Early/Subtle Electrocardiography Features of Acute Coronary Syndrome and ST-Segment Elevation Myocardial Infarction

Abstract

Chest pain is one of the most common presenting complaints in the emergency department. Interpreting a 12-lead electrocardiography (ECG) for evidence of ischemia is always challenging. Frank ECG changes such as ST-segment elevation and ST-segment depression can be easily identified by emergency physicians. However, identifying subtle or early features of ACS in the 12-lead ECG is essential in preventing significant mortality and morbidity from ACS. In the following case series, we describe five of the subtle/early ECG changes of ACS, namely (1) T-wave inversion in lead aVL; (2) terminal QRS distortion; (3) hyperacute T-waves; (4) negative U-waves in precordial leads; and (5) loss of precordial T-wave balance. In all these cases, the initial 12-lead ECG showed only subtle/early ECG changes which were followed up with serial ECGs which progressed to STEMI.

INTRODUCTION

One of the leading causes of emergency department (ED) visits is chest pain and acute coronary syndromes (ACSs). Although the exact data for the Indian scenario are not known, the US data show that about 7 million patients presented to ED with chest pain. Among these only 10% of the patients turn out to have ACS. Approximately 2% of these patients with ACS are missed during initial evaluation in ED which significantly increases the mortality and morbidity and 30-day MACE and is a primary reason for litigation in the United States.[¹] This is primarily because of wrong interpretations of electrocardiography (ECG) or the inability to find the subtle or early ECG features of ACS. In the following case series, we report a series of five cases that had subtle/early ECG features of ACS, namely (1) T-wave inversion (TWI) in lead aVL; (2) terminal QRS distortion; (3) hyperacute T-waves; (4) negative U-waves in precordial leads; and (5) loss of precordial T-wave balance.

CASE REPORT

Case 1 (T-wave inversion in lead aVL)

A 40-year-old male patient presented to our ED with complaints of typical chest pain. A triage ECG [Figure 1a] showed a heart rate 50 beats/min with low atrial rhythm and a negative T-wave in lead aVL. The next ECG [Figure 1b] was taken after 30 min which showed ST segment elevation in lead II, III and aVF and ST depression in lead I and aVL. The patient was thrombolysed with streptokinase and referred to the cardiologist for coronary angiogram.

Figure 1: (a) 12-lead electrocardiography showing negative T-wave in lead aVL; (b) 12-lead electrocardiography of the same patient done subsequently; showing ST elevation in leads II, III, and aVF with ST depression in leads I and aVL; (c) 12-lead-electrocardiography of a patient showing terminal QRS distortion in leads V2 and V3, i.e., the absence of S-wave and J-wave in leads V2 and V3; (d) 12-lead-electrocardiography showing progression into frank anterior wall myocardial infarction with ST-segment elevation in leads V1-V6; (e) 12-lead electrocardiography showing hyperacute T-waves which are asymmetric, broad based, and rounded in precordial leads V2 and V3; (f) 12-lead electrocardiography showing progression of hyperacute T-waves into anterior wall myocardial infarction; (g) 12-lead electrocardiography showing inverted U waves in precordial leads V5 and V6; (h) 12-lead electrocardiography of the same patient showing progression to anterior wall myocardial infarction with ST segment elevation in leads V1–V5; (i) 12-lead electrocardiography showing loss of precordial T-wave balance, i.e., T-wave amplitude in lead V1 more than T wave amplitude in lead V6; (j) 12-lead electrocardiography of the same patient showing progression to frank ST segment elevation myocardial infarction with ST-segment elevation in leads V1–V6

Case 2 (terminal QRS distortion)

A 51-year-old male patient presented to our ED with complaints of typical chest pain for 3 h. A triage ECG [Figure 1c] showed a heart rate of 86 beats/min with normal sinus rhythm and an occasional VPC. The ECG also showed hyperacute T-waves in anterior leads with 1 mm concave upward ST segment elevation and terminal QRS distortion in leads V2 and V3 (which are the absence of S wave or J wave in leads V2 and V3). The next ECG [Figure 1d] was taken after 10 min of initial ECG which showed ST segment elevation in leads V1–V6. The patient was thrombolysed with streptokinase and referred to the cardiologist for coronary angiogram.

