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Atherosclerotic Cardiovascular Disease (ASCVD), Dyslipidemia, and CV Residual Risk: From...
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Atherosclerotic Cardiovascular Disease (ASCVD), Dyslipidemia, and CV Residual Risk: From Mechanisms to Therapeutic Approaches

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 18347

Special Issue Editors

Dr. Chiara Caselli

E-Mail Website
Guest Editor
Council of National Research (CNR), Institute of Clinical Physiology, Pisa, Italy
Interests: cardiovascular disease; atherosclerosis; risk factors; biomarker; molecular biology; personalized medicine
Special Issues, Collections and Topics in MDPI journals
Dr. Danilo Neglia

E-Mail Website
Guest Editor
Fdn CNR Reg Toscana G Monasterio, Cardiovasc Dept., Via G Moruzzi 1, I-56124 Pisa, Italy
Interests: coronary artery disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Adverse cardiovascular (CV) events due to atherosclerotic plaque development and progression have been linked to dyslipidemia, which includes a wide variety of biochemical disorders. Among dyslipidemia factors, the main reason for atherosclerosis development and subsequent CV events is deemed to be low-density lipoprotein cholesterol (LDL-C). Although less evident, other lipids are supposed to contribute to atherosclerosis development, especially in the absence of high LDL-C levels. Plasma triglycerides and TG-rich lipoproteins are emerging new determinants of atherosclerotic cardiovascular disease (ASCVD) risk, predisposing to atherogenesis and involving endothelial dysfunction. In this setting, a number of mechanisms result in lower levels of HDL-C, reduced reverse cholesterol transport (RCT), increased proportion of small, dense HDL and LDL particles with less anti-inflammatory and more pro-atherogenic effects. This specific lipid profile may directly contribute to cause or sustain abnormalities in glucose homeostasis and insulin secretion that characterize the pre-diabetic state. This complex cardiometabolic risk profile, which characterizes the metabolic syndrome, obesity, pre-diabetic and type-2 diabetic states, is considered to predict severe CV events independently of LDL-C levels, thus identifying patients with a “residual CV risk”. In these patients, further strategies may be required to adequately reduce this residual risk. Early identification and screening tools for atherogenic dyslipidemias, particularly in individuals at low to moderate CV risk, could guide interventions to improve primary prevention, including lifestyle modification or drug treatment. New therapeutic strategies based on molecular mechanisms underlying atherogenic dyslipidemias are needed for the treatment of the residual risk profiles. Among them, possible pharmacological targets considered to be relevant, including systemic inflammation and hypertriglyceridaemia, are emerging.

Dr. Chiara Caselli
Dr. Danilo Neglia
Guest Editors

Manuscript Submission Information

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Keywords

  • atherosclerotic cardiovascular disease (ASCVD)
  • dyslipidemia
  • CV residual risk
  • CV mechanisms
  • therapeutic approaches

Related Special Issue

Published Papers (7 papers)

