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Role of lipoprotein (a) and LPA KIV2 repeat polymorphism in bicuspid aortic valve stenosis and calcification: a proof of concept study

  • Elena Sticchi
  • Betti Giusti
  • Antonella Cordisco
  • Anna Maria Gori
  • Alice Sereni
  • Francesco Sofi
  • Fabio Mori
  • Stefania Colonna
  • Maria Pia Fugazzaro
  • Guglielmina Pepe
  • Stefano Nistri
  • Rossella Marcucci
IM - ORIGINAL

Abstract

Hemodynamic valvular impairment is a frequent determinant of the natural history of bicuspid aortic valve (BAV). The role of elevated Lp(a) levels and LPA Kringle IV type 2 (KIV-2) size polymorphism in influencing aortic valve calcification and stenosis development in patients with tricuspid aortic valve was recognized. In this study, we investigate the association between Lp(a) and LPA KIV-2 repeat number, and the presence of calcification and stenosis in BAV patients. Sixty-nine patients [79.7% males; median age 45(30–53) yrs], consecutively referred to Center for Cardiovascular Diagnosis or Referral Center for Marfan syndrome or related disorders, AOU Careggi, from June to November 2014, were investigated. For each patient, clinical (ECG and echocardiography) and laboratory [Lp(a) (Immunoturbidimetric assay) and LPA KIV-2 repeat number (real-time PCR)] evaluation were performed. Patients were compared with 69 control subjects. No significant association between Lp(a) circulating levels and LPA KIV-2 repeat number and BAV was evidenced. Among BAV patients, significantly higher Lp(a) levels according to calcification degree were found [no calcifications:78(42–159) mg/L, mild/moderate: 134(69–189) mg/L; severe: 560(286–1511) mg/L, p = 0.008]. Conversely, lower LPA KIV-2 repeat numbers in subjects with more severe calcification degree were observed. Furthermore, higher Lp(a) levels in patients with aortic stenosis [214(67–501) mg/L vs 104(56–169) mg/L, p = 0.043] were also found. In conclusion, present data suggest the potential role for Lp(a) as a possible risk marker useful to stratify, among BAV patients, those with a higher chance to develop valvular calcifications and aortic stenosis.

Keywords

Lipoprotein (a) Kringle IV type 2 Bicuspid aortic valve Calcification Stenosis 

Notes

Funding

This research was supported by departmental funds (ex-60%) for scientific research 2016 and 2017 to Prof. Betti Giusti.

Compliance with ethical standards

Conflict of interest

The authors declare that there is no conflict of interest.

Statement of human rights

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards.

Informed consent

Written informed consent was obtained from all individual participants included in the study.

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Copyright information

© Società Italiana di Medicina Interna 2018

Authors and Affiliations

  1. 1.Department of Experimental and Clinical Medicine, Section of Critical Medical Care and Medical SpecialitiesUniversity of FlorenceFlorenceItaly
  2. 2.Marfan Syndrome and Related Disorders Regional Referral CenterCareggi HospitalFlorenceItaly
  3. 3.Atherothrombotic Diseases Regional Referral CenterCareggi HospitalFlorenceItaly
  4. 4.Cardiovascular and Perioperative Internal Medicine UnitCareggi HospitalFlorenceItaly
  5. 5.Clinical Nutrition UnitCareggi HospitalFlorenceItaly
  6. 6.Don Carlo Gnocchi Foundation ItalyOnlus Istituto di Ricerca e Cura a Carattere ScientificoFlorenceItaly
  7. 7.Non-Invasive Vascular Diagnosis Regional Referral Center, Cardiovascular Diagnostics UnitCareggi HospitalFlorenceItaly
  8. 8.Outpatient Cardiology UnitHealth District 1 ULSS 6PaduaItaly
  9. 9.Cardiology ServiceCMSR Veneto MedicaAltavilla VicentinaItaly

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