Improved glycemic control may help prevent heart failure, according to a study recently published in The Lancet.
Improved glycemic control may help prevent heart failure, according to a recent study published in The Lancet.
The study enrolled 20,985 patients with type 1 diabetes to assess variables associated with cardiovascular disease, including age, sex, duration of diabetes, HbA1c, body mass index, systolic and diastolic blood pressure, LDL and HDL cholesterol, and smoking status.
Investigators identified the cohort of patients with type 1 diabetes from the Swedish National Diabetes Registry (NDR). Patients 18 years of age or older with no known history of heart failure were registered between January, 1998, and December, 2003. The patients were followed from their first inclusion in the NDR in 1998 to 2003, until hospital admission with a primary or secondary discharge diagnosis for heart failure, death, or the end of follow-up Dec. 31, 2009.
The study revealed 2 key findings. First, 635 (3%) patients had to be admitted to the hospital for heart failure, with an incidence of 3.38 events per 1,000 patient-years. In addition, patients with an HbA1c of at least 10.5% had a risk of heart failure 4 times greater than did those with an HbA1c of less than 6.5%. In the analysis of mean HbA1c as a continuous variable, each 1% increase was associated with a 30% higher risk of heart failure during follow-up, independent of other risk factors for heart failure.
The authors noted the high incidence of heart failure among study participants, despite the relatively youthful mean age at inclusion (38.6 years), and suggested that the substantially increased risk resulting from poor glycemic control indicates an independent role of glycemic control in the pathogenesis of heart failure.
“Because treatment for heart failure improves survival and quality of life, clinicians should be observant of signs of heart failure in management of patients with type 1 diabetes, starting at an early stage,” the report stated.
The study was supported by an unrestricted grant from AstraZeneca, Novo Nordisk Scandinavia, the Swedish Heart and Lung Foundation, and the Swedish Research Council. The authors stated that supporting organizations had no involvement in protocol design, data collection, data analysis, data interpretation, writing of the report, or the decision to submit the report for publication.