Response to Athyros and Colleagues: Inflammation and LDL Reduction

Autores
García, Rodrigo Damián; Asensio, Joana Antonela; Perdicaro, Diahann Jeanette; Peral, Maria de Los Angeles
Año de publicación
2023
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Atyros has discussed the role of statins in different clinical scenarios, doses, and timing of application. In response to your interesting observations, we would like to comment that statins have indeed changed the natural history of atherosclerotic disease in patients with hyperlipaemia and inflammation. Even in patients without hyperlipidemia, and with low-grade systemic inflammation data, studies such as JUPITER [1] demonstrated that statins reduce the risk of major cardiovascular events. In recent years, the use of these lipid-lowering drugs has been extended to patients whose cardiovascular risk is determined by an increased baseline inflammatory rate, such as patients infected with human immunodeficiency virus [2, 3], rheumatoid arthritis [4], systemic lupus erythematosus [5], and heart transplant recipients [6]. As mentioned in our review article [7], innate immunity represents an interesting field of study in the diagnosis and treatment of cardiovascular disease. In fact, innate immunity mechanisms, such as activation of monocytes, T-lymphocytes and platelets, strengthen the local inflammatory response, which contribute to the rupture of the atherosclerotic plaque [8]. These physiopathological events finally lead to acute thrombus formation, the major cause of acute coronary syndromes [9, 10]. The stability of atherosclerotic plaque mainly depends on immune and antiinflammatory pathways [11]. Contemporary studies in stable and unstable coronary artery disease, such as the CANTOS study [12], the COLCOT [13], the LODOCO2 [14], and the OXI trial [15], have supported the inflammatory hypothesis of atherosclerosis. The majority of these studies have demonstrated that the coronary residual inflammatory risk, a crucial prognostic factor of cardiovascular events, could be successfully decreased by inhibition of different proinflammatory interleukins [16]. In conclusion, the horizon in the treatment for atherosclerosis is the prevention of cardiovascular events by targeting the systemic low-grade inflammation and the innate immune response.
Fil: García, Rodrigo Damián. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
Fil: Asensio, Joana Antonela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
Fil: Perdicaro, Diahann Jeanette. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
Fil: Peral, Maria de Los Angeles. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Instituto Superior de Investigaciones Biológicas. Universidad Nacional de Tucumán. Instituto Superior de Investigaciones Biológicas; Argentina
Materia
INFLAMMATION
CARDIOVASCULAR DISEASES
ATYROS
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/233621

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spelling Response to Athyros and Colleagues: Inflammation and LDL ReductionGarcía, Rodrigo DamiánAsensio, Joana AntonelaPerdicaro, Diahann JeanettePeral, Maria de Los AngelesINFLAMMATIONCARDIOVASCULAR DISEASESATYROShttps://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3Atyros has discussed the role of statins in different clinical scenarios, doses, and timing of application. In response to your interesting observations, we would like to comment that statins have indeed changed the natural history of atherosclerotic disease in patients with hyperlipaemia and inflammation. Even in patients without hyperlipidemia, and with low-grade systemic inflammation data, studies such as JUPITER [1] demonstrated that statins reduce the risk of major cardiovascular events. In recent years, the use of these lipid-lowering drugs has been extended to patients whose cardiovascular risk is determined by an increased baseline inflammatory rate, such as patients infected with human immunodeficiency virus [2, 3], rheumatoid arthritis [4], systemic lupus erythematosus [5], and heart transplant recipients [6]. As mentioned in our review article [7], innate immunity represents an interesting field of study in the diagnosis and treatment of cardiovascular disease. In fact, innate immunity mechanisms, such as activation of monocytes, T-lymphocytes and platelets, strengthen the local inflammatory response, which contribute to the rupture of the atherosclerotic plaque [8]. These physiopathological events finally lead to acute thrombus formation, the major cause of acute coronary syndromes [9, 10]. The stability of atherosclerotic plaque mainly depends on immune and antiinflammatory pathways [11]. Contemporary studies in stable and unstable coronary artery disease, such as the CANTOS study [12], the COLCOT [13], the LODOCO2 [14], and the OXI trial [15], have supported the inflammatory hypothesis of atherosclerosis. The majority of these studies have demonstrated that the coronary residual inflammatory risk, a crucial prognostic factor of cardiovascular events, could be successfully decreased by inhibition of different proinflammatory interleukins [16]. In conclusion, the horizon in the treatment for atherosclerosis is the prevention of cardiovascular events by targeting the systemic low-grade inflammation and the innate immune response.Fil: García, Rodrigo Damián. