Abstract
BackgroundWe investigated whether or to what extent the interaction of lipoprotein (a) [Lp(a)] with cholesterol-containing lipids was associated with angiographic coronary collateralization in type 2 diabetic patients with chronic total occlusion.MethodsSerum levels of Lp(a), total cholesterol, low-density lipoprotein–cholesterol (LDL-C), high-density lipoprotein–cholesterol (HDL-C), and triglyceride were determined and non-HDL-C was calculated in 706 type 2 diabetic and 578 non-diabetic patients with stable coronary artery disease and angiographic total occlusion of at least one major coronary artery. The degree of collaterals supplying the distal aspect of a total occlusion from the contra-lateral vessel was graded as poor (Rentrop score of 0 or 1) or good coronary collateralization (Rentrop score of 2 or 3).ResultsFor diabetic and non-diabetic patients, Lp(a), total cholesterol, LDL-C, and non-HDL-C levels were higher in patients with poor coronary collateralization than in those with good collateralization, whereas HDL-C and triglyceride levels were similar. After adjustment for potential confounding factors, tertiles of Lp(a), total cholesterol, LDL-C and non-HDL-C remained independent determinants for poor collateralization. A significant interaction between Lp(a) and total cholesterol, LDL-C or non-HDL-C was observed in diabetic patients (all P interaction < 0.001) but not in non-diabetics. At high tertile of total cholesterol (≥ 5.35 mmol/L), LDL-C (≥ 3.36 mmol/L) and non-HDL-C (≥ 4.38 mmol/L), diabetic patients with high tertile of Lp(a) (≥ 30.23 mg/dL) had an increased risk of poor collateralization compared with those with low tertile of Lp(a) (< 12.66 mg/dL) (adjusted OR = 4.300, 3.970 and 4.386, respectively, all P < 0.001).ConclusionsIncreased Lp(a) confers greater risk for poor coronary collateralization when total cholesterol, LDL-C or non-HDL-C are elevated especially for patients with type 2 diabetes.
Highlights
We investigated whether or to what extent the interaction of lipoprotein (a) [Lp(a)] with cholesterolcontaining lipids was associated with angiographic coronary collateralization in type 2 diabetic patients with chronic total occlusion
Arteriogenesis is likely caused by a combination of mechanical and chemical factors, whereas angiogenesis is thought to be related to tissue hypoxia and the chemical factors produced under these conditions [2, 3]
Baseline characteristics Among overall 1284 patients, poor coronary collateralization occurred in 323 diabetic (45.8%) and 182 nondiabetic patients (31.5%), respectively (P < 0.001)
Summary
We investigated whether or to what extent the interaction of lipoprotein (a) [Lp(a)] with cholesterolcontaining lipids was associated with angiographic coronary collateralization in type 2 diabetic patients with chronic total occlusion. Arteriogenesis is likely caused by a combination of mechanical (shear stress) and chemical factors (related to ischemia and genes activated by ischemia), whereas angiogenesis is thought to be related to tissue hypoxia and the chemical factors produced under these conditions [2, 3] These processes of growth and maturation of coronary collateral vessels are influenced by multiple clinical and biochemical factors, inflammatory cytokines, and growth factors [5,6,7,8,9]. Hypercholesterolemia with high levels of LDL-C and/or low levels of high-density lipoprotein cholesterol (HDL-C) is an established coronary risk factor that induces endothelial cell dysfunction and impairs collateral vessel growth [17]. Non-high-density lipoprotein cholesterol (non-HDL-C)—the sum of cholesterol in other lipoproteins except for high-density lipoprotein—is closely associated with coronary atheroma progression and cardiovascular outcome, and has been proposed to improve risk estimation beyond total cholesterol and/or LDL-C [18, 19], especially for individuals with LDL-C levels that are not high or have already reached the treatment goal when the triglyceride level is elevated [20]
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