Arterial Stiffness in the Heart Disease of CKD

CKD frequently leads to chronic cardiac dysfunction. This complex relationship has been termed as cardiorenal syndrome type 4 or cardio-renal link. Despite numerous studies and reviews focused on the pathophysiology and therapy of this syndrome, the role of arterial stiffness has been frequently ove...

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Veröffentlicht in:Journal of the American Society of Nephrology Jg. 30; H. 6; S. 918
Hauptverfasser: Zanoli, Luca, Lentini, Paolo, Briet, Marie, Castellino, Pietro, House, Andrew A, London, Gerard M, Malatino, Lorenzo, McCullough, Peter A, Mikhailidis, Dimitri P, Boutouyrie, Pierre
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Sprache:Englisch
Veröffentlicht: United States 01.06.2019
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ISSN:1533-3450, 1533-3450
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Abstract CKD frequently leads to chronic cardiac dysfunction. This complex relationship has been termed as cardiorenal syndrome type 4 or cardio-renal link. Despite numerous studies and reviews focused on the pathophysiology and therapy of this syndrome, the role of arterial stiffness has been frequently overlooked. In this regard, several pathogenic factors, including uremic toxins ( , uric acid, phosphates, endothelin-1, advanced glycation end-products, and asymmetric dimethylarginine), can be involved. Their effect on the arterial wall, direct or mediated by chronic inflammation and oxidative stress, results in arterial stiffening and decreased vascular compliance. The increase in aortic stiffness results in increased cardiac workload and reduced coronary artery perfusion pressure that, in turn, may lead to microvascular cardiac ischemia. Conversely, reduced arterial stiffness has been associated with increased survival. Several approaches can be considered to reduce vascular stiffness and improve vascular function in patients with CKD. This review primarily discusses current understanding of the mechanisms concerning uremic toxins, arterial stiffening, and impaired cardiac function, and the therapeutic options to reduce arterial stiffness in patients with CKD.
AbstractList CKD frequently leads to chronic cardiac dysfunction. This complex relationship has been termed as cardiorenal syndrome type 4 or cardio-renal link. Despite numerous studies and reviews focused on the pathophysiology and therapy of this syndrome, the role of arterial stiffness has been frequently overlooked. In this regard, several pathogenic factors, including uremic toxins ( , uric acid, phosphates, endothelin-1, advanced glycation end-products, and asymmetric dimethylarginine), can be involved. Their effect on the arterial wall, direct or mediated by chronic inflammation and oxidative stress, results in arterial stiffening and decreased vascular compliance. The increase in aortic stiffness results in increased cardiac workload and reduced coronary artery perfusion pressure that, in turn, may lead to microvascular cardiac ischemia. Conversely, reduced arterial stiffness has been associated with increased survival. Several approaches can be considered to reduce vascular stiffness and improve vascular function in patients with CKD. This review primarily discusses current understanding of the mechanisms concerning uremic toxins, arterial stiffening, and impaired cardiac function, and the therapeutic options to reduce arterial stiffness in patients with CKD.
CKD frequently leads to chronic cardiac dysfunction. This complex relationship has been termed as cardiorenal syndrome type 4 or cardio-renal link. Despite numerous studies and reviews focused on the pathophysiology and therapy of this syndrome, the role of arterial stiffness has been frequently overlooked. In this regard, several pathogenic factors, including uremic toxins (i.e., uric acid, phosphates, endothelin-1, advanced glycation end-products, and asymmetric dimethylarginine), can be involved. Their effect on the arterial wall, direct or mediated by chronic inflammation and oxidative stress, results in arterial stiffening and decreased vascular compliance. The increase in aortic stiffness results in increased cardiac workload and reduced coronary artery perfusion pressure that, in turn, may lead to microvascular cardiac ischemia. Conversely, reduced arterial stiffness has been associated with increased survival. Several approaches can be considered to reduce vascular stiffness and improve vascular function in patients with CKD. This review primarily discusses current understanding of the mechanisms concerning uremic toxins, arterial stiffening, and impaired cardiac function, and the therapeutic options to reduce arterial stiffness in patients with CKD.CKD frequently leads to chronic cardiac dysfunction. This complex relationship has been termed as cardiorenal syndrome type 4 or cardio-renal link. Despite numerous studies and reviews focused on the pathophysiology and therapy of this syndrome, the role of arterial stiffness has been frequently overlooked. In this regard, several pathogenic factors, including uremic toxins (i.e., uric acid, phosphates, endothelin-1, advanced glycation end-products, and asymmetric dimethylarginine), can be involved. Their effect on the arterial wall, direct or mediated by chronic inflammation and oxidative stress, results in arterial stiffening and decreased vascular compliance. The increase in aortic stiffness results in increased cardiac workload and reduced coronary artery perfusion pressure that, in turn, may lead to microvascular cardiac ischemia. Conversely, reduced arterial stiffness has been associated with increased survival. Several approaches can be considered to reduce vascular stiffness and improve vascular function in patients with CKD. This review primarily discusses current understanding of the mechanisms concerning uremic toxins, arterial stiffening, and impaired cardiac function, and the therapeutic options to reduce arterial stiffness in patients with CKD.
