PMID- 28704465
OWN - NLM
STAT- MEDLINE
DCOM- 20170925
LR  - 20210109
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 7
DP  - 2017
TI  - Lipoprotein(a) in patients with aortic stenosis: Insights from cardiovascular 
      magnetic resonance.
PG  - e0181077
LID - 10.1371/journal.pone.0181077 [doi]
LID - e0181077
AB  - BACKGROUND: Aortic stenosis is the most common age-related valvular pathology. 
      Patients with aortic stenosis and myocardial fibrosis have worse outcome but the 
      underlying mechanism is unclear. Lipoprotein(a) is associated with adverse 
      cardiovascular risk and is elevated in patients with aortic stenosis. Although 
      mechanistic pathways could link Lipoprotein(a) with myocardial fibrosis, whether 
      the two are related has not been previously explored. In this study, we 
      investigated whether elevated Lipoprotein(a) was associated with the presence of 
      myocardial replacement fibrosis. METHODS: A total of 110 patients with mild, 
      moderate and severe aortic stenosis were assessed by late gadolinium enhancement 
      (LGE) cardiovascular magnetic resonance to identify fibrosis. Mann Whitney U 
      tests were used to assess for evidence of an association between Lp(a) and the 
      presence or absence of myocardial fibrosis and aortic stenosis severity and 
      compared to controls. Univariable and multivariable linear regression analysis 
      were undertaken to identify possible predictors of Lp(a). RESULTS: Thirty-six 
      patients (32.7%) had no LGE enhancement, 38 (34.6%) had midwall enhancement 
      suggestive of midwall fibrosis and 36 (32.7%) patients had subendocardial 
      myocardial fibrosis, typical of infarction. The aortic stenosis patients had 
      higher Lp(a) values than controls, however, there was no significant difference 
      between the Lp(a) level in mild, moderate or severe aortic stenosis. No 
      association was observed between midwall or infarction pattern fibrosis and 
      Lipoprotein(a), in the mild/moderate stenosis (p = 0.91) or severe stenosis 
      patients (p = 0.42). CONCLUSION: There is no evidence to suggest that higher 
      Lipoprotein(a) leads to increased myocardial midwall or infarction pattern 
      fibrosis in patients with aortic stenosis.
FAU - Vassiliou, Vassilios S
AU  - Vassiliou VS
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
AD  - Norwich Medical School, University of East Anglia, Bob Champion Research & 
      Education Building, Norwich, United Kingdom.
FAU - Flynn, Paul D
AU  - Flynn PD
AD  - The Lipid Clinic, Addenbrooke's Hospital, Cambridge University Foundation NHS 
      Trust, UK and University of Cambridge, Cambridge, United Kingdom.
FAU - Raphael, Claire E
AU  - Raphael CE
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
FAU - Newsome, Simon
AU  - Newsome S
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
AD  - Department of Statistics, London School of Hygiene and Tropical Medicine, London, 
      United Kingdom.
FAU - Khan, Tina
AU  - Khan T
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
FAU - Ali, Aamir
AU  - Ali A
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
FAU - Halliday, Brian
AU  - Halliday B
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
FAU - Studer Bruengger, Annina
AU  - Studer Bruengger A
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
AD  - Clinic of Cardiology, Stadtspital Triemli, Zurich, Switzerland.
FAU - Malley, Tamir
AU  - Malley T
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
FAU - Sharma, Pranev
AU  - Sharma P
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
FAU - Selvendran, Subothini
AU  - Selvendran S
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
FAU - Aggarwal, Nikhil
AU  - Aggarwal N
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
FAU - Sri, Anita
AU  - Sri A
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
FAU - Berry, Helen
AU  - Berry H
AD  - Department of Biochemistry, Royal Brompton and Harefield NHS Trust, London, 
      United Kingdom.
FAU - Donovan, Jackie
AU  - Donovan J
AD  - Department of Biochemistry, Royal Brompton and Harefield NHS Trust, London, 
      United Kingdom.
FAU - Lam, Willis
AU  - Lam W
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
FAU - Auger, Dominique
AU  - Auger D
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
FAU - Cook, Stuart A
AU  - Cook SA
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
AD  - Duke National University Hospital, Singapore, Singapore.
AD  - Cardiovascular Magnetic Resonance Imaging and Genetics, MRC London Institute of 
      Medical Sciences, Imperial College London, Hammersmith Hospital Campus, London, 
      United Kingdom.
FAU - Pennell, Dudley J
AU  - Pennell DJ
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
FAU - Prasad, Sanjay K
AU  - Prasad SK
AD  - CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal 
      Brompton and Harefield Hospitals and Imperial College London, London, United 
      Kingdom.
LA  - eng
GR  - FS/14/13/30619/BHF_/British Heart Foundation/United Kingdom
GR  - FS/15/29/31492/BHF_/British Heart Foundation/United Kingdom
GR  - MC_U120085815/MRC_/Medical Research Council/United Kingdom
GR  - MR/M003191/1/MRC_/Medical Research Council/United Kingdom
PT  - Journal Article
DEP - 20170713
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Lipoprotein(a))
RN  - K2I13DR72L (Gadolinium DTPA)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Aortic Valve Stenosis/*diagnostic imaging/metabolism
MH  - Female
MH  - Gadolinium DTPA/metabolism
MH  - Humans
MH  - Lipoprotein(a)/*metabolism
MH  - Magnetic Resonance Imaging, Cine/*methods
MH  - Male
MH  - Middle Aged
MH  - Myocardium/*pathology
MH  - Prospective Studies
PMC - PMC5509300
COIS- Competing Interests: Professor Pennell is a consultant to ApoPharma, director of 
      Cardiovascular Imaging Solutions., London, United Kingdom and reports personal 
      fees from Siemens outside the submitted work. Dr Prasad reports personal fees 
      from Bayer outside the submitted work. This does not alter our adherence to PLOS 
      ONE policies on sharing data and materials. The other authors have declared that 
      no competing interests exist.
EDAT- 2017/07/14 06:00
MHDA- 2017/09/26 06:00
PMCR- 2017/07/13
CRDT- 2017/07/14 06:00
PHST- 2016/11/21 00:00 [received]
PHST- 2017/06/26 00:00 [accepted]
PHST- 2017/07/14 06:00 [entrez]
PHST- 2017/07/14 06:00 [pubmed]
PHST- 2017/09/26 06:00 [medline]
PHST- 2017/07/13 00:00 [pmc-release]
AID - PONE-D-16-46237 [pii]
AID - 10.1371/journal.pone.0181077 [doi]
PST - epublish
SO  - PLoS One. 2017 Jul 13;12(7):e0181077. doi: 10.1371/journal.pone.0181077. 
      eCollection 2017.