This study is just published. When looking at this study, there are four key factors to consider:
- This is a study that looks at correlation, it does not specifically test cause. People who had evidence of sustained exposure to higher blood glucose levels had worse outcomes, for whatever mix of reasons.
- This study did not look at micro-vascular disease (such as nerve damage, kidney damage or eye damage) or rate of deterioration of glucose control, so the study does not say that there might not be health benefit from achieving a HgA1c of less than 6.5%
- I’ll have to wait to see the full text of the study (and consider input from others who will doubtless publish commentary) to consider what further might be said of this study. For example, the fact that the results of the study did not suggest a protective effect from having HgA1C below 6.5% could be related to low numbers of the study group reaching such a relatively good level of control – although this was probably accounted for. Only further examination of the full study report will tell.
- Also, HgA1C is only one way of looking at blood glucose levels. It does not give information about aspects of blood glucose that vary between people, such as the degree of elevation of fasting glucose versus glucose spikes after meals.
Relationship between HbA(1c) levels and risk of cardiovascular adverse outcomes and all-cause mortality in overweight and obese cardiovascular high-risk women and men with type 2 diabetes.
Department of Cardiology, Gentofte University Hospital of Copenhagen, Niels Andersens vej 65, 2900, Hellerup, Denmark, email@example.com.
The optimal HbA(1c) concentration for prevention of macrovascular complications and deaths in obese cardiovascular high-risk patients with type 2 diabetes remains to be established and was therefore studied in this post hoc analysis of the Sibutramine Cardiovascular OUTcomes (SCOUT) trial, which enrolled overweight and obese patients with type 2 diabetes and/or cardiovascular disease.
HRs for meeting the primary endpoint (nonfatal myocardial infarction, nonfatal stroke, resuscitated cardiac arrest or cardiovascular death) and all-cause mortality were analysed using Cox regression models.
Of 8,252 patients with type 2 diabetes included in SCOUT, 7,479 had measurements of HbA(1c) available at baseline (i.e. study randomisation). Median age was 62 years (range 51-86 years), median BMI was 34.0 kg/m(2) (24.8-65.1 kg/m(2)) and 44% were women. The median HbA(1c) concentration was 7.2% (3.8-15.9%) (55 mmol/l [18-150 mmol/l]) and median diabetes duration was 7 years (0-57 years). For each 1 percentage point HbA(1c) increase, the adjusted HR for the primary endpoint was 1.17 (95% CI 1.11, 1.23); no differential sex effect was observed (p = 0.12 for interaction). In contrast, the risk of all-cause mortality was found to be greater in women than in men: HR 1.22 (1.10, 1.34) vs 1.12 (1.04, 1.20) for each 1 percentage point HbA(1c) increase (p = 0.02 for interaction). There was no evidence of increased risk associated with HbA(1c) ≤6.4% (≤46 mmol/l). Glucose-lowering treatment regimens, diabetes duration or a history of cardiovascular disease did not modify the associations.
In overweight, cardiovascular high-risk patients with type 2 diabetes, increasing HbA(1c) concentrations were associated with increasing risks of cardiovascular adverse outcomes and all-cause mortality.
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