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; ArgentinaFil: Asensio, Joana Antonela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; ArgentinaFil: Perdicaro, Diahann Jeanette. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; ArgentinaFil: Peral, Maria de Los Angeles. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Instituto Superior de Investigaciones Biológicas. Universidad Nacional de Tucumán. Instituto Superior de Investigaciones Biológicas; ArgentinaBentham Science Publishers2023-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/233621García, Rodrigo Damián; Asensio, Joana Antonela; Perdicaro, Diahann Jeanette; Peral, Maria de Los Angeles; Response to Athyros and Colleagues: Inflammation and LDL Reduction; Bentham Science Publishers; Current Vascular Pharmacology; 21; 1; 1-2023; 71-721570-16111875-6212CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.eurekaselect.com/article/128907info:eu-repo/semantics/altIdentifier/doi/10.2174/1570161121666230118115539info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:03:08Zoai:ri.conicet.gov.ar:11336/233621instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 10:03:08.773CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Response to Athyros and Colleagues: Inflammation and LDL Reduction
title Response to Athyros and Colleagues: Inflammation and LDL Reduction
spellingShingle Response to Athyros and Colleagues: Inflammation and LDL Reduction
García, Rodrigo Damián
INFLAMMATION
CARDIOVASCULAR DISEASES
ATYROS
title_short Response to Athyros and Colleagues: Inflammation and LDL Reduction
title_full Response to Athyros and Colleagues: Inflammation and LDL Reduction
title_fullStr Response to Athyros and Colleagues: Inflammation and LDL Reduction
title_full_unstemmed Response to Athyros and Colleagues: Inflammation and LDL Reduction
title_sort Response to Athyros and Colleagues: Inflammation and LDL Reduction
dc.creator.none.fl_str_mv García, Rodrigo Damián
Asensio, Joana Antonela
Perdicaro, Diahann Jeanette
Peral, Maria de Los Angeles
author García, Rodrigo Damián
author_facet García, Rodrigo Damián
Asensio, Joana Antonela
Perdicaro, Diahann Jeanette
Peral, Maria de Los Angeles
author_role author
author2 Asensio, Joana Antonela
Perdicaro, Diahann Jeanette
Peral, Maria de Los Angeles
author2_role author
author
author
dc.subject.none.fl_str_mv INFLAMMATION
CARDIOVASCULAR DISEASES
ATYROS
topic INFLAMMATION
CARDIOVASCULAR DISEASES
ATYROS
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Atyros has discussed the role of statins in different clinical scenarios, doses, and timing of application. In response to your interesting observations, we would like to comment that statins have indeed changed the natural history of atherosclerotic disease in patients with hyperlipaemia and inflammation. Even in patients without hyperlipidemia, and with low-grade systemic inflammation data, studies such as JUPITER [1] demonstrated that statins reduce the risk of major cardiovascular events. In recent years, the use of these lipid-lowering drugs has been extended to patients whose cardiovascular risk is determined by an increased baseline inflammatory rate, such as patients infected with human immunodeficiency virus [2, 3], rheumatoid arthritis [4], systemic lupus erythematosus [5], and heart transplant recipients [6]. As mentioned in our review article [7], innate immunity represents an interesting field of study in the diagnosis and treatment of cardiovascular disease. In fact, innate immunity mechanisms, such as activation of monocytes, T-lymphocytes and platelets, strengthen the local inflammatory response, which contribute to the rupture of the atherosclerotic plaque [8]. These physiopathological events finally lead to acute thrombus formation, the major cause of acute coronary syndromes [9, 10]. The stability of atherosclerotic plaque mainly depends on immune and antiinflammatory pathways [11]. Contemporary studies in stable and unstable coronary artery disease, such as the CANTOS study [12], the COLCOT [13], the LODOCO2 [14], and the OXI trial [15], have supported the inflammatory hypothesis of atherosclerosis. The majority of these studies have demonstrated that the coronary residual inflammatory risk, a crucial prognostic factor of cardiovascular events, could be successfully decreased by inhibition of different proinflammatory interleukins [16]. In conclusion, the horizon in the treatment for atherosclerosis is the prevention of cardiovascular events by targeting the systemic low-grade inflammation and the innate immune response.
