Mechanisms
First report links elevated Lp(a) to aortic root dilatation specifically in hypertensive patients, in 513 inpatients (Echocardiography 2025)
Original title: Association Between Lipoprotein(a) and Dilatation of Different Aortic Segments in Hypertensive Patients
In 513 consecutive hospitalised patients who underwent echocardiographic measurement of the aortic valve annulus, sinuses of Valsalva (SV), sinotubular junction (STJ), and ascending aorta, Lp(a) showed a positive, independent relationship with SV diameter (beta 0.330, p = 0.002) and STJ diameter (beta 0.253, p = 0.023) in hypertensive but not non-hypertensive patients, adjusted for age, sex, height and other clinical factors. Elevated Lp(a) independently predicted SV dilatation (odds ratio 1.006, 95% CI 1.002-1.009, p = 0.002) and ascending aorta dilatation (odds ratio 1.006, 95% CI 1.000-1.011, p = 0.035) in hypertensive patients, with the ascending aorta association strongest in men and those 65 or younger. Restricted cubic spline analysis showed a linear dose-response relationship between Lp(a) and both dilatation outcomes. This is the first report linking elevated Lp(a) specifically to aortic root and ascending aortic dilatation in hypertension, identifying Lp(a) as a standalone marker of this remodelling.
Original abstract
Purpose: There are limited reports on the potential link between Lp(a) and ARDM. Thus, we examined the relationship between Lp(a) and ARDM among hypertensive patients.
Methods: We used echocardiography to measure ARDM in 513 consecutively hospitalized patients. namely, the aortic valve annulus (Ava), sinuses of Valsalva (SV), sinotubular junction (STJ), and ascending aorta (AA) in 513 consecutive inpatients. We also examined the Lp(a), and other laboratory profiles of all participants.
Results: Lp(a) exhibited a positive and independent relationship with the SV diameter (coefficient [β] = 0.330, p = 0.002) and STJ (coefficient [β] = 0.253, p = 0.023), regardless of age, sex, height, or other clinical factors among hypertensive, but not nonhypertensive patients. We also demonstrated that a marked rise in Lp(a) levels was independently associated with SV dilatation (SVD) (OR: 1.006, 95% CI: 1.002-1.009, p = 0.002) and AA dilatation (AAD) (OR: 1.006, 95% CI: 1.000-1.011, p = 0.035) in patients with hypertension. In the subgroup analysis, elevated Lp(a) levels were significantly associated with SV dilatation in all subgroups, and with AAD in males and patients aged 65 years or younger (p < 0.05). The restricted cubic spline analysis indicated a linear association between Lp(a) levels and the risk of both SV and AAD (p < 0.05).
Conclusions: Herein, we were the first to report that among hypertensive patients, elevated Lp(a) concentrations were intricately linked to the ARDMs at SV and STJ. Moreover, we revealed that the Lp(a) level was a stand-alone indicator of SVD and AAD.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.