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Clinical Updates on Dyslipidemia
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Clinical Updates on Dyslipidemia

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

Deadline for manuscript submissions: 30 September 2026 | Viewed by 3807

Editor

Prof. Dr. Nathan Wong

E-Mail Website
Guest Editor
Division of Cardiology, University of California Irvine, Irvine, CA 92697, USA
Interests: preventive cardiology; cardiovascular epidemiology; dyslipidemia; diabetes; subclinical atherosclerosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Dyslipidemia, especially dyslipidemia featuring elevated LDL-C, low levels of HDL-C, and elevated triglycerides with elevated levels of lipoprotein(a), is a well-established risk factor for atherosclerotic cardiovascular disease (ASCVD). Clinical trials conducted over the past four decades have established the role of LDL-C-lowering therapy in reducing the risk of ASCVD in a wide range of patient populations, with statins being the most common therapy and ezetimibe, PCSK9 inhibitors, and bempedoic acid being explored more recently. Icosapent ethyl also leads to improved ASCVD outcomes. Cardiovascular outcome trials involving the use of inclisiran, obicetrapib, or novel RNA-targeted agents to lower lipoprotein(a) levels are ongoing. However, despite international guidelines and a wide range of therapies for lowering LDL-C to reduce the risk of ASCVD, many people do not undergo lipid testing and are inadequately treated for LDL-C, which makes this an important gap in care. Further efforts are needed to address this clinical inertia if we are to improve ASCVD outcomes, particularly in our highest risk patients.

This Special Issue on dyslipidemia and cardiovascular disease will publish original research, reviews, and commentaries that aim to advance our knowledge on the mechanisms, epidemiology, and existing and newer therapeutic targets for dyslipidemia and cardiovascular disease.

Prof. Dr. Nathan Wong
Guest Editor

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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized 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

  • dyslipidemia
  • cardiovascular disease
  • prevention
  • treatment
  • risk factors

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Published Papers (3 papers)

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Research

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11 pages, 873 KB  
Article
Comparative Proteomic Analysis of Lipoprotein(a): Method-Dependent Profiles and Disease Pathways
by Nelsa Matienzo, Zoe Kress, Sasha A. Singh, Masanori Aikawa, Rajesh K. Soni, Yihao Li and Gissette Reyes-Soffer
J. Clin. Med. 2026, 15(7), 2559; https://doi.org/10.3390/jcm15072559 - 27 Mar 2026
Viewed by 854
Abstract
Background: Lipoprotein(a) [Lp(a)] is a genetically determined risk factor for atherosclerotic cardiovascular disease (ASCVD). Proteomic studies suggest that Lp(a)-associated proteins mediate inflammation, thrombosis, and vascular calcification, but methodological variability may influence proteome definition. Methods: Lp(a) was immunoprecipitated from human plasma using [...] Read more.
Background: Lipoprotein(a) [Lp(a)] is a genetically determined risk factor for atherosclerotic cardiovascular disease (ASCVD). Proteomic studies suggest that Lp(a)-associated proteins mediate inflammation, thrombosis, and vascular calcification, but methodological variability may influence proteome definition. Methods: Lp(a) was immunoprecipitated from human plasma using an apo(a)-specific monoclonal antibody and analyzed by mass spectrometry following either in-gel digestion or automated in-solution proteolysis. Proteins identified by ≥3 unique peptides and consistently detected across all samples by both methods were considered high confidence. Functional enrichment and interaction networks were assessed using STRING. Results: In-solution proteolysis identified 92 proteins and in-gel digestion identified 55 proteins, with 34 proteins shared between methods. These high-confidence proteins were enriched for pathways involved in lipoprotein remodeling, coagulation regulation, vesicle-mediated transport, lipid binding, and extracellular matrix organization, providing biological insight into mechanisms linking Lp(a) to inflammation, thrombosis, and calcification. Conclusions: Proteome composition of Lp(a) is method-dependent; however, a rigorously defined core proteome of 34 proteins was consistently identified across analytical approaches, highlighting biologically relevant pathways that may underlie Lp(a)-mediated ASCVD risk. Full article
(This article belongs to the Special Issue Clinical Updates on Dyslipidemia)
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18 pages, 3698 KB  
Article
A Temporal Validation Study of Diagnostic Prediction Models for the Screening of Elevated Low-Density and Non-High-Density Lipoprotein Cholesterol
by Wuttipat Kiratipaisarl, Vithawat Surawattanasakul, Wachiranun Sirikul and Phichayut Phinyo
J. Clin. Med. 2025, 14(21), 7617; https://doi.org/10.3390/jcm14217617 - 27 Oct 2025
Viewed by 1271
Abstract
Background/Objectives: Limited accessibility to hypercholesterolemia diagnosis hinders the primary prevention of cardiovascular disease. Therefore, we conducted a prospective, temporal validation study of two diagnostic prediction models, targeting endpoints of elevated low-density lipoprotein cholesterol (LDL-C, ≥160 mg/dL) and non-high-density lipoprotein cholesterol (non-HDL-C, ≥160 [...] Read more.
Background/Objectives: Limited accessibility to hypercholesterolemia diagnosis hinders the primary prevention of cardiovascular disease. Therefore, we conducted a prospective, temporal validation study of two diagnostic prediction models, targeting endpoints of elevated low-density lipoprotein cholesterol (LDL-C, ≥160 mg/dL) and non-high-density lipoprotein cholesterol (non-HDL-C, ≥160 mg/dL). Methods: We prospectively recruited workers aged 20–40 years from a single-center, university hospital from March to June 2024 (n = 1099). We determined two diagnostic endpoints: elevated LDL-C and non-HDL-C. The predicted probabilities were derived from the binary logistic regression based on gender, metabolic age, and diastolic blood pressure. We assessed three prediction performances: discrimination from area under the receiver-operating characteristic curve (AuROC); calibration slope (C-slope) and calibration-in-the-large (CITL) from the calibration plot; clinical net benefit from decision curve analysis. Recalibration was based on C-slope and CITL, with a socioeconomic subgroup fairness assessment of AuROC, C-slope, and CITL. Results: From 1099 eligible participants, we identified 135 (12.3%) elevated LDL-C and 251 (22.8%) elevated non-HDL-C cases. The LDL-C model had poor discrimination (AuROC 0.59; 95%-CI, 0.56–0.62), miscalibration (C-slope 0.64; 95%-CI, 0.39–0.88 and CITL −0.14; 95%-CI, −0.27–−0.02), and negligible investigation reduction. The non-HDL-C model had fair discrimination (AuROC 0.67; 95%-CI, 0.64–0.69), miscalibration (C-slope 0.71; 95%-CI, 0.59–0.83 and CITL −0.07; 95%-CI, −0.17–0.03), and 20% investigation reduction at prevalence threshold probability. Updated model fairness improved compared to the original models. Conclusions: Temporal validation demonstrated modest replicability for the elevated non-HDL-C model, with a potential limitation in participants with normal BMI but low muscle and high fat mass. Health practitioners may use updated elevated non-HDL-C models as a non-invasive triage strategy in young adults, with threshold probabilities within the positive clinical net benefit ranges. Further external validation studies in a larger and more diverse population are necessary. Full article
(This article belongs to the Special Issue Clinical Updates on Dyslipidemia)
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Review

