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