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Clinical Significance of Elevated Lipoprotein(a) in Primary and Secondary Prevention: A Multi-institutional Study
Dong-Yi Chen1,2,3, Ming-Lung Tsai4,5, Ming-Jer Hsieh1,4
1Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital at Linkou, Taiwan.
Insights
Elevated lipoprotein(a) [Lp(a)] levels, particularly at 30 mg/dL or higher, significantly increase the risk of major adverse cardiovascular events (MACEs). This finding holds true for individuals both with and without pre-existing atherosclerotic cardiovascular disease (ASCVD).
Area of Science:
- Cardiology
- Biochemistry
- Epidemiology
Background:
- Elevated lipoprotein(a) [Lp(a)] is increasingly recognized as a causal factor in atherosclerotic cardiovascular disease (ASCVD).
- The specific clinical utility of Lp(a) concentration thresholds, such as 30 mg/dL, for risk stratification requires further investigation.
Purpose of the Study:
- To investigate the association between Lp(a) concentrations and cardiovascular outcomes in a Taiwanese population.
- To evaluate the predictive value of an Lp(a) level of 30 mg/dL for major adverse cardiovascular events (MACEs) in individuals stratified by ASCVD status.
Main Methods:
- Retrospective analysis of 51,934 individuals from the Chang Gung Research Database (2004-2019).
- Stratification into groups with and without established ASCVD (2,571 and 49,363 subjects, respectively).
- Primary endpoint: MACEs, including myocardial infarction, stroke, revascularization, and cardiovascular mortality, with follow-up until December 31, 2019.
Main Results:
- Median Lp(a) level was 9.6 mg/dL; mean follow-up was 6.6 years.
- In ASCVD-free individuals, Lp(a) ≥30 mg/dL was linked to increased MACE risk (aSHR: 1.24; 95% CI: 1.07-1.43).
- In the ASCVD cohort, elevated Lp(a) also predicted higher MACE occurrence (aSHR: 1.36; 95% CI: 1.07-1.74); risk increased progressively beyond 30 mg/dL.
Conclusions:
- Lp(a) levels ≥30 mg/dL are an independent predictor of adverse cardiovascular outcomes.
- This 30 mg/dL threshold is effective for cardiovascular risk stratification in both primary and secondary prevention settings.
Aims:
Recent evidence suggests that elevated lipoprotein(a) [Lp(a)] contributes to atherosclerotic cardiovascular disease (ASCVD). The predictive value of specific Lp(a) cutoff points of 30 mg/dL remains to be established. This study investigated the relationship between Lp(a) concentrations and cardiovascular outcomes in Taiwanese individuals, stratified by pre-existing ASCVD status.
Methods:
We conducted a retrospective analysis of 51,934 subjects from the Chang Gung Research Database (January 2004 to June 2019), comprising 49,363 individuals without ASCVD and 2,571 with established ASCVD. The primary outcome was major adverse cardiovascular events (MACEs), encompassing acute myocardial infarction, ischemic stroke, revascularization procedures, peripheral arterial interventions, and cardiovascular mortality. Individuals were followed until their last visit to our institutions or December 31, 2019.
Results:
During a mean follow-up of 6.6 years (standard deviation: 5.0 years), the study population demonstrated a median Lp(a) of 9.6 mg/dL (interquartile range: 4.6-18.5). In ASCVD-free individuals, Lp(a) concentrations ≥30 mg/dL were associated with increased MACE risk (adjusted subdistribution hazard ratio [aSHR]: 1.24; 95% confidence interval [CI]: 1.07-1.43). Similarly, in the ASCVD cohort, elevated Lp(a) predicted higher MACE occurrence (aSHR: 1.36; 95% CI: 1.07-1.74). Restricted cubic spline analysis confirmed a progressive risk elevation beyond the 30 mg/dL threshold in both groups.
Conclusions:
Lp(a) levels ≥30 mg/dL independently predicted adverse cardiovascular outcomes, regardless of baseline ASCVD status. This threshold appears suitable for cardiovascular risk stratification in both primary and secondary prevention settings.
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