Pub Date : 2025-10-18DOI: 10.1016/j.arteri.2025.500870
Rosa Fernández-Olmo, Jesús Lara Mariscal, Ana García Ruano, Alberto Cordero, Juan Manuel Castillo Casas, Diego Franco
Lp(a) is a cardiovascular risk factor influenced by the LPA gene and apo(a) isoforms. Their relationship is not always linear and there are discordant phenotypes, for this reason in our work we evaluated the association between apo(a) isoforms and Lp(a) levels in patients with acute coronary syndrome (ACS). To this end, 43 patients with ACS and Lp(a) >50mg/dL were studied. The isoforms were characterized in 12bands by Western blotting. The association between bands and Lp(a) concentrations was evaluated by statistical analysis. It was observed that the intermediate molecular weight bands (b5-b8) were the most frequent, with band 8 predominating. No significant association was found between isoform size and Lp(a) levels (P>.05). We conclude that in this cohort no correlation was observed between apo(a) and Lp(a) isoforms. Other genetic or regulatory mechanisms could explain the observed variability, supporting the need for larger studies.
{"title":"Relationship between apolipoprotein(a) isoforms and lipoprotein(a) levels in patients with acute coronary syndrome.","authors":"Rosa Fernández-Olmo, Jesús Lara Mariscal, Ana García Ruano, Alberto Cordero, Juan Manuel Castillo Casas, Diego Franco","doi":"10.1016/j.arteri.2025.500870","DOIUrl":"https://doi.org/10.1016/j.arteri.2025.500870","url":null,"abstract":"<p><p>Lp(a) is a cardiovascular risk factor influenced by the LPA gene and apo(a) isoforms. Their relationship is not always linear and there are discordant phenotypes, for this reason in our work we evaluated the association between apo(a) isoforms and Lp(a) levels in patients with acute coronary syndrome (ACS). To this end, 43 patients with ACS and Lp(a) >50mg/dL were studied. The isoforms were characterized in 12bands by Western blotting. The association between bands and Lp(a) concentrations was evaluated by statistical analysis. It was observed that the intermediate molecular weight bands (b5-b8) were the most frequent, with band 8 predominating. No significant association was found between isoform size and Lp(a) levels (P>.05). We conclude that in this cohort no correlation was observed between apo(a) and Lp(a) isoforms. Other genetic or regulatory mechanisms could explain the observed variability, supporting the need for larger studies.</p>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":" ","pages":"500870"},"PeriodicalIF":1.9,"publicationDate":"2025-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145330337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-10-10DOI: 10.1016/j.arteri.2025.500830
Jose María Mostaza, Miquel Camafort Babkowksi, Soraya Sotto Rodriguez, Cristina Vehi Gasol, Juan Carlos Yáñez Wonenburguer, Miguel Chopo Alcubilla, Carlos Escobar, Maria Luisa Fernández Bujia, Fernando Gallo Trébol, Mar Gracia, Marta Martín Millán, Guillermo Pinillos, Juan Pedro Justel Pérez
Background: Arterial hypertension and dyslipidemia are two of the most relevant modifiable cardiovascular risk factors (CVRFs), and they often coexist. No recent studies specifically evaluating the achievement of LDL-C and blood pressure (BP) targets in hypertensive patients with dyslipidemia are available in Spain.
Methods: The SNAPSHOT study was a multicenter, cross-sectional observational study conducted in cardiology and internal medicine (IM) departments/clinics and primary care (PC) centers in Spain. The study enrolled consecutive adult patients (≥18 years of age) diagnosed with both hypertension and dyslipidemia. The primary endpoint was the percentage of patients achieving both the LDL-C goals recommended by the 2021 European Society of Cardiology/European Atherosclerosis Society (ESC/EAS) guidelines and the BP targets established in the 2018 ESC/European Society of Hypertension (ESH) guidelines. Cardiovascular (CV) risk (very high, high, low-to-moderate) was centrally assessed according to the updated Systematic Coronary Risk Evaluation (SCORE2) and SCORE2-Older Person (OP) algorithms recommended in the 2021 ESC guidelines.
Results: Between December 2021 and April 2022, a total of 443 evaluable patients were enrolled (males: 54%; ≥65 years of age: 66.1%; obesity: 37.4%; diabetes mellitus: 37.3%; coronary artery disease [CAD]: 25.7%). Out of the 388 patients in whom CV risk could be assessed, 34.3% and 56.4% were considered as having high and very high risk, respectively. Overall, 24% of the patients had achieved their risk-based LDL-C goals (21.8% of the patients at high-CV risk and 25.1% of those at very high risk), and 30.3% of the patients had reached the recommended BP targets (27.1% of the patients at high risk and 36.1% of those at very high risk). A total of 8.8% of the patients had achieved both the LDL-C and BP targets. Overall, 51.4% of the patients with concurrent diabetes had achieved glycemic control (HbA1c <7%), while only 9.4% of the diabetic patients had reached simultaneous control of LDL-C, BP and HbA1C targets (7.8% of the patients at high risk and 10.4% of those at very high risk).