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Research

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14 pages, 2075 KiB  
Article
Whole-Blood Transcriptional Profiles Enable Early Prediction of the Presence of Coronary Atherosclerosis and High-Risk Plaque Features at Coronary CT Angiography
by Daniele Andreini, Eleonora Melotti, Chiara Vavassori, Mattia Chiesa, Luca Piacentini, Edoardo Conte, Saima Mushtaq, Martina Manzoni, Eleonora Cipriani, Paolo M. Ravagnani, Antonio L. Bartorelli and Gualtiero I. Colombo
Biomedicines 2022, 10(6), 1309; https://doi.org/10.3390/biomedicines10061309 - 2 Jun 2022
Cited by 4 | Viewed by 2305
Abstract
Existing tools to estimate cardiovascular (CV) risk have sub-optimal predictive capacities. In this setting, non-invasive imaging techniques and omics biomarkers could improve risk-prediction models for CV events. This study aimed to identify gene expression patterns in whole blood that could differentiate patients with [...] Read more.
Existing tools to estimate cardiovascular (CV) risk have sub-optimal predictive capacities. In this setting, non-invasive imaging techniques and omics biomarkers could improve risk-prediction models for CV events. This study aimed to identify gene expression patterns in whole blood that could differentiate patients with severe coronary atherosclerosis from subjects with a complete absence of detectable coronary artery disease and to assess associations of gene expression patterns with plaque features in coronary CT angiography (CCTA). Patients undergoing CCTA for suspected coronary artery disease (CAD) were enrolled. Coronary stenosis was quantified and CCTA plaque features were assessed. The whole-blood transcriptome was analyzed with RNA sequencing. We detected highly significant differences in the circulating transcriptome between patients with high-degree coronary stenosis (≥70%) in the CCTA and subjects with an absence of coronary plaque. Notably, regression analysis revealed expression signatures associated with the Leaman score, the segment involved score, the segment stenosis score, and plaque volume with density <150 HU at CCTA. This pilot study shows that patients with significant coronary stenosis are characterized by whole-blood transcriptome profiles that may discriminate them from patients without CAD. Furthermore, our results suggest that whole-blood transcriptional profiles may predict plaque characteristics. Full article
(This article belongs to the Special Issue Atherosclerotic Cardiovascular Disease (ASCVD), Dyslipidemia, and CV Residual Risk: From Mechanisms to Therapeutic Approaches)
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16 pages, 3222 KiB  
Article
The Impact of RIPK1 Kinase Inhibition on Atherogenesis: A Genetic and a Pharmacological Approach
by Pauline Puylaert, Isabelle Coornaert, Cédric H. G. Neutel, Yves Dondelinger, Tom Delanghe, Mathieu J. M. Bertrand, Pieter-Jan Guns, Guido R. Y. De Meyer and Wim Martinet
Biomedicines 2022, 10(5), 1016; https://doi.org/10.3390/biomedicines10051016 - 28 Apr 2022
Cited by 3 | Viewed by 2173
Abstract
RIPK1 (receptor-interacting serine/threonine-protein kinase 1) enzymatic activity drives both apoptosis and necroptosis, a regulated form of necrosis. Because necroptosis is involved in necrotic core development in atherosclerotic plaques, we investigated the effects of a RIPK1S25D/S25D mutation, which prevents activation of RIPK1 kinase, [...] Read more.
RIPK1 (receptor-interacting serine/threonine-protein kinase 1) enzymatic activity drives both apoptosis and necroptosis, a regulated form of necrosis. Because necroptosis is involved in necrotic core development in atherosclerotic plaques, we investigated the effects of a RIPK1S25D/S25D mutation, which prevents activation of RIPK1 kinase, on atherogenesis in ApoE−/− mice. After 16 weeks of western-type diet (WD), atherosclerotic plaques from ApoE−/− RIPK1S25D/S25D mice were significantly larger compared to ApoE−/− RIPK1+/+ mice (167 ± 34 vs. 78 ± 18 × 103 µm2, p = 0.01). Cell numbers (350 ± 34 vs. 154 ± 33 nuclei) and deposition of glycosaminoglycans (Alcian blue: 31 ± 6 vs. 14 ± 4%, p = 0.023) were increased in plaques from ApoE−/− RIPK1S25D/S25D mice while macrophage content (Mac3: 2.3 ± 0.4 vs. 9.8 ± 2.4%, p = 0.012) was decreased. Plaque apoptosis was not different between both groups. In contrast, pharmacological inhibition of RIPK1 kinase with GSK’547 (10 mg/kg BW/day) in ApoE−/− Fbn1C1039G+/− mice, a model of advanced atherosclerosis, did not alter plaque size after 20 weeks WD, but induced apoptosis (TUNEL: 136 ± 20 vs. 62 ± 9 cells/mm2, p = 0.004). In conclusion, inhibition of RIPK1 kinase activity accelerated plaque progression in ApoE−/− RIPK1S25D/S25D mice and induced apoptosis in GSK’547-treated ApoE−/− Fbn1C1039G+/− mice. Thus, without directly comparing the genetic and pharmacological studies, it can be concluded that targeting RIPK1 kinase activity does not limit atherogenesis. Full article
