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Pharmacological Lipid Strategies for Cardiovascular Disease Prevention: Part II
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Pharmacological Lipid Strategies for Cardiovascular Disease Prevention: Part II

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

Deadline for manuscript submissions: closed (30 May 2023) | Viewed by 8960

Special Issue Editors

Dr. Francesca Zimetti

E-Mail Website
Guest Editor
Department of Food and Drugs, University of Parma, Parma, Italy
Interests: high-density lipoprotein (HDL) functions; cardiovascular pharmacology; atherosclerosis; inflammation; lipid metabolism; lipids in neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Maria Pia Adorni

E-Mail Website
Guest Editor
Department of Medicine and Surgery, University of Parma, Via Volturno 39/F, 43125 Parma, Italy
Interests: cholesterol; lipids; macrophage; lipoprotein function
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Although statins have enabled the remarkable reduction of low-density lipoprotein (LDL) cholesterol in blood plasma and a parallel significant reduction in cardiovascular events, cardiovascular disease (CVD) remains the main cause of mortality worldwide due to the so-called “residual cardiovascular risk”. In this context, much effort is being made to identify and develop novel therapeutic approaches. The recent introduction of antibodies targeting PCSK9 has further improved cardiovascular outcomes, and represents a novel alternative therapeutic strategy for many patients, including those intolerant to statins. Moreover, several other promising pharmacological strategies targeting lipid and lipoprotein metabolism are under investigation.

This Special Issue aims to provide researchers with an opportunity to publish both original research and review articles related to recent advances in the CV field, with a particular focus on the pharmacology of novel lipid- and lipoprotein-modifying strategies that have potential use in the clinic for preventing CVD in the near future.

Dr. Francesca Zimetti
Dr. Maria Pia Adorni
Guest Editors

Manuscript Submission Information

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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

  • lipids
  • lipoprotein
  • lipid metabolism
  • cardiovascular disease
  • atherosclerosis

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Published Papers (3 papers)

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Research

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7 pages, 427 KiB  
Article
Patient Selection for Pemafibrate Therapy to Prevent Adverse Cardiovascular Events
by Toshihide Izumida, Teruhiko Imamura, Nikhil Narang and Koichiro Kinugawa
J. Clin. Med. 2023, 12(1), 21; https://doi.org/10.3390/jcm12010021 - 20 Dec 2022
Cited by 1 | Viewed by 1713
Abstract
Background: pemafibrate is a newly-introduced selective peroxisome proliferator-activated receptor-α modulator, which decreases serum triglyceride levels with few drug-related adverse events and may reduce the risk of adverse cardiovascular events in carefully selected patients with hypertriglyceridemia. We aimed to understand which specific cohorts may [...] Read more.
Background: pemafibrate is a newly-introduced selective peroxisome proliferator-activated receptor-α modulator, which decreases serum triglyceride levels with few drug-related adverse events and may reduce the risk of adverse cardiovascular events in carefully selected patients with hypertriglyceridemia. We aimed to understand which specific cohorts may benefit or not from pemafibrate therapy for adverse cardiovascular event risk reduction. Methods: patients with hypertriglyceridemia at baseline received pemafibrate therapy for two years or until October 2022. The factors that were associated with an increased risk of adverse cardiovascular events, defined as heart failure hospitalization, stroke, and acute coronary syndromes, were investigated. Results: a total of 121 patients (median 62 years, 88 men) remained on pemafibrate therapy for a median of 566 days without any drug-related adverse events. During a 3-month therapeutic period, triglyceride levels improved significantly from 302 (205, 581) mg/dL to 178 (117, 253) mg/dL (p < 0.001). During the overall therapeutic period, there were nine cardiovascular events. Comorbid chronic heart failure, comorbid coronary disease, and a lower pemafibrate dosing were independently associated with the primary endpoint (p < 0.05 for all). Those with multiple risk factors (N = 30) had a significantly higher cumulative incidence of the primary endpoint as compared with others (27% versus 3%, p < 0.001). Conclusion: pemafibrate significantly improves hypertriglyceridemia. A higher dose of pemafibrate should be considered to reduce the risk of adverse cardiovascular events, particularly in patients with chronic heart failure or coronary disease. Full article
(This article belongs to the Special Issue Pharmacological Lipid Strategies for Cardiovascular Disease Prevention: Part II)
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15 pages, 306 KiB  
Article
Effects of Antirheumatic Treatment on Cell Cholesterol Efflux and Loading Capacity of Serum Lipoproteins in Spondylarthropathies
by Ingrid Hokstad, Daniela Greco, Gia Deyab, Morten Wang Fagerland, Stefan Agewall, Gunnbjørg Hjeltnes, Francesca Zimetti, Franco Bernini, Nicoletta Ronda and Ivana Hollan
J. Clin. Med. 2022, 11(24), 7330; https://doi.org/10.3390/jcm11247330 - 9 Dec 2022
Cited by 2 | Viewed by 1532
Abstract
Spondyloarthropathies (SpA) are associated with increased cardiovascular risk. Among possible mechanisms is the dysfunction of serum lipoproteins in regulating cell cholesterol homeostasis. Cholesterol efflux capacity (CEC)—the atheroprotective ability of HDL (high density lipoproteins) to accept cholesterol from macrophages—might predict cardiovascular disease independently of [...] Read more.
Spondyloarthropathies (SpA) are associated with increased cardiovascular risk. Among possible mechanisms is the dysfunction of serum lipoproteins in regulating cell cholesterol homeostasis. Cholesterol efflux capacity (CEC)—the atheroprotective ability of HDL (high density lipoproteins) to accept cholesterol from macrophages—might predict cardiovascular disease independently of HDL-cholesterol levels. We aimed at evaluating modifications of CEC and of the atherogenic cholesterol loading capacity (CLC) of serum lipoproteins in psoriatic arthritis (PsA) and ankylosing spondylitis (AS) following anti-rheumatic treatment. A total of 62 SpA patients (37 PsA and 25 AS) were evaluated before and after treatment with tumor necrosis factor inhibitor and/or methotrexate. CEC and CLC were measured by radioisotopic and fluorometric techniques, respectively. Endothelial function was assessed by finger plethysmography (Endopat). In the whole SpA group, total and HDL-cholesterol increased after treatment, while lipoprotein(a) decreased and CLC was unchanged. Treatment was associated with increased Scavenger Receptor class B type I (SR-BI)-mediated CEC in the AS group. SR-BI- and ABCG1-mediated CEC were negatively associated with inflammatory parameters and positively related to coffee consumption. SR-BI CEC and CLC were positively and negatively associated with endothelial function, respectively. Our pilot study suggests that anti-rheumatic treatment is associated with favorable modulation of lipoprotein quality and function in SpA, particularly in AS, in spite of the induced increase in total cholesterol levels. If confirmed in a larger population, this might represent an atheroprotective benefit beyond what is reflected by conventional serum lipid profile. Full article
(This article belongs to the Special Issue Pharmacological Lipid Strategies for Cardiovascular Disease Prevention: Part II)

