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The edict from DCCT/EDIC: Reducing the risk of cardiovascular disease in people with type 1 diabetes

Vinod Patel
Diabetes care has improved substantially in the UK, and we can congratulate ourselves on many of the care processes and clinical outcomes achieved. Unfortunately, the main successes have been in people with type 2 diabetes, with National Diabetes Audit data revealing worse care in people with type 1 versus type 2 diabetes.

Diabetes care has improved substantially in the UK, and we can congratulate ourselves on many of the care processes and clinical outcomes achieved. Unfortunately, the main successes have been in people with type 2 diabetes, with National Diabetes Audit data revealing worse care in people with type 1 versus type 2 diabetes.

Type 1 diabetes carries a high risk of cardiovascular disease (CVD) and is the most common cause of premature CVD morbidity and mortality (Lind et al, 2011; Harding et al, 2014). The DCCT (Diabetes Control and Complications Trial) showed that an average 6.5 years of intensive diabetes treatment achieving a mean HbA1c of 56 mmol/mol (7.2%) substantially reduced microvascular complications compared with conventional treatment achieving an HbA1c of 76 mmol/mol (9.1%; DCCT Research Group, 1993). 

After study closure and an additional 11 years of observational follow-up in the EDIC (Epidemiology of Diabetes Interventions and Complications) study, the risk of major adverse cardiac events (MACE; cardiovascular death, non-fatal myocardial infarction [MI] or non-fatal stroke) was reduced by 58%, and aggregate CVD (MACE plus confirmed angina, silent MI, revascularisation or congestive heart failure) by 42%, in the original intensive treatment group (Nathan et al, 2005).

In the article summarised alongside, the DCCT/EDIC Research Group report their 30-year follow-up data (mean follow-up, 26 years). A substantial 86% of the original cohort were included in this latest analysis. Despite comparable treatment for more than 25 years and near equalisation of achieved HbA1c levels, the benefits of what the authors termed “metabolic memory” were apparent. In the intensive treatment group, 147 cardiovascular events were reported in 82 people, significantly less than the 217 events in 102 people observed in the conventional treatment group. This is equivalent to a rate of 0.81 cardiovascular events per 100 person-years in the intensive group versus 1.18 events per 100 person-years in the conventional group. The average age was only 55 years. This 30% reduction in any CVD was similar to the 32% reduction in MACE that was observed.

The UKPDS (UK Prospective Diabetes Study) showed a similar effect in people with type 2 diabetes, a phenomenon termed the “legacy effect” of good initial glycaemic control (Holman et al, 2008). However, it is important to differentiate this from good control in older people with high CVD risk; in these subjects, implementing very tight glycaemic control in fact resulted in increased mortality and mortality in some studies (Hayward et al, 2015).

A second DCCT/EDIC report (summarised on the facing page) is a detailed analysis of the overall risk factors for CVD at the 30-year follow-up point. Multivariate Cox proportional hazard models were used to assess traditional and novel risk factors for MACE and all CVD. Age and HbA1c were strongly associated with MACE and all CVD. For each 11-mmol/mol (1.0%) increase in mean HbA1c, the risk of all CVD and MACE rose by 31% and 42%, respectively. CVD and MACE were associated with seven other conventional risk factors but not with gender. This makes the point that in type 1 diabetes, the usual protective effect of female gender is lost. The other main significant risk factors were baseline age, mean pulse rate, raised triglyceride levels, systolic blood pressure, smoking, baseline diabetes duration and current LDL-cholesterol level. Current use of an angiotensin-converting enzyme (ACE) inhibitor was protective.

To conclude, people with type 1 diabetes may be the lost tribe caught in the maelstrom of the type 2 diabetes epidemic. Care for this <10% of the diabetes population as always been problematic. The edict? Blood pressure control, ACE inhibitor use and lipid control are all important in reducing CVD risk. However, we must re-focus our attention on achieving early good glycaemic control and maintaining it.

To read the article summaries, please download the PDF

REFERENCES:

Diabetes Control and Complications Trial Research Group (1993) The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med 329: 977–86
Harding JL, Shaw JE, Peeters A et al (2014) Mortality trends among people with type 1 and type 2 diabetes in Australia: 1997–2010. Diabetes Care 37: 2579–86
Hayward RA, Reaven PD, Wiitala WL et al (2015) Follow-up of glycemic control and cardiovascular outcomes in type 2 diabetes. N Engl J Med 372: 2197–206
Holman RR, Paul SK, Bethel MA et al (2008) 10-year follow-up of intensive glucose control in type 2 diabetes. N Engl J Med 359: 1577–89
Lind M, Bounias I, Olsson M et al (2011) Glycaemic control and incidence of heart failure in 20,985 patients with type 1 diabetes: an observational study. Lancet 378: 140–6
Nathan DM, Cleary PA, Backlund JY et al (2005) Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes. N Engl J Med 353: 2643–53

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