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Intensive glycemic control failed to lower heart failure risk in patients with type 2 diabetes
Castagno D. Am Heart J. 2011;162:938-948.
Results of a large meta-analysis involving more than 37,000 patients suggest that intensive glycemic control does not prevent heart failure in patients with type 2 diabetes. In fact, data linked certain treatment regimens to an increased risk for heart failure events.
“This finding contrasts with the large body of epidemiological evidence indicating a relationship between blood glucose level and/or HbA1c and the risk of heart failure,” researchers wrote in the American Heart Journal study.
Researchers studied data from 37,229 patients included in eight randomized trials that compared an intensive glucose-lowering regimen with standard treatment. Follow-up in the trials ranged from 2.3 years to 10.1 years, with 19,562 patients randomly assigned to intensive therapy and 17,667 to standard therapy. Most patients were white men aged older than 60 years with a mean BMI of 30. Mean duration of diabetes was 8 years and nearly half reported experiencing previous cardiovascular events.
Weighted mean HbA1c was 0.9% lower in the intensive treatment arm vs. the standard treatment arm. Fifty-five percent of all 1,469 heart failure-related events occurred in patients assigned to intensive therapy. The overall event rate for either study group was eight per 1,000 person-years of follow-up. Further, risk for heart failure appeared similar between both study groups (OR=1.2; 95% CI, 0.96-1.48). However, there were significant differences in the number of events and the event rates among all studies.
A pooled analysis of trials in which more patients in the intensive group received thiazolidinediones, such as pioglitazone (Actos, Takeda) and rosiglitazone (Avandia, GlaxoSmithKline), indicated that intensive therapy with these medications raised the risk for heart failure (OR=1.33; 95% CI, 1.02-1.72). In contrast, a subgroup analysis of trials in which patients primarily used other drugs, such as sulfonylureas, metformin or insulin, intensive treatment had a neutral effect on HF risk (OR=0.96; 95% CI, 0.81-1.31). Again, the researchers noted significant heterogeneity among results.
“The reason why intensive glucose control does not lead to the reduction in risk of heart failure predicted by epidemiological studies is uncertain but may reflect insufficient duration of treatment or follow-up, treatment intervention too late in the course of the disease, off-target toxicity of the treatments used, or because hyperglycemia per se does not directly cause heart failure in diabetic patients (ie, is a marker rather than a mediator),” they wrote.
Disclosure: The researchers report no relevant financial disclosures.
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Forty-three percent of patients admitted to the hospital with HF in the United States have diabetes. This is due to high incidences of left ventricular hypertrophy and coronary artery disease and a specific diabetic cardiomyopathy. The cardiomyopathy is a consequence of prolonged hyperglycemia, and it is therefore not surprising that glucose control did not affect the outcome [of this study]. The finding of increased heart failure with thiazolidinediones is due to increased salt and water retention in the distal tubule of the kidney, where PPAR-gamma receptors are more plentiful, resulting in an increase of plasma volume of as much as 5% to 6%, which leads to acute heart failure occurring earlier than it normally would have. However, the mortality of heart failure is not increased since, with earlier diagnosis, definitive therapy, such as RAS or beta-blockers, is initiated at an earlier stage.
– David S.H. Bell, MD, FACE, FACP
Endocrine Today Editorial Board member
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