Conclusion: The attainment of LDL-C and BP goals is still suboptimal in patients with dyslipidemia and hypertension in the real-world setting in Spain, with approximately 75% of the patients at very high risk of cardiovascular disease failing to reach their risk-based LDL-C and BP targets. Additionally, the rate corresponding to simultaneous control of LDL-C, BP and HbA1c is likewise very low. The present study thus highlights the current challenge of controlling multiple CVRFs that significantly contribute to atherosclerotic cardiovascular disease events and mortality and emphasizes the need for more effective management of CVRFs in the real-world setting.
{"title":"Real-world characterization of clinical management and achievement of the recommended risk-based low-density lipoprotein cholesterol and blood pressure goals in patients with arterial hypertension and dyslipidemia. The SNAPSHOT study.","authors":"Jose María Mostaza, Miquel Camafort Babkowksi, Soraya Sotto Rodriguez, Cristina Vehi Gasol, Juan Carlos Yáñez Wonenburguer, Miguel Chopo Alcubilla, Carlos Escobar, Maria Luisa Fernández Bujia, Fernando Gallo Trébol, Mar Gracia, Marta Martín Millán, Guillermo Pinillos, Juan Pedro Justel Pérez","doi":"10.1016/j.arteri.2025.500830","DOIUrl":"https://doi.org/10.1016/j.arteri.2025.500830","url":null,"abstract":"<p><strong>Background: </strong>Arterial hypertension and dyslipidemia are two of the most relevant modifiable cardiovascular risk factors (CVRFs), and they often coexist. No recent studies specifically evaluating the achievement of LDL-C and blood pressure (BP) targets in hypertensive patients with dyslipidemia are available in Spain.</p><p><strong>Methods: </strong>The SNAPSHOT study was a multicenter, cross-sectional observational study conducted in cardiology and internal medicine (IM) departments/clinics and primary care (PC) centers in Spain. The study enrolled consecutive adult patients (≥18 years of age) diagnosed with both hypertension and dyslipidemia. The primary endpoint was the percentage of patients achieving both the LDL-C goals recommended by the 2021 European Society of Cardiology/European Atherosclerosis Society (ESC/EAS) guidelines and the BP targets established in the 2018 ESC/European Society of Hypertension (ESH) guidelines. Cardiovascular (CV) risk (very high, high, low-to-moderate) was centrally assessed according to the updated Systematic Coronary Risk Evaluation (SCORE2) and SCORE2-Older Person (OP) algorithms recommended in the 2021 ESC guidelines.</p><p><strong>Results: </strong>Between December 2021 and April 2022, a total of 443 evaluable patients were enrolled (males: 54%; ≥65 years of age: 66.1%; obesity: 37.4%; diabetes mellitus: 37.3%; coronary artery disease [CAD]: 25.7%). Out of the 388 patients in whom CV risk could be assessed, 34.3% and 56.4% were considered as having high and very high risk, respectively. Overall, 24% of the patients had achieved their risk-based LDL-C goals (21.8% of the patients at high-CV risk and 25.1% of those at very high risk), and 30.3% of the patients had reached the recommended BP targets (27.1% of the patients at high risk and 36.1% of those at very high risk). A total of 8.8% of the patients had achieved both the LDL-C and BP targets. Overall, 51.4% of the patients with concurrent diabetes had achieved glycemic control (HbA1c <7%), while only 9.4% of the diabetic patients had reached simultaneous control of LDL-C, BP and HbA1C targets (7.8% of the patients at high risk and 10.4% of those at very high risk).</p><p><strong>Conclusion: </strong>The attainment of LDL-C and BP goals is still suboptimal in patients with dyslipidemia and hypertension in the real-world setting in Spain, with approximately 75% of the patients at very high risk of cardiovascular disease failing to reach their risk-based LDL-C and BP targets. Additionally, the rate corresponding to simultaneous control of LDL-C, BP and HbA1c is likewise very low. The present study thus highlights the current challenge of controlling multiple CVRFs that significantly contribute to atherosclerotic cardiovascular disease events and mortality and emphasizes the need for more effective management of CVRFs in the real-world setting.</p>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":" ","pages":"500830"},"PeriodicalIF":1.9,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145276227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-23DOI: 10.1016/j.arteri.2025.500856
Lídia Puertas-Umbert, Judith Alonso, Laia Blanco-Casoliva, Roger Bentanachs, Lluis Asmarats, Gemma Arderiu, José Martínez-González, Cristina Rodríguez
Background: Inflammation, oxidative stress, and vascular remodeling play a key role in the pathophysiology of abdominal aortic aneurysm (AAA), a severe vascular disease. Previously, we had demonstrated an increase in the phosphorylated form of ATP citrate lyase (p-ACLY) in AAA and that bempedoic acid (BemA), a specific inhibitor of this enzyme, attenuates aneurysm formation in an experimental model. In this study, we further investigated the mechanisms mediating the beneficial effect of BemA.
