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New Frontiers in Atherosclerosis
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New Frontiers in Atherosclerosis

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Cardiovascular Medicine".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 5766

Special Issue Editors

Dr. Iryna Dykun

E-Mail Website
Guest Editor
Department of Cardiology and Vascular Medicine, West German Heart and Vascular Center, University Hospital Essen, 45147 Essen, Germany
Interests: coronary artery disease; atherosclerosis; intravascular ultrasound; echocardiography; secondary prevention; lipids
Dr. Raluca Ileana Mincu

E-Mail Website
Guest Editor
Department of Cardiology and Vascular Medicine, West German Heart and Vascular Center, University Hospital Essen, 45147 Essen, Germany
Interests: coronary artery disease; atherosclerosis; cardio-oncology; congenital heart disease; cardiovascular imaging

Special Issue Information

Dear Colleagues,

Atherosclerosis now encompasses the major contributor to a global epidemic of cardiovascular disease, which is the leading cause of death and disability worldwide. Previously, after lifestyle measures, non-invasive therapeutic intervention for atherosclerosis focused mainly on pharmacologically limiting risk factors such as arterial hypertension and hypercholesterolaemia. Nevertheless, inflammation, endothelial dysfunction, and other novel contributors provide a set of pathways that link traditional risk factors to promote the disease and its complications. Rapidly accelerating knowledge and continued research promise to provide further progress in preventing this common chronic disease.

The special issue on “New Frontiers in Atherosclerosis” welcomes submissions in this field and will focus on the innovative diagnostic and therapeutic strategies on the topic of atherosclerosis. Original research papers, short communications, or focused reviews regarding diagnostic, treatment, prognosis and management of atherosclerosis are invited for submission.

Dr. Iryna Dykun
Dr. Raluca Ileana Mincu
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • atherosclerosis
  • inflammation
  • cardiovascular diseases
  • cardiovascular risk
  • intravascular ultrasound
  • echocardiography
  • prevention
  • lipids
  • diagnosis and prevention

Published Papers (3 papers)

