Lipoprotein(a) and Hypertension-Mediated Organ Damage in Patients with Essential Hypertension: Associations with Carotid Plaque and Impaired Nocturnal Blood Pressure Dipping.
Elevated Lp(a) levels were independently associated with carotid plaque presence and impaired nocturnal blood pressure decline in hypertensive patients, suggesting Lp(a) may be more closely linked to focal macrovascular atherosclerosis and abnormal circadian blood pressure regulation rather than diffuse hypertensive structural remodeling.
Key Findings
Results
Patients with elevated Lp(a) had a significantly higher prevalence of carotid plaque compared to those with lower Lp(a).
Carotid plaque prevalence was 55.0% in the elevated Lp(a) group (≥50 mg/dL, n=20) versus 23.3% in the lower Lp(a) group (<50 mg/dL, n=60), p = 0.008.
In multivariable logistic regression 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).
Study population was 80 nondiabetic patients with essential hypertension in a retrospective cross-sectional design.
Results
Patients with elevated Lp(a) had a significantly higher prevalence of non-dipper hypertension compared to those with lower Lp(a).
Non-dipper hypertension prevalence was 75.0% in the elevated Lp(a) group versus 46.7% in the lower Lp(a) group, p = 0.028.
Non-dipper status was assessed via ambulatory blood pressure monitoring.
All 80 participants underwent ambulatory blood pressure monitoring as part of the study protocol.
Results
Serum Lp(a) concentrations were inversely correlated with nocturnal dipping percentage.
The inverse correlation between Lp(a) and nocturnal dipping percentage was r = -0.362, p = 0.001.
In multiple linear regression 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).
Results
Elevated Lp(a) was not significantly associated with carotid intima-media thickness, left ventricular hypertrophy, hypertensive retinopathy, or renal functional parameters.
No significant associations were observed between Lp(a) and carotid intima-media thickness.
No significant associations were found with left ventricular hypertrophy, hypertensive retinopathy, or renal functional parameters.
All participants underwent carotid ultrasonography, transthoracic echocardiography, and ophthalmologic evaluation to assess these outcomes.
The authors interpret this as suggesting Lp(a) is more linked to focal macrovascular atherosclerosis than diffuse hypertensive structural remodeling.
Methods
The study used a retrospective cross-sectional design with specific patient categorization thresholds for Lp(a).
80 nondiabetic patients with essential hypertension were included.
Patients were divided into elevated Lp(a) (≥50 mg/dL, n=20) and lower Lp(a) (<50 mg/dL, n=60) groups.
Multivariable logistic and linear regression analyses were performed to determine independent associations.
Covariates in regression models included age, sex, LDL cholesterol, active smoking, and office systolic blood pressure.
What This Means
This research suggests that people with high blood pressure who also have elevated levels of a blood particle called lipoprotein(a), or Lp(a), are more likely to develop fatty deposits (plaques) in their carotid arteries — the main arteries supplying the brain — and are more likely to have abnormal blood pressure patterns at night. Specifically, patients with Lp(a) levels at or above 50 mg/dL were more than three times as likely to have carotid plaques and were more likely to be 'non-dippers,' meaning their blood pressure does not drop normally during sleep as it should in healthy individuals. These associations held up even after accounting for other cardiovascular risk factors like age, sex, LDL cholesterol, and smoking.
Interestingly, high Lp(a) was not associated with other common complications of high blood pressure, such as thickening of artery walls (intima-media thickness), enlargement of the heart (left ventricular hypertrophy), eye damage (hypertensive retinopathy), or kidney function problems. This pattern suggests that Lp(a) specifically promotes the formation of discrete plaques and disrupts the body's normal 24-hour blood pressure rhythm, rather than contributing to the general structural damage that high blood pressure causes throughout the body.
This research suggests that measuring Lp(a) in hypertensive patients could help identify those at higher risk for carotid artery disease and abnormal nighttime blood pressure patterns, both of which are associated with increased risk of stroke and heart attack. Because the study was relatively small (80 patients) and cross-sectional in design, larger and longer-term studies are needed to confirm these findings and determine whether treating elevated Lp(a) in hypertensive patients could reduce these specific risks.
Kunak T, Ülgen Kunak A, Başarıcı &. (2026). Lipoprotein(a) and Hypertension-Mediated Organ Damage in Patients with Essential Hypertension: Associations with Carotid Plaque and Impaired Nocturnal Blood Pressure Dipping.. Medicina (Kaunas, Lithuania). https://doi.org/10.3390/medicina62081561