Methods: AAA was induced by angiotensin II (AngII) infusion in ApoE-/- mice, and aneurysm formation was assessed by ultrasonography. Histological analyses (hematoxylin-eosin, orcein staining) and immunohistochemistry were performed. T cell subpopulations in the spleen were characterized by flow cytometry, and superoxide anion production in the vascular wall was evaluated by dihydroethidium (DHE) staining. The expression of enzymes involved in the control of oxidative stress was analyzed by real-time RT-PCR.
Results: Endpoint ultrasonography analyses in AngII-infused ApoE-/- mice confirmed that BemA limits aneurysm formation. Indeed, BemA administration in AngII-infused mice significantly increased both the percentage of animals that did not develop aneurysms and those free of aortic rupture, without altering the pressor effect of AngII. Histologically, BemA preserved the integrity of the aortic wall and reduced the proportion of animals presenting intramural thrombi, with a decrease in hematoma area. Immunohistochemical analyses showed increased levels of p-ACLY in the inflammatory infiltrate of human and murine aneurysmal lesions, as well as BemA's capacity to attenuate the AngII-induced increase in CD3+ T lymphocyte content in the vascular wall. Additionally, analysis of splenic CD8+ T cell subpopulations revealed no significant changes in either AngII-infused animals or those treated with BemA. Finally, ACLY activity inhibition decreased reactive oxygen species production without modifying the expression of key isoforms of the NADPH oxidase (Nox2, Nox4) or superoxide dismutase (Sod1, Sod2) families.
Conclusions: Taken together, these findings position ACLY as a relevant therapeutic target in AAA and BemA as a drug with potential protective effects against the development and progression of this vascular disease.
{"title":"Bempedoic acid attenuates vascular inflammation and oxidative stress in a preclinical model of abdominal aortic aneurysm.","authors":"Lídia Puertas-Umbert, Judith Alonso, Laia Blanco-Casoliva, Roger Bentanachs, Lluis Asmarats, Gemma Arderiu, José Martínez-González, Cristina Rodríguez","doi":"10.1016/j.arteri.2025.500856","DOIUrl":"https://doi.org/10.1016/j.arteri.2025.500856","url":null,"abstract":"<p><strong>Background: </strong>Inflammation, oxidative stress, and vascular remodeling play a key role in the pathophysiology of abdominal aortic aneurysm (AAA), a severe vascular disease. Previously, we had demonstrated an increase in the phosphorylated form of ATP citrate lyase (p-ACLY) in AAA and that bempedoic acid (BemA), a specific inhibitor of this enzyme, attenuates aneurysm formation in an experimental model. In this study, we further investigated the mechanisms mediating the beneficial effect of BemA.</p><p><strong>Methods: </strong>AAA was induced by angiotensin II (AngII) infusion in ApoE<sup>-/-</sup> mice, and aneurysm formation was assessed by ultrasonography. Histological analyses (hematoxylin-eosin, orcein staining) and immunohistochemistry were performed. T cell subpopulations in the spleen were characterized by flow cytometry, and superoxide anion production in the vascular wall was evaluated by dihydroethidium (DHE) staining. The expression of enzymes involved in the control of oxidative stress was analyzed by real-time RT-PCR.</p><p><strong>Results: </strong>Endpoint ultrasonography analyses in AngII-infused ApoE<sup>-/-</sup> mice confirmed that BemA limits aneurysm formation. Indeed, BemA administration in AngII-infused mice significantly increased both the percentage of animals that did not develop aneurysms and those free of aortic rupture, without altering the pressor effect of AngII. Histologically, BemA preserved the integrity of the aortic wall and reduced the proportion of animals presenting intramural thrombi, with a decrease in hematoma area. Immunohistochemical analyses showed increased levels of p-ACLY in the inflammatory infiltrate of human and murine aneurysmal lesions, as well as BemA's capacity to attenuate the AngII-induced increase in CD3<sup>+</sup> T lymphocyte content in the vascular wall. Additionally, analysis of splenic CD8<sup>+</sup> T cell subpopulations revealed no significant changes in either AngII-infused animals or those treated with BemA. Finally, ACLY activity inhibition decreased reactive oxygen species production without modifying the expression of key isoforms of the NADPH oxidase (Nox2, Nox4) or superoxide dismutase (Sod1, Sod2) families.</p><p><strong>Conclusions: </strong>Taken together, these findings position ACLY as a relevant therapeutic target in AAA and BemA as a drug with potential protective effects against the development and progression of this vascular disease.</p>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":" ","pages":"500856"},"PeriodicalIF":1.9,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145138808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-09DOI: 10.1016/j.arteri.2025.500845
Núria Puig, Eduardo Garcia, Montserrat Moncunill, Aleyda Benítez-Amaro, Olga Bautista, Silvia Rodas, Pol Camps-Renom, Jose Luis Sanchez Quesada, Vicenta Llorente-Cortés, Sonia Benitez
Background: Electronegative LDL (LDL(-)) is a circulant modified LDL with inflammatory properties whose proportion raises in ischemic events. The soluble form of LDL receptor related protein 1 (sLRP1) increases in blood in pathological situations, including ischemic stroke. We aimed to evaluate the effect of LDL(-) on sLRP1 release from monocytes and macrophages.
