Management of Diabetes in Patients with Heart Failure

Poorly controlled diabetes should be managed aggressively in any patient with CHF because the attendant metabolic stress can certainly have adverse effects on myocardial function. Stringent control of blood glucose reduces the incidence of several complications of diabetes, specifically retinopathy, neuropathy, and nephropathy, but no data are available pertaining to the long-term effects of stringent control on diabetic cardiomyopathy or CHF in general in patients with diabetes. To the extent that diabetic cardiomyopathy is caused by hyperglycemia per se (e.g., matrix glycosylation) or the intracellular metabolic effects of reduced glucose transport (e.g., free radical damage to membranes), normalization of carbohydrate metabolism makes intuitive sense. Moreover, stringent control has been shown to modestly reduce event rates after an index myocardial infarction. On the other hand, prolonged hyperinsulinemia may be atherogenic and pro-thrombotic in type II diabetic patients. Thus, it is appropriate to achieve stringent control with the lowest possible doses of insulin or secretagogues, including sulfonylureas. The use of insulin sensitizers (thiazoladinediones) and biguanides may facilitate achieving this objective. -o

The use of insulin-sensitizing agents in CHF patients (especially the PPAR |

ligand thiazolidinedione class) has considerable potential attractiveness. Such £

agents should in theory improve the defects in carbohydrate metabolism that are likely significant causes of diabetic cardiomyopathy. In contrast to insulin, their salutary effects on various determinants of and risk factors for atherosclerosis and vasculopathy have obvious potential benefit. Recent preliminary reports also indicate that these agents can inhibit ventricular hypertrophy caused by mechani-

& u cal stimuli. It is interesting to speculate that they might reverse the elevations in left ventricular mass observed in diabetic patients. Despite their promise, troglita-zone, the first thiazolidinedione to be released (and subsequently withdrawn) was relatively contraindicated in symptomatic CHF because it can worsen volume overload and edema. Hopefully, newer thiazolidinediones will be better tolerated. Metformin, which also has insulin-sensitizing properties, is relatively contraindicated in CHF because of potential exacerbation of volume overload, induction of prerenal azotemia, and risk of lactic acidosis.

To reiterate, management of diabetes in patients with CHF should focus on stringent control with minimization of hyperinsulinemia. If insulin therapy cannot be avoided, the overall advantages of stringent control outweigh its potential disadvantages.

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