The American Heart Association (AHA) and Heart Failure Society (HFS) released a joint scientific statement summarizing the epidemiology, pathophysiology, and effects of type 2 diabetes (T2D) control on heart failure (HF) outcomes. The full report was published online in Circulation.1

Epidemiology of T2D and HF

In the past decade, the prevalence of T2D has increased by approximately 30%, with an estimated 30.3 million people in the United States having diabetes in 2015, according to statistics from the Centers for Disease Control and Prevention.1,2 The presence of T2D can be a risk factor for HF, and both diseases increase risk for the other disease. Results from the Framingham Heart Study showed a 2-fold increase in the risk for incident HF in men with T2D and a 4-fold increase in risk for incident HF in women with T2D in analyses adjusted for other cardiovascular risk factors.3

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Inadequate glycemic control also increases HF risk, with each 1% increase in hemoglobin A1c (HbA1c) corresponding to an 8% to 36% increase in risk for incident HF.1

Pathophysiology of T2D and HF

Intrinsic to the pathophysiology of HF is metabolic impairment, with up to 60% of patients with HF having insulin resistance. In addition, T2D itself can contribute to structural heart disease through myocardial ischemia/infarction. Consistently high blood glucose levels can result in excessive inflammation and vascular smooth muscle cell proliferation, causing an acceleration of atherosclerosis. Hyperglycemia may also lead to the production of advanced glycation end products, which form cross-links in collagen and lead to increased myocardial stiffness and fibrosis as well as cardiac relaxation impairment.1

Impact of T2D Management on HF Outcomes

The AHA and HFS emphasized that patients with HF and T2D experience worse clinical outcomes compared with patients with HF but without T2D. Many multivariable risk models, including the MAGGIC (Meta-analysis Global Group in Chronic Heart Failure) risk score, indicate T2D as an independent risk factor for death in HF.1

Research has shown that intensive glycemic control may not reduce all-cause mortality or stroke risk but may reduce the long-term risk for microvascular events. Current data do not support a link between achieving better glycemic control and reducing the risk of developing HF. The majority of clinical guidelines for diabetes recommend HbA1c thresholds ≤7.0% for adults with adequately controlled T2D and no T2D complications or significant comorbidities. In older adults with established microvascular or macrovascular complications and/or comorbidities, recommended HbA1c thresholds are between 8% and 8.5%.1

Comorbidity burden should be taken into account when determining an optimal glycemic target in the context of both T2D and HF. Based on current HF-specific data, a target HbA1c range should be 7% to 8% for most patients with T2D and HF.1

T2D Therapies and Their Impact on HF

The preferred treatment for T2D in the absence of contraindications is metformin. According to the literature, observational studies suggest that metformin is associated with reduced mortality in patients with HF vs controls, despite previously being contraindicated in HF. The scientific statement suggests that use of metformin is reasonable in patients with T2D who are at risk for or have established HF. Patients with acute conditions associated with lactic acidosis, however, should discontinue use.1

This article originally appeared on The Cardiology Advisor