INTRODUCTION

The ST-segment elevation is typical in acute myocardial infarction. In 2011, Littmann et al. reported a particular type of ST-segment elevation, which presented as ST-segment inferior oblique elevation with baseline superior oblique elevation of the QRS wavefront and a sharp R wave. Because of its graphic characteristics similar to the shape of the pointed helmet used by German soldiers, this electrocardiogram (ECG) finding was named the spiked helmet sign (SHS)¹. In the existing literature, SHS is usually associated with critical illnesses such as acute myocardial infarction and predicts very poor clinical outcomes, including death^2,3. However, the mechanism and clinical significance of SHS is still unclear.

ECG artifacts caused by various interferences are often encountered in clinical work ⁴. Although common interferences can be identified in combination with ECG morphology and clinical manifestations of patients, some can also manifest as severe heart diseases, such as acute myocardial infarction, which is difficult for even experienced clinicians to identify. This case reports the ECG manifestations of a patient who initially developed false SHS after an electric shock.

CASE DESCRIPTION

A 60-year-old man with no previous history of critical illness presented with head, chest, hip, and left elbow pain one hour after a fall. The patient was found lying on the ground at work one hour before. The patient’s co-workers claimed that he was injured due to a fall. The patient recalled the scene then and claimed that an electric shock caused it. The patient had an episode of transient coma and recovered spontaneously without nausea, vomiting, convulsions, or dyspnea. At the time of presentation, the patient’s temperature was 36.6 °C, heart rate was 90 beats per minute, blood pressure was 150/70 mmHg,

and oxygen saturation was 95%. The results of the physical examination were mild respiratory sounds in both lungs, normal heart sounds, no evident murmur, warm limbs, about 1% of a third-degree burn area on the forearm of the left upper limb, movable limbs, and palpable dorsalis pedis artery pulsation. A CT scan of the skull revealed swelling of the right scalp soft tissue. Creatine kinase and creatine kinase-MB were 953.7U/L and 27U/L, respectively, which were higher than normal values. A 12-lead electrocardiogram (Fig. 1) revealed an SHS: lead (I, II, AVL, and AVF) showed an ST elevation of 0.05-0.1 mV with T-wave inversion, the lead AVR showed an ST depression of 0.05mm with T-wave bidirectional changes, and QT interval extended to 460 ms. During this period, the radial artery of the patient’s right wrist pulsated strongly, and the SHS phenomenon disappeared after adjusting the contact position of the right arm electrode. After that, the patient received appropriate intravenous rehydration therapy. After 30 minutes, the 12-lead electrocardiogram (Fig. 2) was reviewed, and all the ST-T changes in the electrocardiogram returned to normal. The patient was discharged without any abnormality after 24 hours of observation in the emergency department.

Fig. 1 The patient presented with a 12-lead routine ECG. Arrows indicate ST elevation of 0.05-0.1mv with T- wave inversion in leads I, II, AVL, and AVF, and ST depression of 0.05mv in lead AVR with bidirectional changes in T-wave. 

Fig. 2 The patient’s ECG reviewed after 30 minutes. ST-T in leads I, II, AVR, AVL, and AVF returned to normal. 

DISCUSSION

In the twelve years since the SHS was first reported in 2011, several communications have portrayed the SHS as an indicator of critical illness and poor prognosis, with an alarming post-emergence mortality rate of 59% ⁵. However, recent studies have divided the SHS into two types. The prolongation of the QT interval causes one, and the other is caused by the superposition of mechanical factors, which may be an ECG artifact ⁶.

Experimental data show that physical stretching of the skin can produce a voltage of several millivolts ⁷. The conductivity of ion channels in the heart will be changed under the pull of different tensions, affecting myocardial cells’ action potential and changing the ECG pattern ⁸. In addition, recent studies support the conclusion that mechanical factors contribute to the SHS. When Tomcsányi et al. placed the ECG lead over the arteriovenous fistula in the left arm of a hemodialysis patient, the ECG showed SHS, whereas when the electrodes were placed further on the normal epidermis, the SHS disappeared, meaning that SHS was caused by pulsatile epidermal stretching ⁶. Agarwal et al. reported that an SHS appeared in the ECG of a 77-year-old male patient who used mechanical ventilation when the pressure in the chest cavity increased, obviously due to excessive positive end-expiratory pressure, but disappeared after reducing positive end-expiratory pressure ⁹. In this case, when compared with the ECG image in Fig. 1, we found no dynamic changes in ST-T in Lead III. According to Einstein’s triangle theory, Lead III was the potential difference between the left arm and left leg. When the artifact came to the right arm, there was an interference artifact in leads I and II, and Lead III remained normal. The patient’s right wrist radial artery was beating strongly, and the ECG showed SHS, whereas the ECG disappeared after adjusting the position of the right arm electrode contact, similar to the case reported by Tomcsányi ¹⁰. Therefore, in our case, the SHS was an ECG artifact caused by mechanical traction.

The SHS phenomenon can be produced when limb lead electrodes are placed on the radial artery, indicating acute ST-segment elevation muscular infarction (STEMI). Although an SHS may be an essential indicator of critical diseases, we must identify other conditions that can cause SHS and remain vigilant. Obtaining a complete medical history and the patient’s basic situation during ECG sampling can help clarify the truth of ECG performance, thus avoiding wrong diagnosis and over-treatment.