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Increased cardiac troponin I concentration in diabetic ketoacidosis
Mehmet Emre Atabek1, Ozgur Pirgon, Bülent Oran
1Department of Pediatrics, Selcuk University, Faculty of Medicine, Konya, Turkey. meatabek@hotmail.com
Insights
Diabetic ketoacidosis may harm heart muscle due to high blood sugar and acidosis. Even mild cases show elevated cardiac biomarkers, with severe diabetic ketoacidosis significantly impacting the myocardium.
Area of Science:
- Cardiology
- Endocrinology
- Biochemistry
Background:
- Diabetic ketoacidosis (DKA) is a serious complication of diabetes.
- Potential cardiac muscle injury in DKA is not fully understood.
- Acidosis and hyperglycemia in DKA may contribute to cardiac dysfunction.
Purpose of the Study:
- To investigate the hypothesis that DKA causes myocardial injury.
- To assess the role of acidosis and hyperglycemia in DKA-related cardiac effects.
Main Methods:
- Study included 19 diabetic patients with DKA and 19 healthy children.
- Measured cardiac troponin I (cTnI), CK-MB, and myoglobin levels on admission and after 24 hours.
- Patients were grouped by blood pH (>=7.0 vs <7.0).
Main Results:
- DKA patients had higher cTnI, CK-MB, and myoglobin than controls on admission and at 24 hours.
- cTnI normalized within 24 hours.
- All cardiac markers differed significantly between pH groups; cTnI correlated negatively with pH and HCO3-.
Conclusions:
- DKA, especially severe cases, detrimentally affects the myocardium.
- Elevated cardiac biomarkers suggest myocardial stress or injury during DKA.
- Further research is needed to elucidate mechanisms and long-term cardiac implications.
Objective:
To examine the hypothesis that diabetic ketoacidosis may be associated with some degree of induced injury to heart muscle, related either to acidosis or hyperglycemia.
Methods:
Nineteen diabetic patients with acute ketoacidosis and 19 healthy children were enrolled in this study. Cardiac troponin I (cTnI), creatine kinase (CK)-MB and myoglobin levels were analyzed soon after admission and after 24 h. Patients were subdivided into two groups according to blood pH.
Results:
At the time of admission, the diabetic patients had significantly higher values than the controls for cTnI (0.193+/-0.008 vs 0.176+/-0.006 ng/dl; p <0.001), CK-MB (24.1+/-2.1 vs 22.7+/-1.2 U/l; p = 0.02), and myoglobin (85.5+/-7.4 vs 52.5 +/-8.3 microg/dl; p <0.001). The diabetic patients also had significantly higher values than the controls for CK-MB (24+/-2.1 vs 22.7+/-1.2 U/l; p = 0.02) and for myoglobin (78.5+/-2.5 vs 52.5+/-8.3 microg/dl; p <0.001) at 24 h. cTnI had normalized in patients at 24 h. All parameters were significantly different between patients with pH > or =7.0 and patients with pH <7.0. In addition, serum cTnI levels correlated negatively with blood pH (r = -0.57, p = 0.026) and HCO3- (r = -0.65, p = 0.008) in the patients with diabetic ketoacidosis on admission.
Conclusion:
Our findings suggest that diabetic ketoacidosis, particularly when severe, has a detrimental effect on the myocardium.
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