Case 3 (hyperacute T-waves)

A 68-year-old male patient presented to our ED with complaints of typical chest pain for the past 4 h. A triage ECG [Figure 1e] showed a heart rate of 90 beats/min with atrial fibrillation with controlled ventricular rate with a hyperacute T-waves in leads V2 and V3. The next ECG was taken after 30 min showed ST elevation in leads V1–V6 [Figure 1f]. The patient was thrombolysed with streptokinase and referred to the cardiologist for coronary angiogram.

Case 4 (negative U-waves in precordial leads)

A 55-year-old male patient presented to our ED with complaints of typical chest pain. A triage ECG [Figure 1g] showed a heart rate of 75 beats/min with normal sinus rhythm without any features of STEMI. However, the ECG showed tall T-waves with inverted U-waves in lateral leads (V4–V6). The next ECG [Figure 1h] was taken after 30 min showed ST-segment elevation in leads V1–V6 and lead aVR. This is suggestive of proximal LAD occlusion. The patient was thrombolysed with streptokinase and referred to the cardiologist for coronary angiogram.

Case 5 (loss of precordial T-wave balance)

A 63-year-old male patient presented to our ED with complaints of typical chest pain. Initially he was taken to a private hospital. The ECG [Figure 1i] taken there showed a heart rate of 95 beats/min with normal sinus rhythm. The ECG did not show any features of STEMI. However, the ECG showed a positive T-wave in lead V1 with the T wave amplitude in V1 more than the T-wave amplitude in V6 which is also referred to as loss of precordial T-wave balance. A triage ECG in our ED showed frank ST segment elevation in leads V1–V6 [Figure 1j]. The patient was thrombolysed with streptokinase and referred to the cardiologist for coronary angiogram.

DISCUSSION

ACS is a constellation of signs and symptoms due to an imbalance of myocardial oxygen supply and demand. ACS includes unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction. The principal diagnostic modality in the evaluation of ACS includes a 12-lead electrocardiogram and cardiac biomarkers. 12-lead electrocardiogram as a diagnostic modality has many advantages such as easy, reliable, reproducible, noninvasive, cost-effective, and can be performed by paramedical personnel. It is also an important tool in the management as there are different management plans for STEMI and NSTEMI which is predominantly differentiated by a 12-lead ECG.[²]

Hence, it is essential for the emergency physician to acquire proficiency and sufficient knowledge in interpreting the 12-lead ECG. An emergency physician should not only know about the frank ECG changes of ACS but also about the subtle/early ECG changes of ACS. These subtle/early changes include:

1. TWI in lead aVL
2. Hyperacute T-waves
3. Terminal QRS distortion
4. Negative U-waves in precordial leads
5. Loss of precordial T-wave balance.

T-wave inversion in lead aVL

One of the earliest manifestations of inferior wall myocardial infarction (IWMI) is TWI in lead aVL along with ST depression. This is an isolated finding in an isolated lead which many physicians might regard as normal ECG or nonspecific ST and T wave changes. However, even isolated, TWI in lead aVL signifies the earliest ECG manifestation of IWMI. The current literature also shows that TWI along with ST depression in lead aVL may indicate mid LAD (mLAD) stenosis.[³] A retrospective study done by Nakanishi et al. found out that isolated TWI in lead aVL had a sensitivity of 9.8%, specificity of 86.9%, a positive predictive value of 30.8%, and a negative predictive value of 61.7% for predicting mLAD lesions. Another study done by Hassen et al. found that isolated TWI in lead aVL had an overall sensitivity of 76.7% (95% confidence interval [CI] 0.65–0.86), a specificity of 71.4% (95% CI 0.45–0.88), a positive predictive value of 92%, a negative predictive value of 41.7%, a positive likelihood ratio of 2.7 (95% CI 1.16–6.22), and negative likelihood ratio of 0.32 (95% CI 0.19–0.58) for predicting an mLAD lesion of >50% (P = 0.0011). TWI in lead aVL can also be due to LV strain pattern due to LV hypertrophy, memory T-waves, and hypokalemia.[⁴]