Methods: LDL(-) and native LDL were isolated from total LDL by anion-exchange chromatography. Both fractions were incubated with THP1 monocytes (overexpressing or not CD14) and derived macrophages. Additional conditions were assayed in macrophages: (1) incubation with aggregated LDLs; (2) LDL fractions in the presence/absence of marimastat, a metalloproteinase inhibitor; and (3) presence/absence of HDL from healthy controls and ischemic stroke patients. After incubation, supernatants and cells were collected for sLRP1 determination by ELISA, and for LRP1 expression by real-time PCR, respectively.
Results: LDLs promoted sLRP1 release in monocytes and derived macrophages, regardless of CD14 overexpression. The effect was greater for LDL(-), inducing 6-fold and 3-fold higher sLRP1 release in monocytes and macrophages than native LDL. In macrophages, aggregated LDLs induced greater sLRP1 release than their non-aggregated counterparts. The LDL(-)-induced sLRP1 was not induced by promoting LRP1 expression or cytotoxicity. Otherwise, inhibition of metalloprotease activity and addition of HDL reduced sLRP1 release. However, HDL from ischemic stroke patients showed an impaired ability to decrease sLRP1 secretion.
Conclusions: LDL(-) potently induces sLRP1 in monocytes and macrophages. This action is not mediated by increased LRP1 expression, but may be related to the shedding of the membrane form in macrophages.
{"title":"Electronegative LDL strongly induces LRP1 release from human monocytes and macrophages.","authors":"Núria Puig, Eduardo Garcia, Montserrat Moncunill, Aleyda Benítez-Amaro, Olga Bautista, Silvia Rodas, Pol Camps-Renom, Jose Luis Sanchez Quesada, Vicenta Llorente-Cortés, Sonia Benitez","doi":"10.1016/j.arteri.2025.500845","DOIUrl":"https://doi.org/10.1016/j.arteri.2025.500845","url":null,"abstract":"<p><strong>Background: </strong>Electronegative LDL (LDL(-)) is a circulant modified LDL with inflammatory properties whose proportion raises in ischemic events. The soluble form of LDL receptor related protein 1 (sLRP1) increases in blood in pathological situations, including ischemic stroke. We aimed to evaluate the effect of LDL(-) on sLRP1 release from monocytes and macrophages.</p><p><strong>Methods: </strong>LDL(-) and native LDL were isolated from total LDL by anion-exchange chromatography. Both fractions were incubated with THP1 monocytes (overexpressing or not CD14) and derived macrophages. Additional conditions were assayed in macrophages: (1) incubation with aggregated LDLs; (2) LDL fractions in the presence/absence of marimastat, a metalloproteinase inhibitor; and (3) presence/absence of HDL from healthy controls and ischemic stroke patients. After incubation, supernatants and cells were collected for sLRP1 determination by ELISA, and for LRP1 expression by real-time PCR, respectively.</p><p><strong>Results: </strong>LDLs promoted sLRP1 release in monocytes and derived macrophages, regardless of CD14 overexpression. The effect was greater for LDL(-), inducing 6-fold and 3-fold higher sLRP1 release in monocytes and macrophages than native LDL. In macrophages, aggregated LDLs induced greater sLRP1 release than their non-aggregated counterparts. The LDL(-)-induced sLRP1 was not induced by promoting LRP1 expression or cytotoxicity. Otherwise, inhibition of metalloprotease activity and addition of HDL reduced sLRP1 release. However, HDL from ischemic stroke patients showed an impaired ability to decrease sLRP1 secretion.</p><p><strong>Conclusions: </strong>LDL(-) potently induces sLRP1 in monocytes and macrophages. This action is not mediated by increased LRP1 expression, but may be related to the shedding of the membrane form in macrophages.</p>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":" ","pages":"500845"},"PeriodicalIF":1.9,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145034398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1016/j.arteri.2024.500755
Antón González-Guerrero , Eugenia Navarrete-Rouco , David Benaiges , Eva Giralt-Steinhauer , Lidia Marcos , Anna Oliveras , Lluis Recasens , Juan Pedro-Botet
Objective
To confirm the effectiveness and safety of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors in daily clinical practice.
Methods
Retrospective observational study of patients from hospital registry of PCSK9 inhibitor treatment with a follow-up ≥ 6 months. The lipid-lowering effect and safety were evaluated.
