(p(Homa-IR<2.5 vs. Homa-IR≥2.5)=0,035, p(Homa-IR<2.5 vs. control)=0,238, p(Homa-IR≥2.5 vs. control)=0,002).
Although the diastolic early filling time (E wave duration) was lower in the patient group than the control group, this difference was not statistically significant (p=0.052) . However, the E wave duration with insulin resistance was statistically more down in the group than the control group (68.60±19.24 (Homa-IR≥2.5), 83.50±16.35 (Control)); p=0.020) . It was revealed that the main reason for the significant differences in E/A and E/e’ ratios was the difference in E wave duration, also with the considerable effect of insulin resistance.
Studies conducted with insulin resistance have shown that insulin resistance may lead to subclinical myocardial and vascular irregularities, such as decreased global longitudinal strain values ​​and arterial stiffness in individuals without significant coronary artery disease. Insulin resistance, directly and indirectly, causes adverse effects in the vascular area. Endothelial dysfunction and disruption of the vasomotor response to the pro-inflammatory, pro-coagulant endothelium can be listed among these effects (33). In another study, insulin resistance has been shown to increase the likelihood of ischemia-related cardiac dysfunction (34). It can be thought that the stated effects of insulin resistance may be among the reasons for the differences in diastolic parameters we found in our study.
Prediabetic patients without previous coronary artery disease have been shown to have higher mpi scores than healthy populations, which has been associated with possible subclinical systolic and diastolic dysfunction (35). In our study, the septal mpi score (Tei index) was found to be significantly higher in patients with hypoglycemia, and no significant difference was found in the lateral mpi score (p=0.045 and p=0.474; respectively)
Similar effects of recurrent hypoglycemia have been demonstrated in animal experiments with mice, as demonstrated as increased carotid intima-media thickness due to hyperglycemia in persons with metabolic syndrome (19,36). Interestingly, an increase in the circulating catecholamine levels causes a decrease in the peripheral arterial resistance through β-2 receptor-mediated vasodilation. In the acute phase of hypoglycemia in healthy people, vascular elasticity increases. Additionally, increased catecholamine levels cause a decrease in peripheral arterial resistance with beta-2 receptor-associated vasodilation. However, hypoglycemia episodes (especially in diabetic patients) have been reported in previous studies to cause arterial stiffness. It has been shown that hematological and hemodynamic changes during hypoglycemia may play a role in this situation (12,14,37).
In our study, the patient group observed that the carotid intima-media thickness was more remarkable, and the brachial flow-mediated dilatation value was smaller, which is an indicator of endothelial dysfunction. It was revealed that findings related to carotid intima-media thickness was marked by insulin resistance (p(Homa-IR<2.5 vs. control)=0.027, p(Homa-IR≥2.5 vs. control)<0.001) . Still, in terms of brachial flow-mediated dilatation, when the groups with and without insulin resistance were compared with the control group, the significance levels were found to be similar(p(Homa-IR<2.5 vs. control)=0.027, p(Homa-IR≥2.5 vs. control)=0.028) . We can state that these findings are compatible with the pathophysiological process in related studies (12,14,21,34,37).
Considering the study population’s age group, the findings determined predominantly in terms of diastolic functions (also with endothelial functions) may be predictive for other cardiac pathologies. It was also revealed that the increase in insulin resistance might affect the distinction in diastolic function, septal isovolumetric relaxation time, and carotid intima-media thickness parameters found among the study groups.
We can state that our study will contribute to the literature in the light of echocardiographic findings and peripheral examinations after further evaluations of patients admitted to the emergency department with hypoglycemia. These findings may guide possible future studies that will be conducted with many patients’ participation and in which cardiac involvement can be demonstrated in more detail (such as strain echocardiography, 3D echocardiography).