Lipoprotein(a) and the risk of recurrent coronary heart disease: the Dubbo Study
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Published on: October 12, 2017
Leon A Simons1, Judith Simons2
1School of Clinical Medicine, Faculty of Medicine and Health, UNSW Sydney, Australia.
Insights
Elevated Lipoprotein(a) [Lp(a)] is a significant predictor of recurrent coronary heart disease (CHD) in seniors. Levels of 300 mg/L or 500 mg/L and higher indicate increased risk.
Area of Science:
- Cardiology
- Lipidology
- Geriatrics
Background:
- Elevated Lipoprotein(a) [Lp(a)] is not definitively established as a risk factor for recurrent coronary heart disease (CHD).
- This study investigates the association between Lp(a) levels and recurrent CHD in an elderly population.
Purpose of the Study:
- To determine if elevated Lp(a) independently predicts recurrent CHD in senior citizens.
- To identify appropriate threshold levels of Lp(a) associated with increased risk.
Main Methods:
- A longitudinal study of 607 individuals with prevalent CHD, aged 71 years on average, followed for 16 years.
- Baseline lipid profiles and other CHD risk factors were assessed.
- Proportional hazards regression models were used to analyze the independent contribution of Lp(a) to recurrent CHD events.
Main Results:
- A total of 399 incident CHD cases were recorded.
- Higher Lp(a) levels were observed in cases compared to non-cases (median 130 mg/L vs. 105 mg/L).
- Lp(a) levels ≥300 mg/L and ≥500 mg/L significantly predicted recurrent CHD, independent of other risk factors (HR 1.37 and 1.59, respectively).
Conclusions:
- Elevated Lp(a) is an independent and significant predictor of recurrent CHD in senior citizens.
- Lp(a) levels of 300 mg/L or 500 mg/L appear to be appropriate thresholds for identifying increased risk.
- Further research is needed to confirm the clinical benefit of therapies aimed at reducing elevated Lp(a).
Objective:
Elevated Lipoprotein(a) [Lp(a)] has not been firmly established as a risk factor for recurrent coronary heart disease (CHD). The present analysis explored this relationship in senior citizens.
Methods:
This was a longitudinal study in 607 subjects, all with prevalent CHD, mean age 71 years, followed for 16 years. Baseline examinations of lipids and other CHD risk factors were conducted in 1988-89 in Dubbo, Australia. The independent contribution of Lp(a) to a further CHD event was examined in proportional hazards regression models.
Results:
There were 399 incident CHD cases. Median Lp(a) in CHD cases was 130 mg/L (Interquartile range 60-315) and in non-cases 105 mg/L (45-250) (p < .07, U-Test). 26% of CHD cases and 19% of non-cases had Lp(a) 300 + mg/L; 18% of CHD cases and 8% of non-cases had Lp(a) 500 + mg/L. Lp(a) in Quintile 5 of its distribution (355 + mg/L), using Lp(a) Quintile 1 (<50mg/L) as reference, significantly predicted recurrent CHD with Hazard Ratio 1.53 (95% CI 1.11-2.11, p = .01). Prediction was independent of other risk factors. Lp(a) 500 + mg/L versus lower, significantly predicted recurrent CHD with Hazard Ratio 1.59 (1.16-2.17, p < .01). Prediction was similarly significant for Lp(a) 300 + mg/L versus lower, with Hazard Ratio 1.37 (1.09-1.73, p < .01).
Conclusion:
Elevated Lp(a) is an independent and significant predictor of recurrent CHD in senior citizens. Upper reference Lp(a) levels of 500 mg/L (≈125nmol/L) or 300 mg/L (≈75nmol/L) both appear to be appropriate. The clinical benefit of therapy to reduce elevated Lp(a) remains to be confirmed.
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