Results
Of the 193 patients included in the study, 168 (87%) had cardiovascular disease, and 54 (28%) had familial hypercholesterolemia; 85 (44%) were intolerant to statins/ezetimibe. No differences between alirocumab and evolocumab groups regarding the rate of LDL-C reduction ≥ 50% (82.8% vs. 83.1%), achievement of the therapeutic target (60.9% vs. 65.5%), or complete remission (60.2% vs. 58.5%) were found. An erythema at the injection site in one patient treated with alirocumab and urticaria in one patient treated with evolocumab were recorded. According to the logistic regression analysis, complete remission of LDL-C in subjects treated with PCSK9 inhibitors was positively associated with increased age (OR: 1.045; 95%CI: 1.0-1.092; P=.049) and active smoking (OR: 4.562; 95%CI: 1.434-14.515; P=.010), and negatively associated with female gender (OR: 0.403; 95%CI: 0.171-0.949; P=.038), baseline LDL-C levels (OR: 0.969; 95%CI: 0.957-0.981; P<.001)and statin/ezetimibe intolerance (OR: 0.403; 95%CI: 0.176-0.925; P=.041).
Conclusion
This real-world practice study has confirmed that PCSK9 inhibitors are effective, safe and well tolerated, with lipid-lowering effects comparable to those described in randomized controlled trials, regardless of the monoclonal antibody used.
目的：在临床实践中验证枯草素/可欣9型蛋白转化酶（PCSK9）抑制剂的有效性和安全性。方法：回顾性观察研究医院登记的PCSK9抑制剂治疗患者，随访≥6个月。评价其降脂效果及安全性。结果：纳入研究的193例患者中，168例（87%）患有心血管疾病，54例（28%）患有家族性高胆固醇血症；85例（44%）对他汀类药物/依折麦布不耐受。alirocumab组和evolocumab组在LDL-C降低率≥50% （82.8% vs. 83.1%）、达到治疗目标（60.9% vs. 65.5%）或完全缓解（60.2% vs. 58.5%）方面无差异。一名接受alirocumab治疗的患者在注射部位出现红斑，一名接受evolocumab治疗的患者出现荨麻疹。根据logistic回归分析，接受PCSK9抑制剂治疗的受试者LDL-C完全缓解与年龄增加呈正相关(OR: 1.045；95%置信区间:1.0—-1.092;P= 0.049)和主动吸烟(OR: 4.562；95%置信区间:1.434—-14.515;P= 0.010)，且与女性性别呈负相关(OR: 0.403；95%置信区间:0.171—-0.949;P= 0.038)，基线LDL-C水平(OR: 0.969；95%置信区间:0.957—-0.981;结论：这项现实世界的实践研究证实，PCSK9抑制剂是有效、安全且耐受性良好的，无论使用何种单克隆抗体，其降脂效果与随机对照试验相当。
{"title":"Eficacia y seguridad de los inhibidores de la PCSK9 en la vida real","authors":"Antón González-Guerrero , Eugenia Navarrete-Rouco , David Benaiges , Eva Giralt-Steinhauer , Lidia Marcos , Anna Oliveras , Lluis Recasens , Juan Pedro-Botet","doi":"10.1016/j.arteri.2024.500755","DOIUrl":"10.1016/j.arteri.2024.500755","url":null,"abstract":"<div><h3>Objective</h3><div>To confirm the effectiveness and safety of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors in daily clinical practice.</div></div><div><h3>Methods</h3><div>Retrospective observational study of patients from hospital registry of PCSK9 inhibitor treatment with a follow-up ≥ 6 months. The lipid-lowering effect and safety were evaluated.</div></div><div><h3>Results</h3><div>Of the 193 patients included in the study, 168 (87%) had cardiovascular disease, and 54 (28%) had familial hypercholesterolemia; 85 (44%) were intolerant to statins/ezetimibe. No differences between alirocumab and evolocumab groups regarding the rate of LDL-C reduction ≥ 50% (82.8% vs. 83.1%), achievement of the therapeutic target (60.9% vs. 65.5%), or complete remission (60.2% vs. 58.5%) were found. An erythema at the injection site in one patient treated with alirocumab and urticaria in one patient treated with evolocumab were recorded. According to the logistic regression analysis, complete remission of LDL-C in subjects treated with PCSK9 inhibitors was positively associated with increased age (OR: 1.045; 95%CI: 1.0-1.092; <em>P</em>=.049) and active smoking (OR: 4.562; 95%CI: 1.434-14.515; <em>P</em>=.010), and negatively associated with female gender (OR: 0.403; 95%CI: 0.171-0.949; <em>P</em>=.038), baseline LDL-C levels (OR: 0.969; 95%CI: 0.957-0.981; <em>P</em><.001)and statin/ezetimibe intolerance (OR: 0.403; 95%CI: 0.176-0.925; <em>P</em>=.041).</div></div><div><h3>Conclusion</h3><div>This real-world practice study has confirmed that PCSK9 inhibitors are effective, safe and well tolerated, with lipid-lowering effects comparable to those described in randomized controlled trials, regardless of the monoclonal antibody used.</div></div>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":"37 5","pages":"Article 500755"},"PeriodicalIF":1.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143048217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1016/j.arteri.2024.500756
Pedro Luis Rodríguez García , Juan José Pérez Soto , Eliseo García Cantó , Pedro Javier Tarraga Marcos , Pedro Juan Tárraga López
Background
Physical-sports habits in adulthood constitute one of the predictors of physical, psychological and social health within healthy lifestyles.