(This article belongs to the Special Issue Atherosclerotic Cardiovascular Disease (ASCVD), Dyslipidemia, and CV Residual Risk: From Mechanisms to Therapeutic Approaches)
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11 pages, 542 KiB  
Article
Lipoprotein(a) Serum Levels Predict Pulse Wave Velocity in Subjects in Primary Prevention for Cardiovascular Disease with Large Apo(a) Isoforms: Data from the Brisighella Heart Study
by Arrigo F. G. Cicero, Federica Fogacci, Giuseppe Derosa, Angela D’Angelo, Fulvio Ventura, Elisabetta Rizzoli, Sergio D’Addato, Claudio Borghi and on behalf of the Brisighella Heart Study Group
Biomedicines 2022, 10(3), 656; https://doi.org/10.3390/biomedicines10030656 - 11 Mar 2022
Cited by 5 | Viewed by 2221
Abstract
In the last decades, high serum levels of lipoprotein(a) (Lp(a)) have been associated with increased cardiovascular disease (CVD) risk, in particular among individuals with smaller apolipoprotein(a) (apo(a)) isoforms than those with larger sizes. The aim of our analysis was to evaluate whether Lp(a) [...] Read more.
In the last decades, high serum levels of lipoprotein(a) (Lp(a)) have been associated with increased cardiovascular disease (CVD) risk, in particular among individuals with smaller apolipoprotein(a) (apo(a)) isoforms than those with larger sizes. The aim of our analysis was to evaluate whether Lp(a) levels could predict early vascular aging, and whether smaller apo(a) isoforms had a predictive value for vascular aging different than larger apo(a) isoforms in a cohort of subjects free from CVD. We considered the data of a subset of Brisighella Heart Study (BHS) participants free from CVD (462 men and 516 women) who were clinically evaluated during the 2012 BHS population survey. Predictors of arterial stiffness, measured as carotid-femoral pulse wave velocity (cfPWV) were estimated by the application of a step-wise linear regression model. In our cohort, there were 511 subjects with small apo(a) size and 467 subjects with large apo(a) isoforms. Subjects with larger apo(a) isoform sizes had significantly lower serum levels of Lp(a). In the BHS subpopulation sample, cfPWV was predicted by age, systolic blood pressure (SBP), serum levels of high-density lipoprotein cholesterol (HDL-C), triglycerides (TG) and sex, higher HDL-C serum levels and female sex associated with lower values of cfPWV. In subjects with smaller apo(a) isoform sizes, predictors of cfPWV were age, SBP, sex and serum levels of HDL-C, being higher HDL-C serum levels and female sex associated to lower values of cfPWV. In subjects with larger apo(a) isoform sizes, cfPWV was predicted by age, SBP, serum levels of Lp(a) and sex, with female sex associated with lower values of cfPWV. In our subpopulation sample, Lp(a) did not predict cfPWV. However, in subjects with large apo(a) isoform sizes, Lp(a) was a significant predictor of arterial stiffness. Full article
(This article belongs to the Special Issue Atherosclerotic Cardiovascular Disease (ASCVD), Dyslipidemia, and CV Residual Risk: From Mechanisms to Therapeutic Approaches)
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13 pages, 918 KiB  
Article
Trends in Prediabetes and Non-Alcoholic Fatty Liver Disease Associated with Abdominal Obesity among Korean Children and Adolescents: Based on the Korea National Health and Nutrition Examination Survey between 2009 and 2018
by Kyungchul Song, Goeun Park, Hye Sun Lee, Myeongseob Lee, Hae In Lee, Jungmin Ahn, Eunbyoul Lee, Han Saem Choi, Junghwan Suh, Ahreum Kwon, Ho-Seong Kim and Hyun Wook Chae
Biomedicines 2022, 10(3), 584; https://doi.org/10.3390/biomedicines10030584 - 2 Mar 2022
Cited by 14 | Viewed by 2605
Abstract
