Introduction
Hypoglycemia, also known as low blood sugar, is a condition that can be symptomatic and not very rare. A significant part of it is seen from organic reasons that disrupt the physiological response required for blood sugar. It can cause generally mild symptoms like palpitation, tremor, anxiety, sweating, hunger, dizziness, presyncope, confusion, and fatigue, but severe cerebrovascular symptoms such as seizures and loss of consciousness in acute and chronic processes can also be seen (1,2). Symptoms compatible with hypoglycemia, low plasma glucose concentration, and disappearance of symptoms when plasma glucose level rises are requirements in the primary diagnosis of hypoglycemia, also known as the Whipple triad (3,4,5).
In the pathophysiology of hypoglycemia, it has been shown that increased insulin sensitivity, exaggerated insulin response to insulin resistance or glucagon-related peptide increase, increased adrenergic sensitivity, increased epinephrine levels, and impaired glucagon regulation may occur. Emotional stress, anxiety, depression, as well as after heavy alcohol and high carbohydrate diets. Hypoglycemia is also common in diabetes and especially with drugs used in treatment (6,7,8).
The primary threshold value in the diagnosis of hypoglycemia is accepted as 70 mg/dl and can also be used in hypoglycemia classification. In addition to the blood sugar being below 70 mg/dl, the symptoms of hypoglycemia and the elimination of these symptoms only with the help of another person can be defined as severe, hypoglycemia symptoms and regression of these symptoms after blood glucose-raising agents defined as symptomatic hypoglycemia and the situation had no symptoms can be defined as asymptomatic hypoglycemia. Although the blood sugar is above 70 mg/dl, hypoglycemia-like symptoms can be seen in the condition described as pseudo-hypoglycemia (1,9).
Hypoglycemia induces a stress response that leads to sympathoadrenal activation and the release of hormones such as glucagon, epinephrine, cortisol, and growth hormone (10,11). Hemodynamic changes such as increased heart rate, myocardial contractility, and systolic blood pressure may be observed to glucose formation from the liver and glucose support to the brain (12,13,14). Also, blood viscosity may increase with an increase in platelet cells and increased aggregation and coagulation. Inflammation, leucocytosis, lipid peroxidation, oxidative stress are also increased with hypoglycemia and cause endothelial dysfunction. Disruption of endothelium-related vasodilation and even vascular tone deterioration causes an increased risk of atherosclerosis (15,16,17,18).
When the relevant literature was searched, it was seen that the effects of hypoglycemia on endothelial factors, especially in diabetic patients, were investigated (16,17,18). Besides, in a study conducted in rats, the relationship of recurrent hypoglycemia with carotid intima thickness was shown (19). However, there is no study in the literature evaluating diastolic functions in healthy individuals presenting hypoglycemia attacks. Also, studies on endothelial functions in these individuals are generally conducted at the molecular level to investigate situations that may cause possible future risks (16,17,20).
In the light of these pieces of information, our study aimed to reveal possible cardiac risks by evaluating the cardiac effects (especially in terms of systolic and diastolic functions) and endothelial functions in the presence of echocardiographic findings and peripheral doppler imaging in patients admitted to the emergency department with a diagnosis of hypoglycemia.