Methods
The Acquired Healthy Lifestyle Assessment Scale was applied to a sample of 788 subjects between the ages of 22 and 72 and the dimension that makes up physical-sports practice habits was analyzed.
Results
74.4% of adults have habits of physical-sports practice that are not healthy or unhealthy, 18.8% tend towards health and only 6.9% are healthy. Pearson's 2 tests show a significant association between men and healthy habits, without observing changes associated with the age variable. The t-Student and one-factor ANOVA tests confirm the relationship between the level of health and physical-sports practice habits depending on sex and age.
Conclusions
It is necessary to promote preventive programs to increase participation in the practice of physical and sports exercise in the adult population that has unhealthy or unhealthy levels of lifestyle.
{"title":"Habit of physical-sports practice and the healthy lifestyle among Spanish adults from 22 to 72 years of age","authors":"Pedro Luis Rodríguez García , Juan José Pérez Soto , Eliseo García Cantó , Pedro Javier Tarraga Marcos , Pedro Juan Tárraga López","doi":"10.1016/j.arteri.2024.500756","DOIUrl":"10.1016/j.arteri.2024.500756","url":null,"abstract":"<div><h3>Background</h3><div>Physical-sports habits in adulthood constitute one of the predictors of physical, psychological and social health within healthy lifestyles.</div></div><div><h3>Methods</h3><div>The Acquired Healthy Lifestyle Assessment Scale was applied to a sample of 788 subjects between the ages of 22 and 72 and the dimension that makes up physical-sports practice habits was analyzed.</div></div><div><h3>Results</h3><div>74.4% of adults have habits of physical-sports practice that are not healthy or unhealthy, 18.8% tend towards health and only 6.9% are healthy. Pearson's 2 tests show a significant association between men and healthy habits, without observing changes associated with the age variable. The <em>t</em><span>-Student and one-factor ANOVA tests confirm the relationship between the level of health and physical-sports practice habits depending on sex and age.</span></div></div><div><h3>Conclusions</h3><div>It is necessary to promote preventive programs to increase participation in the practice of physical and sports exercise in the adult population that has unhealthy or unhealthy levels of lifestyle.</div></div>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":"37 5","pages":"Article 500756"},"PeriodicalIF":1.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143060625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1016/j.arteri.2025.500857
Carlos Morillas Ariño
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Pub Date : 2025-09-01DOI: 10.1016/j.arteri.2025.500768
Julio A. Carbayo-Herencia , Marta Simarro Rueda , Luis Miguel Artigao Ródenas , Juan A. Divisón Garrote , Francisca Molina Escribano , Isabel Ponce García , Antonio Palazón Bru , Pilar Torres Moreno , David Caldevilla Bernardo , Rosalina Martínez López , Vicente Francisco Gil Guillén , José R. Banegas , en nombre del Grupo de Enfermedades Vasculares de Albacete (GEVA)
Introduction
Control of the main cardiovascular risk factors had succeeded in reducing cardiovascular diseases (CVD). However, the general increase in the prevalence of type 2 diabetes mellitus (DM2) and obesity has slowed this decline. Both CVRFs are strongly associated, and the term diabesity has been coined to refer to this relationship. The main objective of this study was to assess the influence of diabesity on cardiovascular mortality.
Methods
Prospective cohort study involving 1246 individuals (54.3% women) followed for 20.9 years (SD = 7.31) and selected by random two-stage sampling in a province in southeastern Spain. Diabesity was defined as the combination of DM2 with overweight and obesity. Survival curves (Kaplan-Meier) were calculated and two Cox regression models were used, one unadjusted and the other adjusted by the main explanatory variables in which the diabesity variable consisted of 6 categories (normal weight, overweight, obesity, normal weight+DM2, overweight+DM2 and obesity+DM2).
Results
There were 95 deaths due to CV causes (7.6% of the total; 6.2% women and 9.3% men; p = 0.01). After adjustment, the combination of DM2 and overweight increased the incidence of cardiovascular mortality by 133% (HR = 2.33; 95% CI: 1.18-4.58; p = 0.014) and the combination of DM2 and obesity by 49% (HR = 1.49; 95% CI: 0.64-3.45; p = 0.351), not reaching statistical significance in the latter case.
Conclusions
In the general population, the results of our study show that the combination of overweight and DM2 is associated with higher CV mortality. It seems a priority to intervene intensively in the control of both overweight and DM2.
