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Predictors of the presence and extent of peripheral arterial occlusive disease
H Drexel1, J Steurer, J Muntwyler
1Division of Cardiology, University Hospital Zurich, Switzerland.
Insights
Lipid profiles, including LDL cholesterol and triglycerides, predict peripheral arterial occlusive disease (PAOD) presence. Disease extent relates to HDL cholesterol and non-lipid factors like smoking and glucose.
Area of Science:
- Cardiovascular Medicine
- Atherosclerosis Research
- Lipid Metabolism
Background:
- Limited data exist on lipid associations with peripheral atherosclerosis compared to coronary circulation.
- Peripheral arterial occlusive disease (PAOD) affects limb vasculature, impacting patient mobility and cardiovascular health.
Purpose of the Study:
- To investigate the relationship between lipid profiles and the presence and extent of PAOD.
- To identify key lipid and non-lipid risk factors associated with PAOD.
Main Methods:
- A case-control study involving 102 PAOD patients and 100 healthy controls.
- Angiographic assessment of stenosis presence and extent in peripheral arteries.
- Statistical analysis including logistic regression, simple regression, and discriminant analysis.
Main Results:
- PAOD presence strongly associated with LDL cholesterol, triglycerides, apolipoprotein B, and smoking.
- PAOD presence negatively associated with HDL2 cholesterol and apolipoprotein A-I.
- Disease extent correlated with HDL3 cholesterol, HDL cholesterol, apolipoprotein A-I, smoking, and fasting blood glucose.
Conclusions:
- PAOD presence is predicted by LDL, triglyceride, and HDL2 metabolism parameters.
- The extent of PAOD is influenced by HDL3 and non-lipid risk factors such as smoking and glucose levels.
Background:
Data relating lipids to the angiographic presence and extent of atherosclerosis, as reported for the coronary circulation, are lacking for the peripheral site.
Methods And Results:
This study comprised 102 patients with peripheral arterial occlusive disease (PAOD) referred for elective percutaneous transluminal angioplasty and 100 age-matched control subjects with normal coronary and peripheral angiograms. The presence of PAOD was defined as > or = 1 stenosis with > or = 50% narrowing, and the extent was defined as the total of > or = 50% lesions in the iliac, femoral, popliteal, and crural beds. The relation of lipids and nonlipid risk factors to the presence of PAOD was tested by stepwise logistic regression analysis; their relation to the extent of disease was analyzed by simple regression and stepwise discriminant analysis. The presence of PAOD was significantly and positively associated with LDL cholesterol (P = .0003), triglycerides (P = .0001), apolipoprotein B (P = .0073), and smoking (P = .005) and was significantly and negatively associated with HDL2 cholesterol (P = .0085) and apolipoprotein A-I (P = .021). In the logistic model, LDL cholesterol, triglycerides, smoking, and systolic blood pressure were selected as independent predictors of PAOD presence. The extent of PAOD was significantly and negatively correlated with HDL3 cholesterol (P = .005), HDL cholesterol (P = .013), and apolipoprotein A-I (P = .021) and was significantly and positively associated with smoking and fasting blood glucose. Age, smoking, and blood glucose were selected by the discriminant analysis as independent predictors of the extent of PAOD.
Conclusions:
From this large case-control study, it is concluded that the presence of PAOD is predicted by parameters of LDL, triglyceride, and HDL2 metabolism, whereas the extent of PAOD is related to HDL3 and nonlipid risk factors.