Fil: García, Rodrigo Damián. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
Fil: Asensio, Joana Antonela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas. Instituto de Histología y Embriología de Mendoza Dr. Mario H. Burgos; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
Fil: Perdicaro, Diahann Jeanette. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
Fil: Peral, Maria de Los Angeles. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tucumán. Instituto Superior de Investigaciones Biológicas. Universidad Nacional de Tucumán. Instituto Superior de Investigaciones Biológicas; Argentina
description Atyros has discussed the role of statins in different clinical scenarios, doses, and timing of application. In response to your interesting observations, we would like to comment that statins have indeed changed the natural history of atherosclerotic disease in patients with hyperlipaemia and inflammation. Even in patients without hyperlipidemia, and with low-grade systemic inflammation data, studies such as JUPITER [1] demonstrated that statins reduce the risk of major cardiovascular events. In recent years, the use of these lipid-lowering drugs has been extended to patients whose cardiovascular risk is determined by an increased baseline inflammatory rate, such as patients infected with human immunodeficiency virus [2, 3], rheumatoid arthritis [4], systemic lupus erythematosus [5], and heart transplant recipients [6]. As mentioned in our review article [7], innate immunity represents an interesting field of study in the diagnosis and treatment of cardiovascular disease. In fact, innate immunity mechanisms, such as activation of monocytes, T-lymphocytes and platelets, strengthen the local inflammatory response, which contribute to the rupture of the atherosclerotic plaque [8]. These physiopathological events finally lead to acute thrombus formation, the major cause of acute coronary syndromes [9, 10]. The stability of atherosclerotic plaque mainly depends on immune and antiinflammatory pathways [11]. Contemporary studies in stable and unstable coronary artery disease, such as the CANTOS study [12], the COLCOT [13], the LODOCO2 [14], and the OXI trial [15], have supported the inflammatory hypothesis of atherosclerosis. The majority of these studies have demonstrated that the coronary residual inflammatory risk, a crucial prognostic factor of cardiovascular events, could be successfully decreased by inhibition of different proinflammatory interleukins [16]. In conclusion, the horizon in the treatment for atherosclerosis is the prevention of cardiovascular events by targeting the systemic low-grade inflammation and the innate immune response.
publishDate 2023
dc.date.none.fl_str_mv 2023-01
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/233621
García, Rodrigo Damián; Asensio, Joana Antonela; Perdicaro, Diahann Jeanette; Peral, Maria de Los Angeles; Response to Athyros and Colleagues: Inflammation and LDL Reduction; Bentham Science Publishers; Current Vascular Pharmacology; 21; 1; 1-2023; 71-72
1570-1611
1875-6212
CONICET Digital
CONICET
url http://hdl.handle.net/11336/233621
identifier_str_mv García, Rodrigo Damián; Asensio, Joana Antonela; Perdicaro, Diahann Jeanette; Peral, Maria de Los Angeles; Response to Athyros and Colleagues: Inflammation and LDL Reduction; Bentham Science Publishers; Current Vascular Pharmacology; 21; 1; 1-2023; 71-72
1570-1611
1875-6212
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.eurekaselect.com/article/128907
info:eu-repo/semantics/altIdentifier/doi/10.2174/1570161121666230118115539
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Bentham Science Publishers
publisher.none.fl_str_mv Bentham Science Publishers
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
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instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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