{"title":"Diabesidad y mortalidad de causa cardiovascular en una cohorte prospectiva de origen poblacional seguida más de 20 años","authors":"Julio A. Carbayo-Herencia , Marta Simarro Rueda , Luis Miguel Artigao Ródenas , Juan A. Divisón Garrote , Francisca Molina Escribano , Isabel Ponce García , Antonio Palazón Bru , Pilar Torres Moreno , David Caldevilla Bernardo , Rosalina Martínez López , Vicente Francisco Gil Guillén , José R. Banegas , en nombre del Grupo de Enfermedades Vasculares de Albacete (GEVA)","doi":"10.1016/j.arteri.2025.500768","DOIUrl":"10.1016/j.arteri.2025.500768","url":null,"abstract":"<div><h3>Introduction</h3><div>Control of the main cardiovascular risk factors had succeeded in reducing cardiovascular diseases (CVD). However, the general increase in the prevalence of type 2 diabetes mellitus (DM2) and obesity has slowed this decline. Both CVRFs are strongly associated, and the term diabesity has been coined to refer to this relationship. The main objective of this study was to assess the influence of diabesity on cardiovascular mortality.</div></div><div><h3>Methods</h3><div>Prospective cohort study involving 1246 individuals (54.3% women) followed for 20.9 years (SD<!--> <!-->=<!--> <!-->7.31) and selected by random two-stage sampling in a province in southeastern Spain. Diabesity was defined as the combination of DM2 with overweight and obesity. Survival curves (Kaplan-Meier) were calculated and two Cox regression models were used, one unadjusted and the other adjusted by the main explanatory variables in which the diabesity variable consisted of 6 categories (normal weight, overweight, obesity, normal weight+DM2, overweight+DM2 and obesity+DM2).</div></div><div><h3>Results</h3><div>There were 95 deaths due to CV causes (7.6% of the total; 6.2% women and 9.3% men; p<!--> <!-->=<!--> <!-->0.01). After adjustment, the combination of DM2 and overweight increased the incidence of cardiovascular mortality by 133% (HR<!--> <!-->=<!--> <!-->2.33; 95% CI: 1.18-4.58; p<!--> <!-->=<!--> <!-->0.014) and the combination of DM2 and obesity by 49% (HR<!--> <!-->=<!--> <!-->1.49; 95% CI: 0.64-3.45; p<!--> <!-->=<!--> <!-->0.351), not reaching statistical significance in the latter case.</div></div><div><h3>Conclusions</h3><div>In the general population, the results of our study show that the combination of overweight and DM2 is associated with higher CV mortality. It seems a priority to intervene intensively in the control of both overweight and DM2.</div></div>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":"37 5","pages":"Article 500768"},"PeriodicalIF":1.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143426264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1016/j.arteri.2024.500757
Carlos Santiago Díaz , Francisco J. Medrano , N. Muñoz-Rivas , Luis Castilla Guerra , M. Belén Alonso Ortiz , en representación de los grupos de trabajo de EPOC y de Riesgo Vascular de la Sociedad Española de Medicina Interna
Chronic Obstructive Pulmonary Disease (COPD) usually presents joined to other pathologies we call comorbidities. The more frequent of them are those related to cardiovascular risk, either its risk factors or its clinical manifestations. Cardiovascular risk of these patients grows up with the severity of the airflow obstruction, specially during and after an exacerbation of COPD. Patients with COPD have between 2 and 5 times more risk of ischaemic heart disease than people without COPD, even after adjusting for cofounding factors. Cardiovascular diseases are up to the second cause of mortality in these patients, close to those due to the lung disease. Although COPD is associated to several cardiovascular risk factors such as tobacco, arterial hypertension or Diabetes Mellitus, they don’t explain all the excess in cardiovascular risk these patients have. Despite that excess of cardiovascular risk in COPD patients, most widely used cardiovascular risk scores don’t include COPD as a risk factor itself, so global risk is understimated in these patients. In this review, we make a bibliography revision of the avaliable evidence about COPD and cardiovascular risk factors as well as the excess of cardiovascular risk COPD itself involves.
{"title":"EPOC y riesgo cardiovascular","authors":"Carlos Santiago Díaz , Francisco J. Medrano , N. Muñoz-Rivas , Luis Castilla Guerra , M. Belén Alonso Ortiz , en representación de los grupos de trabajo de EPOC y de Riesgo Vascular de la Sociedad Española de Medicina Interna","doi":"10.1016/j.arteri.2024.500757","DOIUrl":"10.1016/j.arteri.2024.500757","url":null,"abstract":"<div><div>Chronic Obstructive Pulmonary Disease (COPD) usually presents joined to other pathologies we call comorbidities. The more frequent of them are those related to cardiovascular risk, either its risk factors or its clinical manifestations. Cardiovascular risk of these patients grows up with the severity of the airflow obstruction, specially during and after an exacerbation of COPD. Patients with COPD have between 2 and 5 times more risk of ischaemic heart disease than people without COPD, even after adjusting for cofounding factors. Cardiovascular diseases are up to the second cause of mortality in these patients, close to those due to the lung disease. Although COPD is associated to several cardiovascular risk factors such as tobacco, arterial hypertension or Diabetes Mellitus, they don’t explain all the excess in cardiovascular risk these patients have. Despite that excess of cardiovascular risk in COPD patients, most widely used cardiovascular risk scores don’t include COPD as a risk factor itself, so global risk is understimated in these patients. In this review, we make a bibliography revision of the avaliable evidence about COPD and cardiovascular risk factors as well as the excess of cardiovascular risk COPD itself involves.</div></div>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":"37 5","pages":"Article 500757"},"PeriodicalIF":1.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143257004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01DOI: 10.1016/j.arteri.2025.500769
Julius Soudant , Raquel González-Blázquez , Abraham Merino , Constanza Ballesteros-Martínez , Raquel Rodrigues-Diez , Rosa Moreno-Carriles , J. Francisco Nistal , Susana Guerra , Juan Miguel Redondo , Mercedes Salaices , Ana M. Briones , Ana B. García-Redondo
Introduction
Inflammation is a major determinant of abdominal aortic aneurysms (AAA). Interferon stimulated gene 15 (ISG15) has a role in vascular remodelling in AAA. This study investigates the mechanisms whereby ISG15 might affect vascular remodeling and function.
