Department of Cardiovascular Medicine, Mayo Clinic Arizona, Scottsdale, Arizona, USA.
Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Heart. 2024 Jan 29;110(4):299-305. doi: 10.1136/heartjnl-2023-322987.
Lipoprotein(a) (Lp(a)) is associated with an increased incidence of native aortic stenosis, which shares similar pathological mechanisms with bioprosthetic aortic valve (bAV) degeneration. However, evidence regarding the role of Lp(a) concentrations in bAV degeneration is lacking. This study aims to evaluate the association between Lp(a) concentrations and bAV degeneration.
In this retrospective multicentre study, patients who underwent a bAV replacement between 1 January 2010 and 31 December 2020 and had a Lp(a) measurement were included. Echocardiography follow-up was performed to determine the presence of bioprosthetic valve degeneration, which was defined as an increase >10 mm Hg in mean gradient from baseline with concomitant decrease in effective orifice area and Doppler Velocity Index, or new moderate/severe prosthetic regurgitation. Levels of Lp(a) were compared between patients with and without degeneration and Cox regression analysis was performed to investigate the association between Lp(a) levels and bioprosthetic valve degeneration.
In total, 210 cases were included (mean age 74.1±9.4 years, 72.4% males). Median time between baseline and follow-up echocardiography was 4.4 (IQR 3.7) years. Bioprostheses degeneration was observed in 33 (15.7%) patients at follow-up. Median serum levels of Lp(a) were significantly higher in patients affected by degeneration versus non-affected cases: 50.0 (IQR 72.0) vs 15.6 (IQR 48.6) mg/dL, p=0.002. In the regression analysis, high Lp(a) levels (≥30 mg/dL) were associated with degeneration both in a univariable analysis (HR 3.6, 95% CI 1.7 to 7.6, p=0.001) and multivariable analysis adjusted by other risk factors for bioprostheses degeneration (HR 4.4, 95% CI 1.9 to 10.4, p=0.001).
High serum Lp(a) is associated with bAV degeneration. Prospective studies are needed to confirm these findings and to investigate whether lowering Lp(a) levels could slow bioprostheses degradation.
脂蛋白(a)[Lp(a)]与原生主动脉瓣狭窄的发生率增加有关,而后者与生物瓣主动脉瓣(bAV)退行性变具有相似的病理机制。然而,目前缺乏关于 Lp(a)浓度在 bAV 退行性变中的作用的证据。本研究旨在评估 Lp(a)浓度与 bAV 退行性变之间的关系。
在这项回顾性多中心研究中,纳入了 2010 年 1 月 1 日至 2020 年 12 月 31 日期间接受 bAV 置换术且有 Lp(a)测量值的患者。通过超声心动图随访来确定生物瓣是否发生退行性变,其定义为平均梯度较基线增加>10mmHg,同时有效瓣口面积和多普勒速度指数下降,或出现新的中度/重度人工瓣反流。比较退行性变患者和无退行性变患者的 Lp(a)水平,并进行 Cox 回归分析,以研究 Lp(a)水平与生物瓣退行性变之间的关系。
共纳入 210 例患者(平均年龄 74.1±9.4 岁,72.4%为男性)。基线至随访超声心动图的中位时间为 4.4(IQR 3.7)年。随访时,33 例(15.7%)患者的生物瓣发生退行性变。与无退行性变的患者相比,退行性变患者的血清 Lp(a)中位数明显更高:50.0(IQR 72.0)vs 15.6(IQR 48.6)mg/dL,p=0.002。在回归分析中,高 Lp(a)水平(≥30mg/dL)在单变量分析(HR 3.6,95%CI 1.7 至 7.6,p=0.001)和多变量分析(校正其他生物瓣退行性变的危险因素后 HR 4.4,95%CI 1.9 至 10.4,p=0.001)中均与退行性变相关。
高血清 Lp(a)与 bAV 退行性变有关。需要前瞻性研究来证实这些发现,并研究降低 Lp(a)水平是否能减缓生物瓣的降解。