Author Zanoli, Luca
McCullough, Peter A
Castellino, Pietro
London, Gerard M
Mikhailidis, Dimitri P
Malatino, Lorenzo
Lentini, Paolo
Briet, Marie
House, Andrew A
Boutouyrie, Pierre
Author_xml – sequence: 1
  givenname: Luca
  surname: Zanoli
  fullname: Zanoli, Luca
  email: zanoli.rastelli@gmail.com
  organization: Sections of Nephrology and zanoli.rastelli@gmail.com
– sequence: 2
  givenname: Paolo
  surname: Lentini
  fullname: Lentini, Paolo
  organization: Division of Nephrology and Dialysis, St. Bassiano Hospital, Bassano del Grappa, Italy
– sequence: 3
  givenname: Marie
  surname: Briet
  fullname: Briet, Marie
  organization: Institut National de la Santé et de la Recherche Médicale U1083, National Center for Scientific Research Joint Research Unit 6214, Centre Hospitalo-Universitaire d'Angers, Université d'Angers, Angers, France
– sequence: 4
  givenname: Pietro
  surname: Castellino
  fullname: Castellino, Pietro
  organization: Internal Medicine, Department of Clinical and Experimental Medicine, University of Catania, Catania, Italy
– sequence: 5
  givenname: Andrew A
  surname: House
  fullname: House, Andrew A
  organization: Department of Medicine, University of Western Ontario, London, Ontario, Canada
– sequence: 6
  givenname: Gerard M
  surname: London
  fullname: London, Gerard M
  organization: Institut National de la Santé et de la Recherche Médicale U970, Paris, France
– sequence: 7
  givenname: Lorenzo
  surname: Malatino
  fullname: Malatino, Lorenzo
  organization: Internal Medicine, Department of Clinical and Experimental Medicine, University of Catania, Catania, Italy
– sequence: 8
  givenname: Peter A
  surname: McCullough
  fullname: McCullough, Peter A
  organization: Department of Medicine, Baylor University Medical Center, Baylor Heart and Vascular Institute, Baylor Jack and Jane Hamilton Heart and Vascular Hospital, Dallas, Texas
– sequence: 9
  givenname: Dimitri P
  surname: Mikhailidis
  fullname: Mikhailidis, Dimitri P
  organization: Department of Clinical Biochemistry, University College London, London, UK
– sequence: 10
  givenname: Pierre
  surname: Boutouyrie
  fullname: Boutouyrie, Pierre
  organization: Department of Pharmacology, Hôpital Européen Georges-Pompidou, Assistance Publique-Hôpitaux de Paris, Paris, France
BackLink https://www.ncbi.nlm.nih.gov/pubmed/31040188$$D View this record in MEDLINE/PubMed
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Snippet CKD frequently leads to chronic cardiac dysfunction. This complex relationship has been termed as cardiorenal syndrome type 4 or cardio-renal link. Despite...
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SubjectTerms Age Distribution
Aged
Cardio-Renal Syndrome - epidemiology
Cardio-Renal Syndrome - physiopathology
Cardiotonic Agents - therapeutic use
Cardiovascular Diseases - drug therapy
Cardiovascular Diseases - epidemiology
Cardiovascular Diseases - physiopathology
Cause of Death
Comorbidity
Female
Humans
Male
Middle Aged
Prevalence
Prognosis
Renal Dialysis - methods
Renal Insufficiency, Chronic - epidemiology
Renal Insufficiency, Chronic - physiopathology
Renal Insufficiency, Chronic - therapy
Risk Assessment
Severity of Illness Index
Sex Distribution
Survival Analysis
Vascular Stiffness - drug effects
Vascular Stiffness - physiology
Title Arterial Stiffness in the Heart Disease of CKD
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