European Atherosclerosis Journal

The European Atherosclerosis Journal is an official journal of SITeCS (Italian Society for Experimental and Clinical Therapeutics).
The European Atherosclerosis Journal is a new international, peer-reviewed, fully open access, four-monthly journal covering all topics within atherosclerosis and cardiovascular disease areas.The Journal aims to publish high quality research and follows strict rules to assess originality and best practices for authorship and disclosure of potential conflicts of interest.
Open Access
European Atherosclerosis Journal provides immediate open access to its content on the principle that making research freely available to the public supports exchange of knowledge.
All content in European Atherosclerosis Journal are published by SITeCS and are licensed under a Creative Commons Attribution Non-Commercial No Derivatives license (CC BY-NC-ND)

Focus and Scope
European Atherosclerosis Journal is an international journal that publishes papers in the field of atherosclerosis and cardiovascular disease, from basic research to clinical and translational studies. Meta-analysis and systematic reviews will also be accepted. Papers will be considered for publication based on originality and contribution to the field. The journal will consider for publication original articles (experimental and clinical), review articles, methodology papers, editorials, letters to the Editor, viewpoints, congress/conference reports.
Editorial Board
Editor in Chief: Alberto Corsini, Milan, Italy;
Editorial Board: Maurizio Averna, Palermo, Italy; Michel Farnier, Dijon, France; Meral Kayikcioglu, Izmir, Turkey; Luis Masana, Reus, Spain; Andrea Poli, Nutrition Foundation of Italy, Milan, Italy; Evgeny V. Shlyakhto, Saint Petersburg, Russia; Margus Viigimaa, Tallinn, Estonia.
The Editorial Board can invite authors to submit state-of-the-art papers. Authors are encouraged to submit pre-request to the Editor-in-Chief for evaluation of the potential acceptability of their contributions.
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Original article
Abstract 96
Page 27-34
Evaluation of Clinical Features including the frequency of Familial Hypercholesterolemia, and 2-Year Cardiovascular Outcomes in Patients with Early Acute Coronary Syndrome: Real-Life Data from a Retrospective Cohort
Meral Kayikcioglu, Bahadir Alan, Burcu Yağmur
Objective: This retrospective study, based on real-life data, aimed to evaluate the clinical characteristics and 2-year cardiovascular outcomes in patients presenting with early acute coronary syndrome (ACS) in a tertiary healthcare center.
Methods: Information including at least 2-year endpoint data after index ACS event was retrieved from hospital records. Age limit for early ACS was considered <55 years for males and <60 years for females.
Results: Of 985 consecutive ACS patients (770 males; age range, 21-93 years) 361 (36.6%) met early ACS criteria. Frequency familial hypercholesterolemia (FH) was 7.6% and higher in the young-age group (15.5%) than in the old-age group (3%) (p<0.001). During the follow-up (30 monts), the risk predictors for cardiovascular events were the index event being ST-segment elevation myocardial infarction or non-ST-segment elevation myocardial infarction and the presence of hypertension, and the risk predictors for mortality were female sex, older age, in-hospital cardiovascular complications.
Conclusion: A very high rate of early ACS (36.6%) was observed in this retrospective ACS cohort of a single center from Turkey. Compared to older patients, young patients were more smoking, more obese, less diabetic, and less hypertensive. High total cholesterol, high triglycerides, low HDL-cholesterol levels, high non-HDL cholesterol, family history of CAD, and FH were also more commonly observed in the young group. High FH prevalence might be a major factor of the high prevalence of premature ACS in this population. Both the in-hospital and 2-year follow-up mortality rates were significantly lower in the old-age group.
Review
Abstract 153
Page 35-43
PCSK9 in extrahepatic tissues: What can we expect from its inhibition?
Angela Pirillo, Lale Tokgözoğlu, Alberico L. Catapano
Proprotein convertase subtilisin/kexin type 9 (PCSK9) is an enzyme that belongs to the serine protease family and plays a key role in regulating low-density lipoprotein cholesterol (LDL-C) levels in the blood. PCSK9 binds to the LDL receptor (LDLR), targeting it for degradation, resulting in an increase in circulating LDL-C levels. Loss-of-function mutations in the PCSK9 gene are associated with lower LDL-C levels and lower cardiovascular risk; in contrast, gain-of-function mutations are a cause of familial hypercholesterolaemia. The identification of PCSK9 as a pharmacological target led to the development of inhibitors for the treatment of hypercholesterolaemia. To date, the monoclonal antibodies evolocumab and alirocumab (which target plasma PCSK9) and the small-interfering RNA inclisiran (which targets hepatic PCSK9 mRNA) have been approved for the treatment of hypercholesterolaemia. Although hepatic PCSK9 plays a central role in regulating plasma LDL-C levels, this protein is also expressed in other tissues, including the brain, pancreas, heart, kidney, intestine and adipose tissue. In extrahepatic tissues, the functions of PCSK9 are both dependent and independent of LDLR and not necessarily harmful. For this reason, it is essential to uncover any potentially harmful effects of therapies that inhibit PCSK9, beyond their known LDL-C-lowering and CV risk-reducing effects.
Online First

European Atherosclerosis Journal is an international, peer-reviewed, fully open access, four-monthly journal covering all topics within atherosclerosis and cardiovascular disease areas.
European Atherosclerosis Journal is the official journal of SITeCS (Società Italiana di Terapia Clinica e Sperimentale - Italian Society for Experimental and Clinical Therapeutics).
European Atherosclerosis Journal aims to publish high quality research and follows strict rules to assess originality and best practices for authorship and disclosure of potential conflicts of interest.