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.