Methods
We used vascular smooth muscle cells (VSMC) from wild type (ISG15+/+) o ISG15 knockout (ISG15−/−) mice, aorta from ISG15+/+ and ISG15−/− mice infused with angiotensin II (1.44 mg/kg/day, sc, 14 days), and human AAA. We also performed a model of recombinant ISG15 infusion (rISG15, sc, 100 and 500 ng/day, 14 days) in mice.
Results
In VSMC, ISG15 deficiency increased the expression of contractile (Acta2, Tagln) and synthetic (Fn1, Col1a2, Col3, Col4) markers and decreased the expression of the calcification marker Spp1. Ang II infusion changed the expression of phenotype markers differently in aorta from ISG15+/+ or ISG15−/− mice. ISG15 expression showed a negative correlation with expression of contractile markers (ACTA2, CNN1), and with COL3a1, in human samples from patients with AAA or with stenotic aorto-iliac pathology. rISG15 infusion induced hypotrophic vascular remodelling in mesenteric arteries without affecting vascular mechanics. Aorta of ISG15−/− mice contracted more to thromboxane A2 analogue U46619, compared to ISG15−/−mice. Both aorta and mesenteric arteries from rISG15-treated mice showed less contractility than control mice.
Conclusions
ISG15 participates in pathological vascular remodeling probably by modulating VSMC phenotype. These changes could also impact in the vascular function.
{"title":"El gen estimulado por interferón 15 (ISG15) modula el fenotipo de células musculares lisas vasculares y el remodelado vascular patológico","authors":"Julius Soudant , Raquel González-Blázquez , Abraham Merino , Constanza Ballesteros-Martínez , Raquel Rodrigues-Diez , Rosa Moreno-Carriles , J. Francisco Nistal , Susana Guerra , Juan Miguel Redondo , Mercedes Salaices , Ana M. Briones , Ana B. García-Redondo","doi":"10.1016/j.arteri.2025.500769","DOIUrl":"10.1016/j.arteri.2025.500769","url":null,"abstract":"<div><h3>Introduction</h3><div>Inflammation is a major determinant of abdominal aortic aneurysms (AAA). Interferon stimulated gene 15 (ISG15) has a role in vascular remodelling in AAA. This study investigates the mechanisms whereby ISG15 might affect vascular remodeling and function.</div></div><div><h3>Methods</h3><div>We used vascular smooth muscle cells (VSMC) from wild type (ISG15<sup>+/+</sup>) o ISG15 knockout (ISG15<sup>−/−</sup>) mice, aorta from ISG15<sup>+/+</sup> and ISG15<sup>−/−</sup> mice infused with angiotensin II (1.44<!--> <!-->mg/kg/day, sc, 14 days), and human AAA. We also performed a model of recombinant ISG15 infusion (rISG15, sc, 100 and 500<!--> <!-->ng/day, 14 days) in mice.</div></div><div><h3>Results</h3><div>In VSMC, ISG15 deficiency increased the expression of contractile (<em>Acta2</em>, <em>Tagln</em>) and synthetic (<em>Fn1</em>, <em>Col1a2</em>, <em>Col3</em>, <em>Col4</em>) markers and decreased the expression of the calcification marker <em>Spp1</em>. Ang II infusion changed the expression of phenotype markers differently in aorta from ISG15<sup>+/+</sup> or ISG15<sup>−/−</sup> mice. ISG15 expression showed a negative correlation with expression of contractile markers (<em>ACTA2</em>, <em>CNN1</em>), and with <em>COL3a1,</em> in human samples from patients with AAA or with stenotic aorto-iliac pathology. rISG15 infusion induced hypotrophic vascular remodelling in mesenteric arteries without affecting vascular mechanics. Aorta of ISG15<sup>−/−</sup> mice contracted more to thromboxane A<sub>2</sub> analogue U46619, compared to ISG15<sup>−/−</sup>mice. Both aorta and mesenteric arteries from rISG15-treated mice showed less contractility than control mice.</div></div><div><h3>Conclusions</h3><div>ISG15 participates in pathological vascular remodeling probably by modulating VSMC phenotype. These changes could also impact in the vascular function.</div></div>","PeriodicalId":45230,"journal":{"name":"Clinica e Investigacion en Arteriosclerosis","volume":"37 5","pages":"Article 500769"},"PeriodicalIF":1.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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