Diabetic cardiomyopathy is defined as structural and functional myocardial impairment secondary to diabetes mellitus, in the absence of coronary artery disease, hypertension, or other causes of heart disease. (1) Its prevalence is uncertain, but it is estimated that approximately 12–22% of diabetic patients develop diabetic cardiomyopathy after 10 years of disease duration. (1) Therefore, it is essential to identify clinical, laboratory, and imaging markers that enable early diagnosis, allowing timely initiation of appropriate treatment and preventing disease progression.

Pathophysiologically, hyperglycemia, insulin resistance, and lipotoxicity induce oxidative stress, inflammation, cardiomyocyte apoptosis, and interstitial fibrosis, initially resulting in impaired ventricular relaxation, followed by left ventricular hypertrophy and, in advanced stages, impaired systolic function. (2)

Consequently, echocardiography is a useful, accessible, and reproducible imaging technique. It enables the identification of patients with diastolic dysfunction, an early marker of diabetic cardiomyopathy, (1) as well as patients with reduced global longitudinal strain before changes in ejection fraction occur, an early marker of systolic dysfunction. (3)

In the study entitled *“Differences in Diastolic Function and Global Longitudinal Strain on Stress Echocardiography between Elderly Diabetic and Nondiabetic* Patients” by Kufert et al., 176 diabetic patients and 771 non-diabetic patients underwent stress echocardiography. The researchers found that the group with diabetes had a higher prevalence of significant diastolic dysfunction, both at rest and during exercise, and that although left ventricular ejection fraction was normal and similar between the two groups, global longitudinal strain was significantly lower in diabetic patients. (4)

The study’s strengths include the number of patients enrolled, the systematic exclusion of coronary artery disease as a potential confounder, the incorporation of conventional echocardiographic parameters alongside global longitudinal strain, and the assessment of impaired diastolic reserve during exercise, thereby unmasking an abnormality that is often not apparent at rest.

As a limitation, considering this was a cross-sectional study, the true prognostic impact of the observed abnormalities cannot be established. Although the association of diabetes with diastolic dysfunction and reduced global longitudinal strain is consistent, this does not address whether these findings identify patients at higher risk of developing heart failure with preserved ejection fraction. In this context, it would have been of interest to examine variables related to the course of diabetes, particularly whether patients were receiving SGLT2 inhibitors or GLP-1 receptor agonists, given that these therapies have been shown to modify the risk of heart failure and could influence echocardiographic parameters. (2;3)

As suggested by this study, diabetes mellitus is independently associated with a higher prevalence of diastolic dysfunction and reduced global longitudinal strain, even in the presence of preserved ejection fraction, reinforcing the concept of subclinical myocardial involvement. Awareness of these findings allows the echocardiographer to focus the examination on assessing these parameters and provides the clinical cardiologist with a broader perspective when initiating or modifying treatment in this population, rather than focusing solely on coronary or peripheral vascular disease.