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Persistent endothelial dysfunction is related to elevated C-reactive protein (CRP) levels in Type II diabetic
Thomas Nyström1, Arne Nygren, Ake Sjöholm
1Department of Internal Medicine, Karolinska Institute, Stockholm South Hospital, SE-118 83 Stockholm, Sweden. thomas.nystrom@sos.sll.se
Insights
Type II diabetes patients show persistent endothelial dysfunction and inflammation after acute myocardial infarction, unlike non-diabetic patients. This may explain their poorer outcomes in coronary artery disease.
Area of Science:
- Cardiology
- Endocrinology
- Vascular Biology
Background:
- Type II diabetes is linked to poor outcomes in acute coronary artery disease, beyond traditional risk factors.
- Endothelial dysfunction and inflammation are key aspects of atherosclerosis.
Purpose of the Study:
- To compare non-traditional risk factors, including endothelial function and inflammatory markers, in Type II diabetic versus non-diabetic patients post-acute myocardial infarction (AMI).
Main Methods:
- Assessed brachial artery flow-mediated vasodilatation (FMD) and nitroglycerine-induced vasodilatation (NTG) via ultrasound.
- Measured plasma levels of C-reactive protein (CRP) and adiponectin using ELISA.
- Compared Type II diabetic (n=20) and non-diabetic (n=25) patients at baseline and 60-day follow-up after AMI.
Main Results:
- At baseline, adiponectin levels were lower in diabetic patients; FMD and CRP did not differ.
- At 60 days, diabetic patients exhibited significantly lower FMD, higher CRP, and lower adiponectin compared to non-diabetic patients.
- Both groups showed improved NTG responses, indicating preserved endothelium-independent function.
Conclusions:
- Type II diabetes is associated with persistent endothelium-dependent dysfunction and elevated inflammatory activity following AMI.
- These non-traditional risk factors may contribute to the adverse outcomes observed in diabetic patients with coronary artery disease.
Abstract:
The atherosclerotic process is an ongoing dynamic and progressive state arising from endothelial dysfunction and inflammation. Although suffering from an acute coronary artery disease, patients with Type II diabetes have a poor outcome compared with non-diabetic patients, which may only partly be explained by traditional risk factors. Our purpose was to compare non-traditional risk factors, such as endothelial function, C-reactive protein (CRP) and adiponectin, in Type II diabetic and non-diabetic patients following AMI (acute myocardial infarction). Twenty Type II diabetic patients were compared with 25 non-diabetic patients at baseline (1-3 days from the onset of chest pain) and at 60 days follow-up after an AMI. Using high-resolution ultrasound, brachial artery responses to FMD (flow-mediated vasodilatation; endothelium-dependent vasodilatation) and NTG (nitroglycerine-induced vasodilatation; endothelium-independent vasodilatation) were measured. Plasma levels of CRP and adiponectin were measured by ELISA. At baseline, FMD (1.9 compared with 3.2%; P=0.22) and CRP levels (6.95 compared with. 5.51 mg/l; P=0.40) did not differ between Type II diabetic and non-diabetic patients, whereas adiponectin levels were lower in Type II diabetic patients (2.8 compared with 5.0 ng/ml; P<0.05). At 60 days follow-up, there were significant differences in FMD (1.5 compared with 4.1%; P<0.02), CRP (4.23 compared with 1.46 mg/ml; P<0.01) and adiponectin (3.3 compared with 5.3 ng/ml; P<0.05) levels between Type II diabetic and non-diabetic patients. In contrast, NTG responses improved in both groups between baseline and follow-up (Type II diabetic patients, 9.7 compared with 13.2% respectively, P<0.05; non-diabetic patients, 7.9 compared with 12.4% respectively, P<0.01). These results show a persistent endothelium-dependent dysfunction and inflammatory activity in patients with Type II diabetes, but not in non-diabetic patients, after AMI. These findings may, in part explain, the poor outcome in coronary artery disease seen in Type II diabetes.
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