Low adiponectin levels are an independent predictor of mixed and non-calcified coronary atherosclerotic plaques.
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vor 15 Jahren
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. 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
(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. 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
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