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Diabetes mellitus in patients with myocardial infarction complicated by heart failure: a ‘low ejection fraction’ equivalent?

Diabetes mellitus (DM) is a public health problem of massive and rising proportions; the estimated global prevalence of DM increased from 135 million in 1995 to over 220 million in 2009, and is projected to surpass 366 million by 2030. Compounded with the markedly increased risk of coronary heart disease (CHD) associated with DM, and with the high incidence of CHD-associated heart failure (HF) in patients with DM, the increase in prevalence of DM equates to more and more patients requiring concomitant management of DM, CHD, and HF. In this context, understanding the interactions among these conditions—from pathophysiology to epidemiology to clinical practice—has never been more imperative. More than a decade ago, it was postulated that diabetic patients with no history of CHD have a risk of myocardial infarction (MI) similar to that of non-diabetic patients with prior MI. Although the original study underpinning this concept had limited statistical power and precision, the concept that DM is a ‘CHD equivalent’ for long-term cardiovascular disease prognosis has contributed to more directed and intensive CHD risk mitigation efforts targeting the patient population with DM, for example, in specific guideline recommendations for more intensive management of lipids and blood pressure. More recent data from several large randomized trials suggest that the risk of CHD events in patients with DM, most of which comprised DM patients with prevalent CHD or clustered CHD risk factors, is significantly lower than the risk traditionally used to define ‘CHD equivalency’; that is, about 1% annualized CHD risk in most of the recent DM trials, contrasted with a 2% annualized CHD risk traditionally considered ‘CHD equivalent risk’. The lower risk observed in the DM trials likely reflects some degree of clinical success attributable to the more specifically targeted and aggressive risk intervention applied over the past decade. In a similar construct, the study by Shah et al. published in this issue of the European Journal of Heart Failure suggests that following an acute MI complicated by signs and/or symptoms of HF, DM is a ‘low left-ventricular ejection fraction (LVEF) equivalent’ with regard to subsequent clinical risk prediction. Analysing data from the Valsartan in Acute Myocardial Infarction (VALIANT) trial, a study of 14 703 patients with MI complicated by signs or symptoms of HF with or without compromised LVEF, DM was associated with an increased risk of adverse clinical events across the LVEF strata, including all-cause death, cardiovascular death, death or recurrent MI, and death or hospitalization for HF, such that non-diabetic patients with lower LVEF and diabetic patients with preserved LVEF had similar risks of adverse outcomes. Aside from potential implications for post-MI risk stratification, the concept of DM independent of EF as low-LVEF equivalent may prove useful with regard to clinical decision-making in the management of patients with DM and acute MI, much has been incorporated into guidelines and practice for the chronic ambulatory management of CHD risk in DM patients. For example, the long-term use of angiotensin-converting enzyme (ACE)-inhibitors post-MI is currently recommended in patients with low LVEF (,40%) as well as in patients with DM across the spectrum of ACS events, both in Europe and in the United States (class I, level of evidence A). 14 However, ACE-inhibitors continue to be under-used post-MI especially in patients with DM when compared with non-DM patients. The present findings of Shah et al. underscore the imperative to more equitably use evidence-based therapies, including but extending beyond ACE-inhibitors, post-MI in patients with DM with the goal of eroding the residual risk associated with DM in this population. Furthermore, while most guidelines specifically indicate that ACE-inhibitors should be started within 24 h of admission for MI in patients with decreased EF, 13 no such indication exists for patients with DM in the absence of decreased EF. Therefore, if DM is indeed a low-LVEF equivalent, perhaps early vs. later initiation of ACE-inhibitor therapy could yield incremental benefit in patients