Michel Pompeu Barros de Oliveira Sá1,2,3, Luiz Rafael P Cavalcanti4,5, Álvaro M Perazzo4,5, Rafael A F Gomes4,5,6, Marie-Annick Clavel7, Philippe Pibarot7, Giuseppe Biondi-Zoccai8,9, Konstantin Zhigalov10, Alexander Weymann10, Arjang Ruhparwar10, Ricardo Carvalho Lima4,5,6. 1. Division of Cardiovascular Surgery of Pronto Socorro Cardiológico de Pernambuco, PROCAPE, Av. Eng. Domingos Ferreira n°4172. Edf. Paquetá, apt° 405, Recife, Pernambuco, 51021-040, Brazil. michel_pompeu@yahoo.com.br. 2. University of Pernambuco, UPE, Recife, Brazil. michel_pompeu@yahoo.com.br. 3. Nucleus of Postgraduate and Research in Health Sciences of Faculty of Medical Sciences and Biological Sciences Instituite, FCM/ICB, Recife, Brazil. michel_pompeu@yahoo.com.br. 4. Division of Cardiovascular Surgery of Pronto Socorro Cardiológico de Pernambuco, PROCAPE, Av. Eng. Domingos Ferreira n°4172. Edf. Paquetá, apt° 405, Recife, Pernambuco, 51021-040, Brazil. 5. University of Pernambuco, UPE, Recife, Brazil. 6. Nucleus of Postgraduate and Research in Health Sciences of Faculty of Medical Sciences and Biological Sciences Instituite, FCM/ICB, Recife, Brazil. 7. Québec Heart and Lung Institute/Institut Universitaire de Cardiologie et de Pneumologie de Québec, Université Laval, 2725 Chemin Sainte Foy, #A-2075, Quebec, QC, G1V4G5, Canada. 8. Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy. 9. Mediterranea Cardiocentro, Naples, Italy. 10. Department of Thoracic and Cardiovascular Surgery, West German Heart and Vascular Center Essen, University Hospital of Essen, University Duisburg-Essen, Essen, Germany.
Abstract
PURPOSE OF REVIEW: This review summarizes the pathophysiology of calcific aortic valve stenosis (CAVS) and surveys relevant clinical data and basic research that explain how CAVS arises. RECENT FINDINGS: Lipoprotein(a) [Lp(a)], lipoprotein-associated phospholipase A2 (Lp-PLA2), oxidized phospholipids (OxPL), autotaxin, and genetic driving forces such as mutations in LPA gene and NOTCH gene seem to play a major role in the development of CAVS. These factors might well become targets of medical therapy in the coming years. CVAS seems to be a multifactorial disease that has much in common with coronary artery disease, mainly regarding lipidic accumulation and calcium deposition. No clinical trials conducted to date have managed to answer the key question of whether Lp(a) lowering and anti-calcific therapies confer a benefit in terms of reducing incidence or progression of CAVS, although additional outcome trials are ongoing.
PURPOSE OF REVIEW: This review summarizes the pathophysiology of calcific aortic valve stenosis (CAVS) and surveys relevant clinical data and basic research that explain how CAVS arises. RECENT FINDINGS:Lipoprotein(a) [Lp(a)], lipoprotein-associated phospholipase A2 (Lp-PLA2), oxidized phospholipids (OxPL), autotaxin, and genetic driving forces such as mutations in LPA gene and NOTCH gene seem to play a major role in the development of CAVS. These factors might well become targets of medical therapy in the coming years. CVAS seems to be a multifactorial disease that has much in common with coronary artery disease, mainly regarding lipidic accumulation and calcium deposition. No clinical trials conducted to date have managed to answer the key question of whether Lp(a) lowering and anti-calcific therapies confer a benefit in terms of reducing incidence or progression of CAVS, although additional outcome trials are ongoing.
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