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Research

7 pages, 631 KiB  
Article
Association between Pemafibrate Therapy and Triglyceride to HDL-Cholesterol Ratio
by Teruhiko Imamura, Nikhil Narang and Koichiro Kinugawa
J. Clin. Med. 2022, 11(10), 2820; https://doi.org/10.3390/jcm11102820 - 17 May 2022
Cited by 3 | Viewed by 1825
Abstract
Background: Pemafibrate is a novel selective peroxisome proliferator-activated receptor-α modulator, which was demonstrated to reduce serum triglyceride level with few drug-related adverse events in phase II and III clinical trials. However, its clinical implication in real-world practice remains unknown. Triglyceride/HDL-cholesterol ratio is a [...] Read more.
Background: Pemafibrate is a novel selective peroxisome proliferator-activated receptor-α modulator, which was demonstrated to reduce serum triglyceride level with few drug-related adverse events in phase II and III clinical trials. However, its clinical implication in real-world practice remains unknown. Triglyceride/HDL-cholesterol ratio is a surrogate of small dense LDL-cholesterol, which is a newly proposed cardiovascular risk factor independent of LDL-cholesterol levels. Methods: Consecutive patients who received pemafibrate between April 2020 and September 2021 and continued therapy for at least 3 months were included in this retrospective analysis. The primary outcome was the trend in triglyceride/HDL-cholesterol ratio during the 3-month treatment period. The change in cardiovascular event rate between the one-year pre-treatment period and the on-treatment period was also analyzed. Results: A total of 19 patients (median age 63 years, 74% men) were included and continued pemafibrate therapy for 3 months without any drug-related adverse events. Sixteen were add-on and three were conversions from other fibrates. Triglyceride/HDL-cholesterol ratio decreased significantly from 5.85 (4.19, 16.1) to 3.14 (2.39, 4.62) (p < 0.001). The cardiovascular event rate decreased significantly from 0.632 events/year to 0.080 events/year (p < 0.001). Conclusions: Pemafibrate therapy might have the potential to lower triglyceride/HDL-cholesterol ratio and decrease cardiovascular events. Full article
(This article belongs to the Special Issue New Frontiers in Atherosclerosis)
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22 pages, 2786 KiB  
Article
Relationships between Indicators of Lower Extremity Artery Disease and miRNA Expression in Peripheral Blood Mononuclear Cells
by Daniel P. Zalewski, Karol P. Ruszel, Andrzej Stępniewski, Dariusz Gałkowski, Marcin Feldo, Janusz Kocki and Anna Bogucka-Kocka
J. Clin. Med. 2022, 11(6), 1619; https://doi.org/10.3390/jcm11061619 - 15 Mar 2022
Cited by 1 | Viewed by 2059
Abstract
Lower extremity artery disease (LEAD) is an underdiagnosed and globally underestimated vascular disease caused by the progressive and chronic formation of atherosclerotic plaques in the arteries of the lower limbs. Much evidence indicates that the abnormal course of pathophysiological processes underlying LEAD development [...] Read more.
Lower extremity artery disease (LEAD) is an underdiagnosed and globally underestimated vascular disease caused by the progressive and chronic formation of atherosclerotic plaques in the arteries of the lower limbs. Much evidence indicates that the abnormal course of pathophysiological processes underlying LEAD development is associated with altered miRNA modulatory function. In the presented study, relationships between miRNA expression and clinical indicators of this disease (ABI, claudication distance, length of arterial occlusion, Rutherford category, and plaque localization) were identified. MiRNA expression profiles were obtained using next-generation sequencing in peripheral blood mononuclear cells (PBMCs) of 40 LEAD patients. Correlation analysis performed using the Spearman rank correlation test revealed miRNAs related to ABI, claudication distance, and length of arterial occlusion. In the DESeq2 analysis, five miRNAs were found to be dysregulated in patients with Rutherford category 3 compared to patients with Rutherford category 2. No miRNAs were found to be differentially expressed between patients with different plaque localizations. Functional analysis performed using the miRNet 2.0 website tool determined associations of selected miRNAs with processes underlying vascular pathology, such as vascular smooth muscle cell differentiation, endothelial cell apoptosis, response to hypoxia, inflammation, lipid metabolism, and circadian rhythm. The most enriched functional terms for genes targeted by associated miRNAs were linked to regulation of the cell cycle, regulation of the transcription process, and nuclear cellular compartment. In conclusion, dysregulations of miRNA expression in PBMCs of patients with LEAD are indicative of the disease and could potentially be used in the prediction of LEAD progression. Full article
(This article belongs to the Special Issue New Frontiers in Atherosclerosis)
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15 pages, 1941 KiB  
Article
Left Ventricular Diastolic Function Following Anthracycline-Based Chemotherapy in Patients with Breast Cancer without Previous Cardiac Disease—A Meta-Analysis
by Raluca I. Mincu, Lena F. Lampe, Amir A. Mahabadi, Rainer Kimmig, Tienush Rassaf and Matthias Totzeck
J. Clin. Med. 2021, 10(17), 3890; https://doi.org/10.3390/jcm10173890 - 29 Aug 2021
Cited by 11 | Viewed by 2312
Abstract
Background: Anthracycline-based chemotherapy (ANT) remains among the most effective therapies for breast cancer. Cardiotoxicity from ANT represents a severe adverse event and may predominantly manifest as heart failure. While it is well-recognised that left ventricular systolic heart failure assessment is key in ANT-treated [...] Read more.
Background: Anthracycline-based chemotherapy (ANT) remains among the most effective therapies for breast cancer. Cardiotoxicity from ANT represents a severe adverse event and may predominantly manifest as heart failure. While it is well-recognised that left ventricular systolic heart failure assessment is key in ANT-treated patients, less is known about the relevance of LV diastolic functional impairment and its characterisation. Methods: Studies reporting on echocardiographic diastolic function parameters before and after ANT in breast cancer patients without cardiac disease were included. We evaluated pulsed wave (E/A ratio and mitral E-wave deceleration time (EDT)) and tissue Doppler (mean velocities of the mitral ring in the early diastole (e′) and E/e′ ratio) echocardiographic parameters. Results: A total of 892 patients from 13 studies were included. E/A ratio was significantly reduced at the end of ANT while EDT was not influenced by ANT. Additionally, e’ and E/e’ ratio showed no significant change after ANT. A modest reduction in LV ejection fraction and global longitudinal strain was observed at the end of ANT therapy. Conclusions: ANT had a modest early impact on E/A ratio, without changing EDT, e’, or E/e’ in patients with breast cancer without cardiac disease. Randomised studies on larger populations, using new parameters are required to define the role of diastolic dysfunction in the early diagnosis of ANT-induced cardiotoxicity. Full article
(This article belongs to the Special Issue New Frontiers in Atherosclerosis)
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