Lipoprotein(a) in patients with aortic stenosis: Insights from cardiovascular magnetic resonance
Vassilios S Vassiliou1,2, Paul D Flynn3, Claire E Raphael1
1CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal Brompton and Harefield Hospitals and Imperial College London, London, United Kingdom.
Insights
This study found no link between elevated Lipoprotein(a) and myocardial fibrosis in patients with aortic stenosis. Further research is needed to understand the mechanisms behind worse outcomes in these patients.
Area of Science:
- Cardiology
- Biochemistry
- Medical Imaging
Background:
- Aortic stenosis is a common age-related heart valve disease.
- Myocardial fibrosis in aortic stenosis patients is linked to poorer outcomes, but the cause is unknown.
- Lipoprotein(a) is a cardiovascular risk factor often elevated in aortic stenosis.
Purpose of the Study:
- To investigate the association between elevated Lipoprotein(a) and myocardial replacement fibrosis in patients with aortic stenosis.
Main Methods:
- 110 patients with varying degrees of aortic stenosis underwent cardiovascular magnetic resonance with late gadolinium enhancement (LGE) to detect fibrosis.
- Statistical analyses, including Mann Whitney U tests and regression, were used to assess the relationship between Lipoprotein(a) levels and fibrosis presence/severity.
Main Results:
- 32.7% of patients showed no fibrosis, 34.6% had midwall fibrosis, and 32.7% had subendocardial fibrosis.
- Aortic stenosis patients had higher Lipoprotein(a) than controls, but levels did not differ significantly across stenosis severity.
- No association was found between Lipoprotein(a) and midwall or infarction-pattern fibrosis in any stenosis group.
Conclusions:
- The study found no evidence that higher Lipoprotein(a) levels contribute to myocardial fibrosis in patients with aortic stenosis.
- The underlying mechanisms connecting Lipoprotein(a), aortic stenosis, and adverse outcomes remain unclear.
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.
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