Lipoprotein(a) and Hypertension-Mediated Organ Damage in Patients with Essential Hypertension: Associations with Carotid Plaque and Impaired Nocturnal Blood Pressure Dipping

Background and Objectives: Lipoprotein(a) [Lp(a)] is an established cardiovascular risk factor associated with atherosclerosis, vascular inflammation, and endothelial dysfunction. However, data regarding its relationship with hypertension-mediated organ damage and circadian blood pressure abnormalities remain limited. We aimed to investigate the association of elevated Lp(a) levels with carotid atherosclerosis and nocturnal blood pressure dipping patterns in patients with hypertension. Materials and Methods: This retrospective cross-sectional study included 80 nondiabetic patients with essential hypertension. Patients were categorized according to serum Lp(a) levels into elevated Lp(a) (≥50 mg/dL, n = 20) and lower Lp(a) (<50 mg/dL, n = 60) groups. All participants underwent carotid ultrasonography, transthoracic echocardiography, ambulatory blood pressure monitoring, and ophthalmologic evaluation. Multivariable logistic and linear regression analyses were performed to determine independent associations between Lp(a), carotid plaque presence, and nocturnal dipping percentage. Results: Patients with elevated Lp(a) levels had a significantly higher prevalence of carotid plaque (55.0% vs. 23.3%, p = 0.008) and non-dipper hypertension (75.0% vs. 46.7%, p = 0.028) compared with patients with lower Lp(a) levels. Serum Lp(a) concentrations were inversely correlated with nocturnal dipping percentage (r = −0.362, p = 0.001). In multivariable logistic regression analysis adjusted for age, sex, LDL cholesterol, and active smoking, elevated Lp(a) remained independently associated with carotid plaque presence (OR 3.24, 95% CI 1.06–9.80, p = 0.039). In multiple linear regression analysis adjusted for age, sex, LDL cholesterol, and office systolic blood pressure, higher Lp(a) levels remained independently associated with lower nocturnal dipping percentage (β = −0.294, p = 0.008). No significant associations were observed between Lp(a) and carotid intima–media thickness, left ventricular hypertrophy, hypertensive retinopathy, or renal functional parameters. Conclusions: Elevated Lp(a) levels were independently associated with carotid plaque presence and impaired nocturnal blood pressure decline in hypertensive patients. These findings suggest that Lp(a) may be more closely linked to focal macrovascular atherosclerosis and abnormal circadian blood pressure regulation rather than diffuse hypertensive structural remodeling.