Severe hypoglycemia due to insulin self-injection as a cause of acute ST elevation myocardial infarction

Abstract

Introduction

The role of hypoglycemia in cardiovascular disease still needs to be evaluated. Incidental case studies provide direct, but so far limited, evidence for the direct impairment of heart caused by hypoglycemia. We present a case of severe hypoglycemia manifesting with acute ST elevation myocardial infarction (STEMI).

Case presentation

A 48-year old man committed a suicidal attempt by insulin self-injection. The emerged hypoglycemia was accompanied by ECG changes and positive troponins confirming the diagnosis of STEMI. Urgent coronary angiography was performed, but no acute coronary artery closure/critical stenosis was found. After resolution of hypoglycemia all signs of ischemia diminished. Insulin and C-peptide levels confirmed exogenous hyperinsulinemia, confirming insulin self-injection. Sadly, the patient suffered irreversible brain damage.

Conclusion

This patient case shows that severe hypoglycemia can precipitate acute STEMI.

Introduction

Severe hypoglycemia is connected with a higher mortality rate [1, 2]. Now, several reports suggested that severe hypoglycemia may cause acute myocardial ischemia. Two previously published case studies [3, 4] reported patients evolving myocardial infarction during severe hypoglycemia which ensued from insulin injection. Additionally, insulin self-injection is a relatively rare cause of a suicidal attempt [5]. We present a case study of patient presenting with severe hypoglycemia, coma and acute ST-elevation myocardial infarction, in whom exogenous hyperinsulinemia was confirmed as a cause of severe hypoglycemia.

Severe hypoglycemia as a cause of acute STEMI: Clinical case report

48 - year old patient with a history of untreated depression, and type 2 diabetes on diet (with no hypoglycemic drugs), having a son with a history of type 1 diabetes on multiple daily injections insulin therapy, was admitted to our emergency department with a rapid development of unconsciousness. The first examination in the ambulance went as follows: Glasgow coma scale (GCS) was 3 points, the point of care glycemia was 0.8 mmol/L, and his electrocardiogram (ECG) showed ST segment elevations on anterior wall (Fig. 1). The patient according to his wife was not drinking alcohol, smoking or taking illegal drugs. During the initial examination the patient was intubated, 60 ml of 40% solution of glucose was given intravenously. First laboratory examination showed elevation of cardiac troponin I (94.7 ng/L), and low level of plasma C-peptide (0.06 μg/L). The diagnosis of acute ST segment elevation myocardial infarction (STEMI) was made according to the ECG changes and elevated troponin, urgent coronary angiography was preformed, but no acute coronary occlusion or critical coronary stenosis was found (Fig. 2). Another examination of plasma glucose showed persistent severe hypoglycemia (1.2 mmol/L), and the patient needed a continuous infusion of 40% solution of glucose to achieve satisfactory plasma glucose levels. The control level of cardiac troponin I was 117.6 ng/L. After the stabilization of glycaemia ECG changes diminished. Nevertheless, the patient developed persistent cerebral damage which was confirmed with a brain CT scan. The examination of serum insulin and C-peptide confirmed exogenous hyperinsulinemia, suggesting insulin self-injection as a most probable cause of severe hypoglycemia (Fig. 3).

Fig. 1.

Diagnostic electrocardiogram showing anterior ST elevation myocardial infarction prior urgent coronary angiography

Fig. 2.

Urgent coronary angiography showing left (a) and right coronary artery (b)

Fig. 3.

Insulin and C-peptide levels during the first 36 h (h) after admission

Discussion

First, insulin self-injection is a rare cause of a suicide attempt. Although insulin overdose had been occasionally used as a mode of suicide since its introduction in 1921 [6], the last case of a suicide attempt with insulin was reported in 2016 [7]. In our patient case, the examination of serum insulin and C-peptide confirmed exogenous hyperinsulinemia, suggesting insulin self-injection as a most probable cause of severe hypoglycemia. In addition, our patient was not treated with insulin, but had a son who was on multiple daily injections intensified insulin therapy. Therefore, this case study points on the fact that insulin self-injection might occur not only in insulin-treated diabetics, but also in individuals who have different access to insulin (such as relatives of diabetic patients on insulin, health care professionals, etc.).

Second, insulin-induced hypoglycemia is a rare cause of myocardial infarction, and the mechanism of hypoglycemia-induced myocardial infarction is not fully explained. It is suggested that its potential harmful effect consists of autonomic activation, which exaggerates the supply-demand mismatch in an already affected myocardium, and inflammatory response which causes endothelial dysfunction and coagulation abnormalities [8, 9]. Incidental case studies of patients suffering severe hypoglycemia caused by insulin injection support this indirect evidence. Furthermore, sever hypoglycemia may cause vascular (coronary) spasm [10], or may be directly associated with coronary thrombosis [11]. In our case, myocardial infarction was diagnosed according to ECG abnormalities, and positive cardiac troponins. As the coronary catheterization showed no signs of coronary occlusion, plaque rupture or critical stenosis, and the control troponin was significantly increased, we established the diagnosis of myocardial infarction type 2, most probably caused by severe hypoglycemia. In our case, we can definitely exclude acute coronary thrombosis or instable coronary plaque rupture, as urgent coronary angiography showing normal coronary arteries was performed. This corresponds with previously published observations in several other cases of patients with hypoglycemia-induced myocardial infarction in whom delayed coronary catheterization was performed, and no critical stenosis or coronary occlusion was found [3, 4, 12]. However, we cannot exclude coronary spasm, although no spasm was found on coronary arteries, but the spasm could reverse after initial glucose administration prior urgent coronary angiography. Finally, endothelial dysfunction and/or cellular ischemia due to severe hypoglycemia might play their role, as the restoration of normal glucose plasma levels led to the normalization of ECG ischemic changes. Concluding, based on these data, further research would be needed for the clarification of the mechanism of hypoglycemia-induced myocardial infarction.

Funding

This study was funded by research project APVV (Slovak Research and Development Agency) 16–0020.

Compliance with ethical standards

Conflict of interest

Jakub Benko, Tomáš Bolek, Dana Prídavková, Peter Galajda, Matej Samoš, and Marián Mokáň declare that they have no conflicts of interest that might be relevant to the contents of this manuscript.

Ethical approval and inform consent

This research was done according to ethical standards. The patient relatives (as patient suffered irreversible brain damage and was not able to sign any form) agreed to participate in the research and to publish this case study and signed informed consent for study participation.