Diabetes is a potent risk factor for adverse outcomes following acute myocardial infarction,1 but the mechanisms responsible for this association are not well understood.
Diabetes is a potent risk factor for adverse outcomes following acute myocardial infarction,1 but the mechanisms responsible for this association are not well understood. Factors that may contribute to worse outcomes in patients with diabetes include more extensive coronary disease, preexisting left ventricular systolic and/or diastolic dysfunction, impaired infarct healing, and altered myocardial substrate utilization and metabolism.
It has also long been recognized that clinical heart failure occurring in the setting of acute myocardial infarction substantially increases both short- and long-term mortality, and that more severe heart failure translates to a correspondingly worse prognosis.2 Further, patients with diabetes who suffer acute myocardial infarction are at increased risk for developing heart failure,1 and it therefore seems likely that the presence of acute heart failure, implying a tenuous hemodynamic state, is an important mediator of the adverse outcomes associated with diabetes.
Until recently, a noninvasive, inexpensive, and clinically useful “window” into the internal state of cardiac hemodynamics was not readily available. However, with the advent of assays for measuring circulating levels of B-type natriuretic peptide (BNP) and its precursor, N-terminal pro-BNP (Nt-pro-BNP), which are released by the cardiac ventricles in response to increased wall stress, it is now possible to use these markers as indexes of acute cardiac stress. Indeed, as anticipated, elevated levels of these peptides have been consistently shown to be associated with worse prognosis, both in patients with acute coronary syndromes,3,4 as well as in those with acute decompensated heart failure in the absence of ischemia.5,6
In the present study, Vergès measured Nt-pro-BNP levels in 199 patients with diabetes and 361 without who were hospitalized with acute myocardial infarction.7 As in prior studies, hospital mortality was substantially higher in the diabetic subgroup—by 4.7-fold. Nt-pro-BNP levels were also significantly higher among those with diabetes than those without diabetes (mean 245 pmol/L vs 130 pmol/L, < .001), as well as in patients who died compared to those who survived. In multivariate analysis, diabetes was an independent predictor of increased mortality, but the magnitude of this effect was diminished when Nt-pro-BNP was introduced into the model. The author concluded that the increased mortality following acute myocardial infarction in patients with diabetes is partially accounted for by elevated Nt-pro-BNP, reflecting significant myocardial decompensation.
The key message from this analysis is that diabetes and elevated Nt-pro-BNP are both strong independent predictors of increased short-term mortality following acute myocardial infarction. Thus, although it is true that the impact of diabetes was decreased after Nt-pro-BNP levels were taken into account, diabetes nonetheless remained an independent predictor of increased hospital mortality ( = .01). Additional research is therefore required to elucidate other mechanisms contributing to worse outcomes in patients with diabetes.
What are the clinical implications of this report? The findings of Vergès are important because they show that both diabetes and elevated Nt-pro-BNP levels are strong, interrelated, but nonetheless independent predictors of increased mortality following acute myocardial infarction. Each marker thus identifies a high-risk subgroup, and patients who have both diabetes and an elevated Nt-pro-BNP level are at highest risk; as such, these patients should be targeted for maximally intensive therapy.