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Lipoprotein(a) and calcific aortic valve stenosis: A systematic review.
Guddeti, Raviteja R; Patil, Shantanu; Ahmed, Aiza; Sharma, Arindam; Aboeata, Ahmed; Lavie, Carl J; Alla, Venkata Mahesh.
Afiliación
  • Guddeti RR; Division of Cardiovascular Diseases, Creighton University School of Medicine, Omaha, NE, USA. Electronic address: ravitejaguddeti@creighton.edu.
  • Patil S; Division of Cardiovascular Diseases, Creighton University School of Medicine, Omaha, NE, USA.
  • Ahmed A; Division of Internal Medicine, Creighton University School of Medicine, Omaha, NE, USA.
  • Sharma A; Division of Cardiovascular Diseases, Creighton University School of Medicine, Omaha, NE, USA.
  • Aboeata A; Division of Cardiovascular Diseases, Creighton University School of Medicine, Omaha, NE, USA.
  • Lavie CJ; John Ochsner Heart and Vascular Institute, Ochsner Clinical School, The University of Queensland School of Medicine, New Orleans, LA, USA.
  • Alla VM; Division of Cardiovascular Diseases, Creighton University School of Medicine, Omaha, NE, USA.
Prog Cardiovasc Dis ; 63(4): 496-502, 2020.
Article en En | MEDLINE | ID: mdl-32526213
Calcific aortic valve stenosis (AS) is the most common form of acquired valvular heart disease needing intervention and our understanding of this disease has evolved from one of degenerative calcification to that of an active process driven by the interplay of genetic factors and chronic inflammation modulated by risk factors such as smoking, hypertension and elevated cholesterol. Lipoprotein(a) [Lp (a)] is a cholesterol rich particle secreted by the liver which functions as the major lipoprotein carrier of phosphocholine-containing oxidized phospholipids. Lp(a) levels are largely genetically determined by polymorphisms in the LPA gene. While there is an extensive body of evidence linking Lp(a) to atherosclerotic cardiovascular disease, emerging evidence now suggests a similar association of Lp(a) to calcific AS. In this article, we performed a systematic review of all published literature to assess the association between Lp(a) and calcific aortic valve (AV) disease. In addition, we review the potential mechanisms by which Lp(a) influences the progression of valve disease. Our review identified a total of 21 studies, varying from case-control studies, prospective or retrospective observational cohort studies to Mendelian randomized studies that assessed the association between Lp(a) and calcific AS. All but one of the above studies demonstrated significant association between elevated Lp(a) and calcific AS. We conclude that there is convincing evidence supporting a causal association between elevated Lp(a) and calcific AS. In addition, elevated Lp(a) predicts a faster hemodynamic progression of AS, and increased risk of AV replacement, especially in younger patients. Further research into the clinical utility of Lp(a) as a marker for predicting the incidence, progression, and outcomes of sclerodegenerative AV disease is needed.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Válvula Aórtica / Estenosis de la Válvula Aórtica / Calcinosis / Lipoproteína(a) Tipo de estudio: Clinical_trials / Observational_studies / Prognostic_studies / Risk_factors_studies / Systematic_reviews Límite: Humans Idioma: En Revista: Prog Cardiovasc Dis Año: 2020 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Válvula Aórtica / Estenosis de la Válvula Aórtica / Calcinosis / Lipoproteína(a) Tipo de estudio: Clinical_trials / Observational_studies / Prognostic_studies / Risk_factors_studies / Systematic_reviews Límite: Humans Idioma: En Revista: Prog Cardiovasc Dis Año: 2020 Tipo del documento: Article Pais de publicación: Estados Unidos