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Stroke mortality and the apoB/apoA-I ratio: results of the AMORIS prospective study
G Walldius1, A H Aastveit, I Jungner
1King Gustaf V Research Institute, Karolinska Institute, Stockholm, Sweden. goran.walldius@astrazeneca.com
Insights
The apoB/apoA-I ratio, reflecting cholesterol balance, is a strong predictor of stroke risk, similar to its association with heart attacks. This ratio is a reliable marker for most ischemic events.
Area of Science:
- Cardiovascular Medicine
- Lipid Metabolism
- Stroke Research
Background:
- Low-density lipoprotein (LDL) cholesterol is a known risk factor for myocardial infarction but not stroke.
- The relationship between stroke risk and the balance of proatherogenic apolipoprotein B (apoB) and antiatherogenic apolipoprotein A-I (apoA-I) particles is not well-established.
Purpose of the Study:
- To investigate if the apoB/apoA-I ratio, representing cholesterol balance, is associated with stroke risk.
- To compare the predictive power of the apoB/apoA-I ratio with traditional lipid ratios for stroke.
Main Methods:
- Prospective analysis of over 175,000 individuals (98,722 men, 76,831 women).
- Examination of relationships between fatal stroke types, lipid fractions, apoB, apoA-I, and the apoB/apoA-I ratio.
- Comparison of stroke risk with other ischemic and non-ischemic fatalities.
Main Results:
- High apoB and low apoA-I levels were significantly associated with stroke risk.
- The apoB/apoA-I ratio was a stronger predictor of stroke than total/HDL and LDL/HDL cholesterol ratios.
- The apoB/apoA-I ratio showed a linear relationship with stroke risk, particularly for ischemic stroke, and was not linked to cancer risk.
Conclusions:
- The apoB/apoA-I ratio is linked to fatal stroke risk, mirroring its association with myocardial infarction and other ischemic events.
- The apoB/apoA-I ratio serves as a robust and specific biomarker for nearly all ischemic events.
- This ratio provides valuable insight into cholesterol balance and cardiovascular risk.
Objectives:
LDL cholesterol is a well-established risk factor for myocardial infarction, but not for stroke. The main objective of the present study was to determine if the risk of stroke is related to the balance between the proatherogenic apoB lipoprotein particles and the antiatherogenic apoA-I particles as is the case for myocardial infarction.
Subjects And Design:
A total of 98 722 men and 76 831 women were recruited from screening programmes. The prospective risk and the relationships between five different types of fatal strokes and the lipid fractions, apoB, apoA-I and the apoB/apoA-I ratio (automated immunoturbidimetry) were examined. The results were compared with the risks of other ischaemic and non-ischaemic fatalities.
Results:
Mean follow-up was 10.3 years. High apoB and low apoA-I values were significantly related to risk of stroke. The odds ratio comparing the upper 10th versus the 1st decile of the apoB/apoA-I ratio for all strokes adjusted for age, gender, total cholesterol (TC) and triglycerides (TG) was 2.07 (95% CI: 1.49-2.88), P < 0.0001. The strongest association was for ischaemic stroke. Low apoA-I was a common abnormality in all stroke subtypes including subarachnoidal and haemorrhagic strokes. In multivariate analyses the apoB/apoA-I ratio was a stronger risk predictor than total/HDL and LDL/HDL cholesterol ratios. The apoB/apoA-I ratio was linearly related to the risk of stroke although the slope was less than observed for the risk of fatal myocardial infarction. For all ischaemic events pooled together the age-, gender-, TC- and TG-adjusted odds ratio, 10th vs. 1st decile, was 3.13 (95% CI: 2.66-3.69), P < 0.0001. By contrast, there was no relationship between the apoB/apoA-I ratio and risk of cancer or any other non-ischaemic causes of death.
Conclusions:
These observations link the apoB/apoA-I ratio to the risk of fatal stroke in a similar fashion as for myocardial infarction and other ischaemic events. Our findings indicate that the apoB/apoA-I ratio, which indicates the 'cholesterol balance', is a robust and specific maker of virtually all ischaemic events.
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