Heart failure in diabetes: are we late?

Abstract

Heart failure (HF) affects between 2% and 3% of the general population, but its prevalence can exceed 10% in people over 70 years of age. Diabetes mellitus (DM) is an independent risk factor for the development of HF, increasing the risk 2- to 4-fold in both men and women.

In patients with DM, HF is not only a common cardiovascular complication but may also represent the first clinical manifestation, even in the absence of prior coronary artery disease. This association translates into an increased risk of hospitalization, functional decline, and cardiovascular mortality¹.

From a pathophysiological perspective, DM contributes to the development of HF through multiple mechanisms, including myocardial ischemia, microvascular dysfunction, chronic inflammation, oxidative stress, mitochondrial dysfunction, alterations in cardiomyocyte energy metabolism, collagen glycation, and dysfunctional epicardial adipose tissue, among others. The current classification of HF is based on ejection fraction (EF): HF with reduced EF (HFrEF), mildly reduced EF, and HF with preserved EF (HFpEF). Although they present different clinical profiles, all share an adverse prognosis²

The universal definition of HF establishes structured criteria for its diagnosis, including typical symptoms and signs, objective evidence of cardiac structural or functional abnormality associated with signs of systemic or pulmonary congestion through echocardiographic signs of pressure overload or elevated natriuretic peptides³. However, diagnosis remains especially challenging in patients with HFpEF, in whom symptoms may be nonspecific and overlap with other conditions common in people with DM, such as obesity, chronic obstructive pulmonary disease (COPD), or functional impairment.

In this setting, pharmacological treatment has evolved significantly. Sodium-glucose cotransporter 2 inhibitors (SGLT-2 inhibitors) have been shown to reduce the combined risk of HF hospitalization and cardiovascular death in various patient profiles, with or without DM, and in any HF phenotype⁴.

Meanwhile, GLP-1 receptor agonists (GLP-1 RAs) showed benefits in HFpEF, while finerenone demonstrated efficacy in reducing cardiovascular and renal events in patients with T2DM and chronic kidney disease⁵.

Managing patients with T2DM and HF requires a multidimensional strategy. Beyond glycemic and hemodynamic control, it is essential to incorporate therapies with robust evidence of reducing major clinical events. This paradigm shift transcends traditional metabolic control and guides treatment toward preventing cardiovascular and renal complications, prioritizing a personalized approach that optimizes long-term clinical outcomes.