Vassiliou Vassilios S, Flynn Paul D, Raphael Claire E, Newsome Simon, Khan Tina, Ali Aamir, Halliday Brian, Studer Bruengger Annina, Malley Tamir, Sharma Pranev, Selvendran Subothini, Aggarwal Nikhil, Sri Anita, Berry Helen, Donovan Jackie, Lam Willis, Auger Dominique, Cook Stuart A, Pennell Dudley J, Prasad Sanjay K
CMR Unit, Royal Brompton Hospital and NIHR Biomedical Research Unit, Royal Brompton and Harefield Hospitals and Imperial College London, London, United Kingdom.
Norwich Medical School, University of East Anglia, Bob Champion Research & Education Building, Norwich, United Kingdom.
PLoS One. 2017 Jul 13;12(7):e0181077. doi: 10.1371/journal.pone.0181077. eCollection 2017.
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.
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).
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).
There is no evidence to suggest that higher Lipoprotein(a) leads to increased myocardial midwall or infarction pattern fibrosis in patients with aortic stenosis.
主动脉瓣狭窄是最常见的与年龄相关的瓣膜病变。主动脉瓣狭窄合并心肌纤维化的患者预后较差，但其潜在机制尚不清楚。脂蛋白(a)与不良心血管风险相关，在主动脉瓣狭窄患者中升高。尽管机制途径可能将脂蛋白(a)与心肌纤维化联系起来，但此前尚未探讨两者是否相关。在本研究中，我们调查了脂蛋白(a)升高是否与心肌替代性纤维化的存在有关。
通过延迟钆增强（LGE）心血管磁共振对110例轻度、中度和重度主动脉瓣狭窄患者进行评估，以识别纤维化。采用曼-惠特尼U检验评估脂蛋白(a)与心肌纤维化的存在与否、主动脉瓣狭窄严重程度之间的关联证据，并与对照组进行比较。进行单变量和多变量线性回归分析，以确定脂蛋白(a)的可能预测因素。
36例患者（32.7%）无LGE增强，38例（34.6%）有提示中层纤维化的中层增强，36例（32.7%）患者有梗死典型的心内膜下心肌纤维化。主动脉瓣狭窄患者的脂蛋白(a)值高于对照组，然而，轻度、中度或重度主动脉瓣狭窄患者的脂蛋白(a)水平之间无显著差异。在轻度/中度狭窄（p = 0.91）或重度狭窄患者（p = 0.42）中，未观察到中层或梗死型纤维化与脂蛋白(a)之间的关联。
没有证据表明脂蛋白(a)升高会导致主动脉瓣狭窄患者心肌中层或梗死型纤维化增加。
