Lipoprotein(a) in patients with aortic stenosis: Insights from cardiovascular magnetic resonance

Vassiliou, Vassilios; Flynn, Paul D; Raphael, Claire E.; Khan, Taha; Ali, Aamir; Halliday, Brian P; Bruengger, Annina Studer; Malley, Tamir; Sharma, Podila Satya Venkata Narasimha; Selvendran, Subothini; Aggarwal, Nikhil; Anita, Sri; Berry, Helen K.; Donovan, Jackie; Lam, Willis; Auger, Dominique; Cook, Stuart A.; Pennell, Dudley J.; Prasad, Sanjay K.

doi:10.1371/journal.pone.0181077

Cited by 13 publications

(14 citation statements)

References 34 publications

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“…Studies and guidelines also need to address the role of Lp(a) and its treatments in various high-risk ethnic groups, including non-Caucasian populations and people with diabetes. Lastly, the role of Lp(a) in the development of CAVD [137] strongly supports the need for trials of apo(a)-targeting ASOs and the developing siRNA therapies in these populations.…”

Section: Future Challenges: Resarch Questionsmentioning

confidence: 89%

Molecular, Population, and Clinical Aspects of Lipoprotein(a): A Bridge Too Far?

Ward

Kostner

Sullivan

et al. 2019

JCM

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There is now significant evidence to support an independent causal role for lipoprotein(a) (Lp(a)) as a risk factor for atherosclerotic cardiovascular disease. Plasma Lp(a) concentrations are predominantly determined by genetic factors. However, research into Lp(a) has been hampered by incomplete understanding of its metabolism and proatherogeneic properties and by a lack of suitable animal models. Furthermore, a lack of standardized assays to measure Lp(a) and no universal consensus on optimal plasma levels remain significant obstacles. In addition, there are currently no approved specific therapies that target and lower elevated plasma Lp(a), although there are recent but limited clinical outcome data suggesting benefits of such reduction. Despite this, international guidelines now recognize elevated Lp(a) as a risk enhancing factor for risk reclassification. This review summarises the current literature on Lp(a), including its discovery and recognition as an atherosclerotic cardiovascular disease risk factor, attempts to standardise analytical measurement, interpopulation studies, and emerging therapies for lowering elevated Lp(a) levels.

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Section: Future Challenges: Resarch Questionsmentioning

confidence: 89%

Molecular, Population, and Clinical Aspects of Lipoprotein(a): A Bridge Too Far?

Ward

Kostner

Sullivan

et al. 2019

JCM

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“…There is, however, a strong need for randomized controlled trials in secondary prevention due to the residual risk in patients with elevated Lp(a) despite reduced LDL-c [60]. Furthermore, the role of Lp(a) in the development of calcific aortic stenosis [61] strongly supports the need for trials of apo(a) targeting ASOs and siRNA in these populations.…”

Section: Discussionmentioning

confidence: 99%

What’s new on therapies for elevated lipoprotein(a)

Ward

Schultz

Watts

2019

Expert Review of Clinical Pharmacology

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“…CMR was performed using a 1.5 T scanner (Sonata or Avanto, Siemens, Erlangen, Germany) and a standardised protocol as described previously. 11…”

Section: Methodsmentioning

confidence: 99%

A model based on clinical parameters to identify myocardial late gadolinium enhancement by magnetic resonance in patients with aortic stenosis: An observational study

Kuk

Alpendurada

Dweck

et al. 2020

JRSM Cardiovascular Disease

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Objective With increasing age, the prevalence of aortic stenosis grows exponentially, increasing left heart pressures and potentially leading to myocardial hypertrophy, myocardial fibrosis and adverse outcomes. To identify patients who are at greatest risk, an outpatient model for risk stratification would be of value to better direct patient imaging, frequency of monitoring and expeditious management of aortic stenosis with possible earlier surgical intervention. In this study, a relatively simple model is proposed to identify myocardial fibrosis in patients with a diagnosis of moderate or severe aortic stenosis. Design Patients with moderate to severe aortic stenosis were enrolled into the study; patient characteristics, blood work, medications as well as transthoracic echocardiography and cardiovascular magnetic resonance were used to determine potential identifiers of myocardial fibrosis. Setting The Royal Brompton Hospital, London, UK Participants One hundred and thirteen patients in derivation cohort and 26 patients in validation cohort. Main outcome measures Identification of myocardial fibrosis. Results Three blood biomarkers (serum platelets, serum urea, N-terminal pro-B-type natriuretic peptide) and left ventricular ejection fraction were shown to be capable of identifying myocardial fibrosis. The model was validated in a separate cohort of 26 patients. Conclusions Although further external validation of the model is necessary prior to its use in clinical practice, the proposed clinical model may direct patient care with respect to earlier magnetic resonance imagining, frequency of monitoring and may help in risk stratification for surgical intervention for myocardial fibrosis in patients with aortic stenosis.

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Lipoprotein(a) in patients with aortic stenosis: Insights from cardiovascular magnetic resonance

Cited by 13 publications

References 34 publications

Molecular, Population, and Clinical Aspects of Lipoprotein(a): A Bridge Too Far?

Molecular, Population, and Clinical Aspects of Lipoprotein(a): A Bridge Too Far?

What’s new on therapies for elevated lipoprotein(a)

A model based on clinical parameters to identify myocardial late gadolinium enhancement by magnetic resonance in patients with aortic stenosis: An observational study

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