NEW YORK (Reuters Health) – More intensive blood glucose lowering won’t reduce the risk of heart failure in patients with type 2 diabetes, and when achieved with a thiazolidinedione, may actually increase the risk, according to results of a meta-analysis of relevant studies.
Heart failure is a “common and important complication of diabetes,” John J. V. McMurray, from BHF Glasgow Cardiovascular Research Centre, University of Glasgow, United Kingdom, who worked on the study, told Reuters Health.
“Observational data have suggested that higher blood glucose and haemoglobin A1c are associated with a greater risk of heart failure,” he explained. Yet, large randomized trials testing whether tight glucose control might reduce the risk of heart failure have yielded inconclusive and conflicting results.
The meta-analysis Dr. McMurray and colleagues performed failed to show a benefit of tight glycemic control on heart failure risk reduction. The study was published online October 10 in the American Heart Journal.
Their analysis included 8 studies that compared a more intensive glucose-lowering regimen to a standard one in 37,229 patients with type 2 diabetes, with follow-up ranging from 2 to 10 years. The overall number of heart failure-related events was 1,469 – more than half of these (55%) in the intensive treatment arm.
The investigators report that the average difference in glycated hemoglobin level between patients given standard treatment and those allocated to a more intensive regimen was 0.9%.
In the pooled analysis, when compared with conventional treatment, intensive glucose control did not influence the overall occurrence of heart failure-related events, with a nonsignificant 20% increase in risk (odds ratio 1.20).
They note, however, that the “the effect estimate was highly heterogeneous, with almost 70% of variability across studies attributable to heterogeneity rather than chance.”
A subgroup analysis found an odds ratio of 1.33 for heart failure-related events when intensive glycemic control was achieved using a thiazolidinedione.
There are several possible reasons why intensive glucose control does not lead to the reduction in risk of heart failure “predicted by epidemiological studies,” the authors note.
It 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 (i.e., is a marker rather than mediator).”
The current findings, Dr. McMurray said, “add to recent evidence of lack of macrovascular benefit (heart attacks, strokes, and now heart failure) of more intensive glycaemic control.”
“It is also important to point out,” he said, “that better glycaemic control does seem to reduce the risk of microvascular complications” such as diabetic eye disease, nephropathy and neuropathy.
Am Heart J 2011.