Review

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13 pages, 1937 KiB  
Review
Mechanistic View on the Effects of SGLT2 Inhibitors on Lipid Metabolism in Diabetic Milieu
by Habib Yaribeygi, Mina Maleki, Željko Reiner, Tannaz Jamialahmadi and Amirhossein Sahebkar
J. Clin. Med. 2022, 11(21), 6544; https://doi.org/10.3390/jcm11216544 - 4 Nov 2022
Cited by 22 | Viewed by 5242
Abstract
Chronic hyperglycemia induces pathophysiologic pathways with negative effects on the metabolism of most substrates as well as lipids and lipoproteins, and thereby induces dyslipidemia. Thus, the diabetic milieu is commonly accompanied by different levels of atherogenic dyslipidemia, which is per se a major [...] Read more.
Chronic hyperglycemia induces pathophysiologic pathways with negative effects on the metabolism of most substrates as well as lipids and lipoproteins, and thereby induces dyslipidemia. Thus, the diabetic milieu is commonly accompanied by different levels of atherogenic dyslipidemia, which is per se a major risk factor for subsequent complications such as atherosclerosis, coronary heart disease, acute myocardial infarction, ischemic stroke, and nephropathy. Therefore, readjusting lipid metabolism in the diabetic milieu is a major goal for preventing dyslipidemia-induced complications. Sodium-glucose cotransporter-2 (SGLT2) inhibitors are a class of relatively newly introduced antidiabetes drugs (including empagliflozin, canagliflozin, dapagliflozin, etc.) with potent hypoglycemic effects and can reduce blood glucose by inducing glycosuria. However, recent evidence suggests that they could also provide extra-glycemic benefits in lipid metabolism. It seems that they can increase fat burning and lipolysis, normalizing the lipid metabolism and preventing or improving dyslipidemia. Nevertheless, the exact mechanisms involved in this process are not well-understood. In this review, we tried to explain how these drugs could regulate lipid homeostasis and we presented the possible involved cellular pathways supported by clinical evidence. Full article
(This article belongs to the Special Issue Pharmacological Lipid Strategies for Cardiovascular Disease Prevention: Part II)
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