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Published on: January 28, 2020
LP(a) phenotypes and levels in angiographically proven coronary heart disease patients and controls
K Luthra1, S Vasisht, S Chhabra
1Department of Biochemistry, CN Centre, All India Institute of Medical Sciences, 110029 New Delhi.
Insights
Elevated Lipoprotein (a) levels, particularly smaller apo(a) isoforms, significantly increase the risk of coronary artery disease (CAD) in North India. This study highlights Lp(a) as a key predictor for cardiovascular events in this population.
Area of Science:
- Cardiovascular Medicine
- Genetics
- Biochemistry
Background:
- Elevated Lipoprotein (a) [Lp(a)] is a recognized risk factor for atherosclerotic vascular diseases.
- Understanding Lp(a) variations in diverse populations is crucial for risk stratification.
Purpose of the Study:
- To investigate the association between Lipoprotein (a) levels, apo(a) isoforms, and coronary artery disease (CAD) in a North-Indian population.
- To determine if Lp(a) concentration and size correlate with CAD risk in this demographic.
Main Methods:
- Analysis of 130 CAD patients and 130 controls from North India.
- Assessment of plasma Lp(a) concentrations and apo(a) phenotypic isoform sizes.
- Statistical comparison of Lp(a) levels and isoform distribution between patient and control groups.
Main Results:
- Mean Lp(a) levels were significantly higher in CAD patients (42±34 mg/dl) compared to controls (27±27 mg/dl).
- A higher frequency of elevated Lp(a) levels (>20 mg/dl) was observed in patients (73%) versus controls (43%).
- Inverse correlation found between apo(a) isoform size and Lp(a) concentration, with smaller isoforms linked to higher levels.
Conclusions:
- Low molecular weight apo(a) isoforms are significantly associated with an increased risk of CAD in the North-Indian population.
- Lp(a) concentration and apo(a) isoform heterogeneity are important factors in CAD pathogenesis within this ethnic group.
Abstract:
Lipoprotein Lp(a) excess has been identified as a powerful predictor of premature atherosclerotic vascular diseases. To evaluate this in a North-Indian population, 130 CAD patients and 130 controls were analyzed. The size of the apo(a) phenotypic isoforms was inversely proportional to Lp(a) concentrations. The mean concentration of Lp(a) in the CAD patients was 42±34 mg/dl whereas in the normal subjects it was much lower, 27±27 mg/dl. 157 subjects out of the total 260 subjects showed plasma levels of >20mg/dl. The frequency of high Lp(a) levels was much higher in patients(73%) than controls (43%). These data suggest (1) that there is heterogeneity of the Lp(a) polymorphism, (2) Higher Lp(a) levels were found in patients than in the controls, (3) Patients showed 1.5 fold increase in Lp(a) levels as compared to the controls. We conclude that low molecular weight apo(a) isoforms are significantly associated with increased risk of CAD in the North-Indian population.
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