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Published on: October 12, 2017
Lipoprotein(a) in Essential Hypertension: Associations with Blood Pressure and Hypertension-Mediated Organ Damage
Giulia Nardoianni1, Giuliano Tocci2,3,4, Barbara Pala1,5
1Division of Cardiology, Department of Clinical and Molecular Medicine, Sant'Andrea Hospital, University of Rome Sapienza, Rome, Italy.
Insights
Lipoprotein(a) [Lp(a)] levels were not linked to blood pressure (BP) in hypertensive outpatients. Further research is needed to understand Lp(a)’s role in hypertension and cardiovascular risk.
Area of Science:
- Cardiology
- Hypertension Research
- Lipidology
Background:
- Lipoprotein(a) [Lp(a)] is recommended for cardiovascular (CV) risk stratification in adults.
- Its specific role in hypertension remains under investigation.
- Understanding Lp(a) in hypertension is crucial for comprehensive CV risk assessment.
Purpose of the Study:
- To evaluate lipoprotein(a) [Lp(a)] levels in adult outpatients diagnosed with essential arterial hypertension.
- To explore the association between Lp(a) levels and blood pressure (BP) parameters.
- To investigate potential links between Lp(a) and hypertension phenotypes.
Main Methods:
- Retrospective observational study of adult outpatients with essential hypertension.
- Inclusion criteria: age ≥18 years, treated or untreated hypertension.
- Assessment included office/out-of-office BP, hypertension-mediated organ damage (HMOD), and Lp(a) levels.
- Hypertension phenotypes classified per 2023 European guidelines; Lp(a) stratified at ≥50 mg/dL.
Main Results:
- 230 patients included; 32.2% had Lp(a) ≥50 mg/dL.
- High Lp(a) group showed higher proportions of men, dyslipidemia, and comorbidities.
- No significant association found between Lp(a) levels and office or out-of-office BP values.
- Lp(a) levels did not differ significantly across hypertension phenotypes.
Conclusions:
- Lipoprotein(a) [Lp(a)] levels were not associated with blood pressure (BP) in this hypertensive outpatient cohort.
- The findings suggest Lp(a) may not be a direct marker for BP levels in hypertension.
- Further research is warranted to elucidate the precise role of Lp(a) in hypertension and its cardiovascular implications.
Introduction:
Although recommended for cardiovascular (CV) risk stratification in adults, the role of lipoprotein(a) [Lp(a)] in hypertension is not fully established.
Aim:
To evaluate Lp(a) levels in adult outpatients with essential arterial hypertension.
Methods:
A retrospective, observational study was conducted in outpatients of both sexes, aged ≥ 18 years, with treated or untreated essential hypertension, who were consecutively evaluated at the Hypertension Unit, Excellence Hypertension Center, Sant'Andrea Hospital, Rome, Italy. Participants underwent office and out-of-office blood pressure (BP) measurements, as well as assessment of hypertension-mediated organ damage (HMOD). BP measurements were performed, and hypertension phenotypes were classified according to 2023 European hypertension guidelines. Lp(a) levels were measured, and the study population was stratified according to a Lp(a) cut-off value of ≥50 mg/dl. Due to the non-uniform distribution, absolute Lp(a) values were logarithmically transformed.
Results:
A total of 230 patients with available Lp(a) values were included (42.6% women, mean age 66.3 ± 11.5 years, BMI 27.1 ± 4.5 kg/m2, office BP 137.1 ± 18.1/83.7 ± 11.0 mmHg, 24-hour BP 129.8 ± 14.5/79.6 ± 9.8 mmHg, Lp(a) 51.4 ± 65.3 mg/dL), among whom 32.2% had Lp(a) ≥50 mg/dl. There were significantly higher proportions of men (74.3% vs. 49.4%; P < 0.001), dyslipidaemia (97.3% vs. 75.0%; P < 0.001) and comorbidities (55.4% vs. 30.8%; P < 0.001) in patients with high Lp(a) than in those with normal Lp(a), who also received more frequently lipid lowering therapies (P < 0.001) and aspirin (P = 0.003). However, lower office systolic BP values (133.5±18.8 vs. 138.8±17.6 mmHg: P = 0.036) were observed in patients with Lp(a) ≥50 mg/dL than in those with < 50 mg/dl. Also, no significant differences for Lp(a) levels were observed among various hypertension phenotypes, as defined by office (P = 0.156) or out-of-office BP values (P = 0.065). No significant correlations were found between Lp(a) and office or out-of-office BP levels, both in treated and untreated hypertensive outpatients.
Conclusions:
In our population, Lp(a) levels were not associated with either office or out-of-office BP values, irrespective of antihypertensive treatment status. The role of Lp(a) in hypertension warrants further investigation.
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