Broedl Uli C, Lebherz Corinna, Lehrke Michael, Stark Renee, Greif Martin, Becker Alexander, von Ziegler Franz, Tittus Janine, Reiser Maximilian, Becker Christoph, Göke Burkhard, Parhofer Klaus G, Leber Alexander W
Department of Internal Medicine II, University of Munich, Munich, Germany.
PLoS One. 2009;4(3):e4733. doi: 10.1371/journal.pone.0004733. Epub 2009 Mar 6.
Atherosclerosis is the primary cause of coronary artery disease (CAD). There is increasing recognition that lesion composition rather than size determines the acute complications of atherosclerotic disease. Low serum adiponectin levels were reported to be associated with coronary artery disease and future incidence of acute coronary syndrome (ACS). The impact of adiponectin on lesion composition still remains to be determined.
METHODOLOGY/PRINCIPAL FINDINGS: We measured serum adiponectin levels in 303 patients with stable typical or atypical chest pain, who underwent dual-source multi-slice CT-angiography to exclude coronary artery stenosis. Atherosclerotic plaques were classified as calcified, mixed or non-calcified. In bivariate analysis adiponectin levels were inversely correlated with total coronary plaque burden (r = -0.21, p = 0.0004), mixed (r = -0.20, p = 0.0007) and non-calcified plaques (r = -0.18, p = 0.003). No correlation was seen with calcified plaques (r = -0.05, p = 0.39). In a fully adjusted multivariate model adiponectin levels remained predictive of total plaque burden (estimate: -0.036, 95%CI: -0.052 to -0.020, p<0.0001), mixed (estimate: -0.087, 95%CI: -0.132 to -0.042, p = 0.0001) and non-calcified plaques (estimate: -0.076, 95%CI: -0.115 to -0.038, p = 0.0001). Adiponectin levels were not associated with calcified plaques (estimate: -0.021, 95% CI: -0.043 to -0.001, p = 0.06). Since the majority of coronary plaques was calcified, adiponectin levels account for only 3% of the variability in total plaque number. In contrast, adiponectin accounts for approximately 20% of the variability in mixed and non-calcified plaque burden.
CONCLUSIONS/SIGNIFICANCE: Adiponectin levels predict mixed and non-calcified coronary atherosclerotic plaque burden. Low adiponectin levels may contribute to coronary plaque vulnerability and may thus play a role in the pathophysiology of ACS.
动脉粥样硬化是冠状动脉疾病(CAD)的主要病因。人们越来越认识到,病变的组成而非大小决定了动脉粥样硬化疾病的急性并发症。据报道,血清脂联素水平低与冠状动脉疾病及急性冠状动脉综合征(ACS)的未来发病率相关。脂联素对病变组成的影响仍有待确定。
方法/主要发现:我们测量了303例有典型或非典型胸痛症状的稳定型患者的血清脂联素水平,这些患者接受了双源多层CT血管造影以排除冠状动脉狭窄。动脉粥样硬化斑块被分类为钙化斑块、混合斑块或非钙化斑块。在双变量分析中,脂联素水平与冠状动脉总斑块负荷呈负相关(r = -0.21,p = 0.0004),与混合斑块(r = -0.20,p = 0.0007)和非钙化斑块(r = -0.18,p = 0.003)呈负相关。与钙化斑块无相关性(r = -0.05,p = 0.39)。在一个完全调整的多变量模型中,脂联素水平仍然可预测总斑块负荷(估计值:-0.036,95%置信区间:-0.052至-0.020,p<0.0001)、混合斑块(估计值:-0.087,95%置信区间:-0.132至-0.042,p = 0.0001)和非钙化斑块(估计值:-0.076,95%置信区间:-0.115至-0.038,p = 0.0001)。脂联素水平与钙化斑块无关(估计值:-0.021,95%置信区间:-0.043至-0.001,p = 0.06)。由于大多数冠状动脉斑块是钙化的,脂联素水平仅占总斑块数变异性的3%。相比之下,脂联素约占混合斑块和非钙化斑块负荷变异性的20%。
结论/意义:脂联素水平可预测混合和非钙化冠状动脉粥样硬化斑块负荷。低脂联素水平可能导致冠状动脉斑块易损性增加,因此可能在ACS的病理生理学中起作用。