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J Am Coll Cardiol, 2006; 47:2124-2126, doi:10.1016/j.jacc.2006.02.033
(Published online 20 April 2006). © 2006 by the American College of Cardiology Foundation |
* Heidelberg University Hospital, Department of Medicine, INF 410, 69120 Heidelberg, Germany (Email: maximilian.eynatten{at}med.uni-heidelberg.de).
Two hundred forty-seven individuals, ages 31 to 83 years, who were undergoing clinically indicated coronary angiography at the University Hospital Heidelberg were enrolled. Treatment with peroxisome proliferator-activated receptor (PPAR)-alpha or PPAR-gamma agonists, known to affect adiponectin levels, was an exclusion criterion. Serum samples were obtained before angiography and frozen at 70°C until analyses were performed. Serum adiponectin was determined by enzyme-linked immunosorbent assay (B-Bridge-International, San Jose, California). The extent of angiographically documented CAD was quantified by two independent investigators as follows: 1) the SS as one-vessel, two-vessel, or three-vessel disease, defined as stenosis of more than 50% of the luminal diameter (3); and 2) the ES, in which atherosclerotic wall irregularities in 10 defined segments of the coronary arteries were evaluated (4). Two-tailed bivariate correlations were determined by the Spearman correlation coefficient, and comparisons between two sets of patients were performed with the Mann-Whitney U test. Comparisons between quartiles (SS) and quintiles (ES) were performed with the Kruskal-Wallis test. The study was approved by the ethics committee of Heidelberg University. All patients gave written informed consent.
Coronary artery disease was found in 172 patients. Compared with the 75 patients without CAD, the 172 men with CAD were older, more likely to be a current smoker, and had higher blood pressure and lower high-density lipoprotein cholesterol (data not shown). Adiponectin levels were significantly lower in patients with CAD than in those without (4.8 vs. 7.5 µg/ml; p < 0.001). The severity of CAD as quantified by SS correlated significantly with serum adiponectin (p < 0.001 by Kruskal-Wallis test) (Fig. 1A). In addition to severity of CAD, we further found a significant inverse correlation between serum adiponectin and the more sensitive ES (r = 0.23; p < 0.001). When patients were divided into quintiles of increasing ES, a stepwise decrease in adiponectin levels was associated with increasing extent of atherosclerotic wall irregularities (p < 0.001 by Kruskal-Wallis test) (Fig. 1B).
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Serum adiponectin was lower among patients with PPAR-gamma-2Pro12Ala (Ala-allele: 3.9 ± 0.4 µg/ml vs. Pro-allele: 5.9 ± 0.4 µg/ml; p = 0.001) and was increased in patients with adiponectin-T94G (G-allele: 7.6 ± 0.6 µg/ml vs. T-allele: 5.1 ± 0.5 µg/ml; p < 0.001). Moreover, patients with PPAR-gamma-2Pro12Ala showed increased CAD in ES (Ala-allele: 34.4 ± 4.0 vs. Pro-allele: 26.0 ± 2.7; p = 0.03) and a tendency toward increased CAD in SS (Ala-allele: 1.60 ± 0.19 vs. Pro-allele: 1.34 ± 0.09; p = 0.09). Patients with the adiponectin-T94G variant had significantly less CAD in both angiographic scores: ES (G-allele: 21.9 ± 3.1 vs. T-allele: 30.7 ± 2.3; p = 0.03) and SS (G-allele: 1.02 ± 0.14 vs. T-allele: 1.53 ± 0.10; p = 0.01). In an additional linear regression analysis with SS or ES as dependent variable, only adiponectin remained a significant predictor of CAD, with the two polymorphisms being inter-correlated with adiponectin (data not shown).
In summary, these data demonstrate that serum adiponectin levels and the extent of CAD show a significant correlation in men. These results were obtained with two established scores of which the ES in particular has been demonstrated to better correlate with cardiovascular risk factors than other scores (4). Furthermore, we demonstrate that genetic variations known to affect adiponectin levels were significantly associated with the extent of CAD. This is in accordance with a recent study reporting a genetic variability of the adiponectin gene (G276T) to be associated with a reduced cardiovascular risk in patients with T2D (7). Our results indicate that the measurement of serum adiponectin might represent a novel diagnostic tool to stratify patients at risk for CAD and to identify those patients who would benefit most from preventive strategies.
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