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.