MD Conference Express AHA 2013 - (Page 39)

The 2013 ACCF/AHA guideline for the management of HF provides some guidance for how to treat patients with diabetes and HF [Yancy CW et al. J Am Coll Cardiol 2013]. Among patients with Stage A HF, the 2013 guidelines recommend that clinicians make every effort to control hyperglycemia (Class I, Level of Evidence [LoE] C), even though control has not yet been shown to reduce the subsequent risk of HF. The reason for this is that many of the standard diabetes therapies can prevent the development of other HF risk factors and may by themselves directly lower the likelihood of HF. The guidelines recommend angiotensin-converting-enzyme (ACE) inhibitors (or angiotensin II receptor blockers [ARBs] in patients intolerant of ACE inhibitors) for all patients (regardless of diabetes status) with Stage C HF with reduced ejection fraction (HFrEF) and current or prior symptoms (both Class I, LoE A). With respect to β-blockers, the current guidelines recommend the use of bisoprolol, carvedilol, or sustained-release metoprolol succinate for all patients with current or prior symptoms of HFrEF (Class I, LoE A). In HF patients with diabetes, the marked clinical benefits of these therapies are considered to outweigh the risks of hypoglycemia and dyslipidemia or decreased insulin sensitivity. Clear benefit has also been shown for aldosterone receptor antagonists in HF patients with a history of diabetes (Class I, LoE B). Patients with diabetes, left ventricular dysfunction, mildly symptomatic HF, and wide QRS complex derive similar benefit from cardiac resynchronization therapy defibrillation compared with patients without diabetes [Martin D et al. Circ Heart Fail 2011], and those without significant diabetic complications are eligible for transplantation [Russo M et al. Circulation 2006]. There are no differences in the recommendations for patients with diabetes and HF with preserved ejection fraction. Daniel Kelly, MD, Sanford-Burnham Medical Research Institute at Lake Nona, Orlando, Florida, USA, discussed an emerging theory in diabetic cardiac dysfunction-lipotoxic cardiomyopathy, which he believes reflects a more systemic problem driven by caloric excess. For centuries, pathologists have noted an accumulation of neutral lipids in cardiac myocytes during autopsy of morbidly obese individuals, many of whom had diabetes. More recently imaging studies in living patients with obesity and diabetes have shown evidence of increased myocardial fatty acid utilization and cardiac steatosis [Herrero P et al. J Am Coll Cardiol 2006; Szczepaniak LS et al. Magn Reson Med 2003]. These results, along with other studies focused on glucose toxicity and microvascular disease have led to a general view of the metabolic disturbances that occur in diabetic cardiac dysfunction. This view begins with insulin resistance in type 2 diabetes that reduces the ability of the heart to use glucose as fuel and consequently forces increased fatty acid burning, which in turn results in lipid accumulation that is associated with early-stage diastolic and then systolic ventricular dysfunction, and sensitivity to ischemic insult. The rationale for serum lipid-lowering strategies in the treatment of diabetic cardiomyopathy has been demonstrated in several preclinical mouse models [Duncan JG et al. Circulation 2010; Yang J et al. Circ Res 2007; Finck BN et al. Proc Natl Acad Sci USA 2003]. Dr. Kelly presented a model for lipotoxic organ dysfunction (Figure 1) in which the adipocytes have no more capacity to store fat and the calories end up in other tissues as neutral lipid droplets-including the heart. To define the mechanism and perhaps identify targets for metabolic modulator therapy that would be given along with traditional HF therapy, Dr. Kelly and colleagues have embarked on a small-molecule high throughput screen. One promising compound has been shown to reduce myocyte triglyceride accumulation and increases fat burning capacity, fatty acid oxidation rates, and glucose uptake. Further studies are needed to determine if this compound has the potential improve clinical outcomes in patients with diabetes and warrents further study. Figure 1.Figure 1 Systemic Model of Lipotoxic Organ Dysfunction 18. Diabetes; Insulin Resistance Heart Failure Obesity Insulin Resistance Diabetes Reproduced with permission from D Kelly, MD. Although the exact mechanism remains unclear there is little doubt that there is a relationship between diabetes and HF and that the incidence of both of these life altering diseases is increasing. Patients with diabetes should be encouraged manage their risk through lifestyle changes and adherence to their treatment regimen. Clinicians treating patients with HF should manage their patients according to published guidelines. Official Peer-Reviewed Highlights From the American Heart Association Scientific Sessions 2013 39 

Table of Contents for the Digital Edition of MD Conference Express AHA 2013

Contents

MD Conference Express AHA 2013

https://www.nxtbook.com/nxtbooks/md_conference_express/AHA2013
https://www.nxtbookmedia.com