal promoter -with previously reported significant polymorphy in 63 angiographically diagnosed CAD patients and 63 age and sex matched controls with negative coronary angiography.

Interleukin 8 gene polymorphisms and susceptibility to restenosis after percutaneous coronary intervention.

Interleukin-8 is a strong mediator of inflammation and has been implicated in the biochemical pathways involved in a wide range of inflammatory diseases including atherosclerosis. We investigated the potential influence of two common functional polymorphisms of the interleukin (IL)-8 gene: -251A/T and 781C/T on susceptibility to in stent restenosis (ISR) following percutaneous coronary intervention (PCI). The hypothesis was tested by screening for the prevalence of the above polymorphisms in 201 coronary artery disease (CAD) patients subjected to PCI and presenting with symptoms or signs of recurrent ischemia.

Genetic diversity of RANTES gene promoter and susceptibility to coronary artery disease and restenosis after percutaneous coronary intervention.

Regulated on activation, normal T cell expressed and secreted (RANTES) gene promoter is a regulatory region and a site of notable genetic diversity. In order to explore a possible interaction between RANTES promoter genetic diversity and susceptibility to coronary artery disease (CAD) and in stent restenosis (ISR), we initially sequenced a locus extending from -516 to 40 covering the entire region of the RANTES promoter in 100 subjects randomly selected from our cohort. Four single nucleotide polymorphisms (SNPs) were identified: -403G/A, -256G/A, -109C/T and -28C/G.

Interleukin 8 and susceptibility to coronary artery disease: a population genetics perspective.

Introduction: Interleukin 8 is a strong chemoattractant factor for neutrophils and T lymphocytes. We investigated the potential influence of two common polymorphisms of the interleukin-8 gene, -251A/T, and 781C/T on susceptibility to coronary artery disease.

Materials And Methods: The hypothesis was tested by screening for the prevalence of the above polymorphisms in 241 angiographically diagnosed coronary artery disease patients compared to 157 selected controls with negative coronary angiography.

CX3CR1 receptor is up-regulated in monocytes of coronary artery diseased patients: impact of pre-inflammatory stimuli and renin-angiotensin system modulators.

Fractalkine/CX3CR1 pathway is considered a major modulator of atherosclerosis. In the present study, expression of CX3CR1 on PBMCs/monocytes of healthy individuals and coronary artery diseased patients was initially assessed by flow cytometry. Effects of pre-inflammatory cytokines interferon (INF)-gamma and tumor necrosis factor (TNF)-alpha on expression of CX3CR1 and a single representative of each major chemokine family (CCR5 and CXCR4) were further assessed in three cell models: THP-1 monocytes, Jurkat T lymphocytes and primary monocytes isolated from healthy donors.

Effects of polymorphisms in chemokine ligands and receptors on susceptibility to coronary artery disease.

Introduction: Atherosclerosis, the underlying disorder of coronary artery disease (CAD), is an inflammatory process involving multiple molecular pathways. Chemokine-mediated mechanisms are potent regulators of atherosclerosis. Genetic variations that alter such signaling pathways could affect susceptibility to CAD.