Artigo Acesso aberto Revisado por pares

C-Reactive Protein Levels Following Acute Myocardial Infarction

2004; American Diabetes Association; Volume: 27; Issue: 12 Linguagem: Inglês

10.2337/diacare.27.12.2971

ISSN

1935-5548

Autores

Vincent Wong, Mark McLean, Steven Boyages, N. Wah Cheung,

Tópico(s)

Cardiovascular Function and Risk Factors

Resumo

Acute myocardial infarction (AMI) triggers an inflammatory reaction, which plays an important role in myocardial injury (1). Inflammatory markers such as C-reactive protein (CRP) reflect the extent of myocardial necrosis and correlate with cardiac outcomes following AMI (2–4). Hyperglycemia has proinflammatory effects, inducing the release of inflammatory cytokines (5) and is associated with increased mortality from AMI (6,7). Conversely, insulin-based therapy in patients following AMI may confer survival benefits, but the mechanism is unclear (8–11). Insulin suppresses the inflammatory response (12), but it is uncertain if the anti-inflammatory effect of insulin therapy depends on glycemic status. The Hyperglycemia: Intensive Insulin Infusion In Infarction (HI-5) study is a multicentered randomized trial of insulin infusion for hyperglycemic patients with AMI. In this substudy, we examined the relationship between blood glucose levels (BGLs) and the inflammatory response (CRP levels) following AMI and evaluated the effect of insulin-based infusion therapy. In the HI-5 study, patients presenting with AMI within 24 h who either had known diabetes or admission BGL ≥7.8 mmol/l were recruited. AMI was defined by a plasma troponin T level of 0.1 μg/l. Following written consent, patients were randomized to either intensive or conventional therapy. Intensive therapy consisted of insulin-dextrose infusion for at least 24 h. Patients were given 5% dextrose at 80 ml/h, while …

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