Investigations on the trends of prediabetes and non-alcoholic fatty liver disease (NAFLD) among children are scarce. We aimed to analyze the trends of prediabetes and NAFLD, as well as their association, among Korean children and adolescents from 2009 to 2018. This study investigated [...] Read more.
Investigations on the trends of prediabetes and non-alcoholic fatty liver disease (NAFLD) among children are scarce. We aimed to analyze the trends of prediabetes and NAFLD, as well as their association, among Korean children and adolescents from 2009 to 2018. This study investigated the prevalence of prediabetes, NAFLD, and abdominal obesity among 6327 children and adolescents aged 10–18 years according to age, sex, and body mass index (BMI) using a nationally representative survey. The prevalence of prediabetes, NAFLD, and abdominal obesity increased from 5.14%, 8.17%, and 5.97% respectively, in 2009 to 10.46%, 12.05%, and 10.51% respectively, in 2018. In age-specific analyses, an adverse trend in NAFLD was significant only in participants aged 16–18 years while the prevalence of prediabetes worsened significantly in all age groups. In BMI-specific analyses, the prevalence of prediabetes and NAFLD increased significantly only in participants with normal BMI. In logistic regression analysis, the odds ratio of prediabetes for NAFLD was 1.85 and those of abdominal obesity for prediabetes and NAFLD was 1.85 and 9.34, respectively. Our results demonstrated that the prevalence of prediabetes and NAFLD was increasing in association with abdominal obesity in Korean children and adolescents. Full article
(This article belongs to the Special Issue Atherosclerotic Cardiovascular Disease (ASCVD), Dyslipidemia, and CV Residual Risk: From Mechanisms to Therapeutic Approaches)
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14 pages, 473 KiB  
Article
Postprandial Hyperlipidemia: Association with Inflammation and Subclinical Atherosclerosis in Patients with Rheumatoid Arthritis
by Natalia Mena-Vázquez, Rocío Redondo-Rodríguez, José Rioja, Francisco Gabriel Jimenez-Nuñez, Sara Manrique-Arija, Jose Manuel Lisbona-Montañez, Laura Cano-García, Marta Rojas-Gimenez, Inmaculada Ureña, Pedro Valdivielso and Antonio Fernández-Nebro
Biomedicines 2022, 10(1), 133; https://doi.org/10.3390/biomedicines10010133 - 8 Jan 2022
Cited by 7 | Viewed by 1856
Abstract
Objective: To describe postprandial lipidemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis and inflammatory activity. Methods: Observational study of 80 cases of RA and 80 sex- and age-matched controls. We excluded individuals with dyslipidemia. Postprandial hyperlipidemia [...] Read more.
Objective: To describe postprandial lipidemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis and inflammatory activity. Methods: Observational study of 80 cases of RA and 80 sex- and age-matched controls. We excluded individuals with dyslipidemia. Postprandial hyperlipidemia (PPHL) was defined as postprandial triglycerides >220 mg/dL and/or postprandial ApoB48 levels >75th percentile (>p75). Plasma lipids, cholesterol, triglycerides, ApoB48, and total ApoB were evaluated at baseline and after a meal. Other variables analyzed included subclinical atherosclerosis (defined as presence of carotid atheromatous plaque), inflammatory activity (disease activity score (DAS28-ESR)), cytokines, apolipoproteins, and physical activity. A multivariate analysis was performed to identify factors associated with PPHL in patients with RA. Results: A total of 75 patients with RA and 67 healthy controls fulfilled the inclusion criteria. PPHL was more frequent in patients with RA than controls (No. (%), 29 (38.70) vs. 15 (22.40); p = 0.036), as was subclinical atherosclerosis (No. (%), 22 (30.10) vs. 10 (14.90); p = 0.032). PPHL in patients with RA was associated with subclinical atherosclerosis (OR (95% CI) 4.69 (1.09–12.11); p = 0.037), TNF-α (OR (95% CI) 2.00 (1.00–3.98); p = 0.048), high-sensitivity C-reactive protein (OR (95% CI) 1.10 (1.01–1.19); p = 0.027), and baseline triglycerides (OR (95% CI) 1.02 (1.00–1.04); p = 0.049). Conclusion: PPHL was more frequent in patients with RA than in controls. PPHL in patients with RA was associated with inflammation and subclinical atherosclerosis. Full article
(This article belongs to the Special Issue Atherosclerotic Cardiovascular Disease (ASCVD), Dyslipidemia, and CV Residual Risk: From Mechanisms to Therapeutic Approaches)
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Review

