Discussion
Hypoglycemia causes several homeostatic changes to balance falling blood sugar (11). Changes in hemodynamic response can be seen in healthy individuals, especially in diabetic patients, with sympathoadrenal response after hypoglycemia. Also, an increase in inflammatory and pro-atherogenic markers was detected as a result of oxidative stress. Combining these factors revealed a rise in blood viscosity, endothelial dysfunction, and acceleration of the atherosclerotic process. It has been shown that insulin resistance can accelerate cardiac morbidity and mortality caused by hypoglycemia by worsening these processes, especially in diabetic patients (16,17,18,20,21).
Due to the lack of a detailed study showing the impact of hypoglycemia on diastolic functions and the conditions mentioned above, it was aimed to reveal possible cardiac risks in patients who applied to the emergency department with hypoglycemia and who were referred to cardiology with complaints of palpitations, dizziness, and presyncope. For this purpose, brachial flow-mediated dilatation and carotid intima-media thickness were examined to show endothelial dysfunction, and essential echocardiographic and tissue doppler evaluation was performed to reveal systolic and diastolic effects.
When looking in the literature regarding systolic and diastolic parameters, an increase in myocardial contractility secondary to transient sympathoadrenal response during acute hypoglycemia after insulin administration in healthy subjects was detected by multiple-gated radionuclide ventriculography (27). A study found that hypoglycemia worsened survival in diabetic patients with systolic heart failure (28). In large-scale ADVANCE, ORIGIN, NICE-SUGAR studies conducted in patients with type 2 diabetes, the relationship of hypoglycemia with outcomes of heart failure, coronary artery disease, and peripheral artery disease has been demonstrated (29,30,31). From these studies, it can be inferred that systolic dysfunction outcomes due to hypoglycemia may be observed. Fasting blood glucose was shown to be one of the markers in the Young Finns study conducted in a population aged between 34 and 49 years to show the determinants of diastolic dysfunctions. However, in this study, high blood glucose, the diagnostic criterion for metabolic syndrome, was mentioned (32).
In our study, in terms of systolic functions, there was no difference(mean LVEF: 65.85±3.75 (patient), 64.57±5.55 (control); p=0.285) . The deceleration time did not differ between the groups in terms of diastolic parameters (p=0.058) . When the E/A ratio was examined, it was observed that it was lower in the patient group(Patient (1.33±0.34), control (1.52±0.34), p=0.020). It was shown that insulin resistance was influential in the formation of this significant difference (p(Homa-IR<2.5 vs. control)=0.249, p(Homa-IR≥2.5 vs. control)=0.013) . Similarly, when the E/e’ ratios were examined, it was significantly lower in the patient group (Patient (median 4,53), control (median 5.10), p=0.026) . Besides, this rate was considerably more down in the patient group with insulin resistance than the patient group without insulin resistance