Key result
Type II diabetes is linked to persistent endothelial dysfunction and elevated CRP 60 days post-MI.
Why the study?
Do Type II diabetic patients have worse endothelial function and inflammatory profiles compared to non-diabetic patients following acute myocardial infarction?
Observational (n=45)
Do Type II diabetic patients have worse endothelial function and inflammatory profiles compared to non-diabetic patients following acute myocardial infarction?
Absolute Event Rate: 1.5% vs 4.1%
p-value: p=<0.02
Type II diabetic patients exhibit persistent endothelium-dependent dysfunction and inflammatory activity 60 days after an acute myocardial infarction compared to non-diabetic patients, which may contribute to their poorer clinical outcomes.
Persistent endothelial dysfunction and inflammation may drive excess post-MI risk in type 2 diabetes; hypothesis-generating for targeted endothelial therapies.
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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Nyström et al. (2005) conducted an observational in Acute myocardial infarction (n=45). Type II diabetes vs. Non-diabetic patients was evaluated on Flow-mediated vasodilatation (FMD) at 60 days follow-up (p=<0.02). Type II diabetes was associated with persistent endothelial dysfunction (FMD 1.5% vs 4.1%, P<0.02) and elevated CRP (4.23 vs 1.46 mg/ml, P<0.01) at 60 days post-myocardial infarction.
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