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17 pages, 526 KiB  
Review
Cardiovascular Risk in Childhood Cancer Survivors
by Francesca Mainieri, Cosimo Giannini and Francesco Chiarelli
Biomedicines 2022, 10(12), 3098; https://doi.org/10.3390/biomedicines10123098 - 1 Dec 2022
Cited by 3 | Viewed by 1651
Abstract
Cancer is a prominent cause of death worldwide in the pediatric population. Since childhood cancer is not possible to prevent, it is essential to focus on a prompt and correct diagnosis followed by effective, evidence-based therapy with individualized supportive care. Given the enhancement [...] Read more.
Cancer is a prominent cause of death worldwide in the pediatric population. Since childhood cancer is not possible to prevent, it is essential to focus on a prompt and correct diagnosis followed by effective, evidence-based therapy with individualized supportive care. Given the enhancement of childhood cancer management over the past decades, survival rate has significantly improved, thus leading to the progression of several late effects, including metabolic derangements. These metabolic imbalances are associated with the underlying disease and the cancer treatments. As a result, the metabolic state may contribute to a high risk of cardiovascular morbidity and premature mortality among childhood cancer survivors. This review aims to summarize the potential pathophysiological mechanisms linked to the risk of diabetes and metabolic syndrome and screening recommendations. Further investigations are needed to clarify the underlying mechanisms of such metabolic abnormalities and to improve long-term cardiometabolic survival among these patients. Full article
(This article belongs to the Special Issue Atherosclerotic Cardiovascular Disease (ASCVD), Dyslipidemia, and CV Residual Risk: From Mechanisms to Therapeutic Approaches)
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15 pages, 548 KiB  
Review
Recent Advances on Familial Hypercholesterolemia in Children and Adolescents
by Francesca Mainieri, Veronica Maria Tagi and Francesco Chiarelli
Biomedicines 2022, 10(5), 1043; https://doi.org/10.3390/biomedicines10051043 - 30 Apr 2022
Cited by 10 | Viewed by 4336
Abstract
Familial hypercholesterolemia is a common autosomal hereditary disorder characterized by elevated concentrations of low-density lipoprotein cholesterol and the development of premature atherosclerosis and cardiovascular disease. Early diagnosis, as well as prompt and aggressive treatment, are fundamental steps to prevent cardiovascular complications and a [...] Read more.
Familial hypercholesterolemia is a common autosomal hereditary disorder characterized by elevated concentrations of low-density lipoprotein cholesterol and the development of premature atherosclerosis and cardiovascular disease. Early diagnosis, as well as prompt and aggressive treatment, are fundamental steps to prevent cardiovascular complications and a high rate of premature mortality in children and adolescents. Clinics and genetics are the two main aspects on which diagnosis is based. Widespread screening programs are a respectable option for the early detection of familial hypercholesterolemia. Different types of screening have been proposed so far; however, the optimal screening program has not yet been found. The treatment approach for both heterozygous and homozygous familial hypercholesterolemia in the pediatric population is multidisciplinary, including lifestyle modifications, standard lipid-lowering medications, and novel pharmacological agents. The latter show promising results, especially for patients who experience intolerance to other treatment or present with more severe conditions. Our purpose is to focus on the importance of the early detection of familial hypercholesterolemia, and to highlight the best therapeutic strategies, including the recent approaches based on current clinical evidence, that need to be adopted from the earliest stages of life. Full article
(This article belongs to the Special Issue Atherosclerotic Cardiovascular Disease (ASCVD), Dyslipidemia, and CV Residual Risk: From Mechanisms to Therapeutic Approaches)
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