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Lipoprotein(a) as a key target in combined therapeutic approaches for cardiovascular disease
Joaquim A Meireles Brandão1, Lúcia R Meireles-Brandão2, Rui Coelho3
1Faculdade de Medicina do Porto, Universidade do Porto (FMUP), Porto, Portugal; Starmedica.Clinica, Paredes, Portugal.
Insights
Combined therapy significantly reduces Lipoprotein(a) [Lp(a)] levels and improves vascular risk markers in high-risk patients. This approach is crucial for primary prevention and delaying atherosclerosis.
Area of Science:
- Cardiology
- Metabolic Disorders
- Vascular Health
Background:
- Lipoprotein(a) [Lp(a)] is an independent cardiovascular risk factor.
- Lp(a)] is closely associated with other manageable cardiovascular risk factors.
- High cardiovascular risk patients require effective primary prevention strategies.
Purpose of the Study:
- To evaluate the impact of combined therapy on managing Lp(a) levels.
- To assess cardiovascular risk reduction in primary prevention.
- To investigate the effect on metabolic variables and vascular markers.
Main Methods:
- Retrospective observational study of 516 high-risk patients.
- Analysis of metabolic disorders and pharmacological therapies.
- Assessment of cardiovascular risk scores and lifestyle changes.
Main Results:
- Significant reduction in Lp(a) levels (p<0.001) and improved carotid intima-media thickness.
- Lipid-lowering therapy, particularly statins, effectively decreased Lp(a).
- Synergistic benefits observed with combined drug therapies.
Conclusions:
- Lp(a) is a critical therapeutic target for vascular risk.
- Combined drug therapies are essential for primary prevention.
- Addressing all cardiovascular risk factors delays the atherosclerotic process.
Introduction And Objective:
Lipoprotein(a) [Lp(a)] is an independent cardiovascular risk factor but is closely associated with other similar risk factors that are manageable with appropriate treatment and guidance. We aimed to study the impact of using combined therapy for managing Lp(a) levels in patients at high cardiovascular risk but without major adverse cardiovascular events, in primary prevention.
Methods:
We conducted a retrospective observational study in 516 patients randomly selected from a group of 1677 patients who attended cardiovascular risk and metabolism consultations between 1995 and 2015. The disorders observed and therapies used were classified into nosological and pharmacological groups, respectively. Cardiovascular risk was calculated based on the Framingham risk score, the European Society of Cardiology's SCORE and the American College of Cardiology's ASCVD Risk Estimator, and changes in patients' lifestyle were assessed.
Results:
Significant differences (p<0.001) were found in almost all metabolic variables, except fasting insulin and C-peptide. Lp(a) levels were also significantly reduced (p<0.001). Carotid intima-media thickness improved, decreasing from 2.90 mm to 1.40 mm; however, there was no reduction in the number of cases of vascular stenosis. Of patients with hepatic steatosis (85.5%), 40.7% presented hepatomegaly, but liver function was only altered in a few patients (14.5%). Lipid-lowering therapy, especially statins, significantly decreased Lp(a), benefiting from synergy with other treatments.
Conclusions:
Lp(a) is a key overall indicator of vascular risk and should be considered a therapeutic target. Besides a healthy lifestyle, primary prevention should include combined drug therapies to address all cardiovascular risk factors and to delay the atherosclerotic process.
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