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16 pages, 676 KB  
Review
Therapeutic Inertia in Lipid-Lowering Treatment: A Narrative Review
by Marco Vatri, Andrea Faggiano, Elisabetta Angelino, Marco Ambrosetti, Pompilio Massimo Faggiano and Francesco Fattirolli
J. Clin. Med. 2026, 15(3), 1075; https://doi.org/10.3390/jcm15031075 - 29 Jan 2026
Cited by 3 | Viewed by 1188
Abstract
Therapeutic inertia in lipid-lowering treatment remains a striking paradox of modern cardiovascular medicine: at a time when the causal role of LDL-cholesterol in atherosclerotic disease is unequivocal and potent therapies are widely available, a substantial proportion of high- and very-high-risk patients still fail [...] Read more.
Therapeutic inertia in lipid-lowering treatment remains a striking paradox of modern cardiovascular medicine: at a time when the causal role of LDL-cholesterol in atherosclerotic disease is unequivocal and potent therapies are widely available, a substantial proportion of high- and very-high-risk patients still fail to receive timely treatment intensification. Contemporary European and international data consistently show fewer than one in three patients in secondary prevention achieve guideline-recommended LDL-C targets, revealing a persistent and unacceptable gap between scientific evidence and clinical reality. This narrative review examines therapeutic inertia as a key explanatory framework for this gap, describing its epidemiology, mechanisms, and clinical consequences in secondary cardiovascular prevention. We summarize the main physician-, patient-, and system-level determinants and propose recurrent clinician “phenotypes” of inertia that may help explain why opportunities are missed even in the highest-risk patients. The consequences are profound: therapeutic inertia contributes to what we propose as the conceptual framework of an “avoidable atherosclerotic burden”, the cumulative vascular injury that accrues each period in which LDL-C remains above target, translating into higher rates of avoidable cardiovascular events, and increased healthcare costs. Emerging strategies such as upfront combination therapy, decision-support systems, structured lipid pathways, and the integration of artificial intelligence offer practical tools to shift lipid management from reactive to proactive care. Overcoming therapeutic inertia is therefore not merely a matter of improving process metrics, but a clinical and ethical imperative. Closing the gap between evidence and practice requires transforming optimal lipid management from an exception into a system-level default, ensuring that every patient receives the full benefit of therapies proven to save lives. This work proposes a novel characterization of clinician ‘phenotypes’ and the concept of ‘avoidable atherosclerotic burden’ as a framework to understand and address this gap. Full article
(This article belongs to the Special Issue Clinical Updates on Dyslipidemia)
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