Hyperacute T-waves

Hyperacute T-waves are classically known as the earliest manifestation of ACS and were first described in 1947.[⁵] Hyperacute T-waves are defined as straightening of ST-segment or increase in the amplitude of T-waves wherein the QRS complex fits into the T-wave. The other differentials include hyperkalemia, early repolarization, LV hypertrophy, and acute myopericarditis. Hyperacute T-waves are wide-based, asymmetric with a gradual upstroke than downstroke, localize to the anatomic area of infarction and are always followed by ST-segment changes within 5 − 30 min. Hyperacute T-waves are one of the earliest manifestations of STEMI in myocardial infarction.[⁵⁶⁷⁸⁹] Hyperacute T-waves can be normal variants in young Negro adults. A study done by Collins et al. found out that a combination of J-point position/T-wave amplitude of more than 25%, T-wave amplitude/QRS amplitude of more than 75%, J-point position of more than 0.30 mV, and age of more than 45 years predicted HATWs from a control group with a specificity of 98.0% and a sensitivity of 61.9% and with positive and negative predictive values of 92.9% and 86.2%, respectively.

Terminal QRS distortion

Terminal QRS distortion is defined as an absence of both S-wave and J-wave in either of leads V2 and V3. Terminal QRS distortion is one of the earliest or sometimes the only manifestations of anterior wall myocardial infarction.[¹⁰¹¹¹²] The presence of terminal QRS distortion distinguishes STEMI from benign early repolarization (BER).[¹³] Furthermore, the presence of terminal QRS distortion signifies a very severe disease with greater infarct size and severe LV dysfunction. A study done by Lee et al. found that terminal QRS distortion was 100% specific for ACS and zero cases of BER had terminal QRS distortion. A study done by Prasitlumkum et al. found that the QRS distortion was associated with 1.81 times more risk compared to non-QRS distortion ACS. It also increased the all-cause mortality by 81%.

Negative U-waves

A negative U-wave is defined as a deflection below the isoelectric line after the T-wave. The negative U-wave is almost always pathological. It is one of the earliest or sometimes the only manifestation of anterior wall myocardial infarction.[¹⁴¹⁵¹⁶] It signifies critical stenosis of proximal left anterior descending artery occlusion. It has low sensitivity and specificity.[¹⁷] A negative U-wave is sometimes misinterpreted as a biphasic T-wave. However, this can be easily appreciated if we measure the QT interval in the limb leads and then approximate the QT interval in the anterior leads. If any extranegative deflection after the QT interval in the precordial leads was found, it can be reliably named as a negative U-wave. A negative U-wave can also be seen in hypokalemia. A study done by Gerson et al. found out that the resting U-wave inversion predicted the presence of LAD disease or LMCA occlusion with a sensitivity of 8.2% and a specificity of 99% with a positive predictive value of 92%.

Loss of precordial T-wave balance

Loss of precordial T-wave balance is defined as “amplitude of T-wave in lead V1 more than the amplitude of T wave in V6.” This is a type of hyperacute T wave. Normally, the T-wave in V1 is flat or negative. The T-wave can be tall in lead V1 in LVH and LBBB. However, in such scenarios, the amplitude of the T-wave in V1 will be less than the amplitude of the T-wave in V6. Loss of precordial T-wave balance is one of the earliest manifestations of an anterior wall myocardial infarction.[¹⁸¹⁹²⁰] A new upright T-wave in lead V1 can also be considered as a hyperacute nature of T-wave if we have previous ECG evidence that the T wave was inverted in lead V1. A study done by Barthwal et al. found out that the TV1 > TV6 sign has sensitivity, specificity and false positivity of 72.9%, 84.4%, and 15.6%, respectively.

CONCLUSION

The 12-lead ECG is simple, noninvasive, and cost-effective. Identifying the subtle/early ECG features of ACS can avoid significant cardiovascular mortality and morbidity Figure 2. Hence, all emergency physicians must be trained to identify the subtle/early ECG features of ACS namely (1) TWI in lead aVL; (2) Terminal QRS distortion; (3) Hyperacute T-waves; (4) Negative U-waves in precordial leads; and (5) Loss of precordial T-wave balance. The identification of these early/subtle features of ACS can decrease immediate and 30-day MACE on this population. An institute level or multi-departmental weekly or monthly ECG club or educational activities can reinforce these early/subtle features of ACS. Along with that a retrospective analysis of ECGs of patients with chest pain who died unexpectedly during the mortality meeting can also help us close the knowledge gap.

Figure 2: Summary of the early/subtle features of acute coronary syndrome

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patients have given their consent for their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Research quality and ethics statement

The authors followed applicable EQUATOR Network (http://www.equator-network.org/) guidelines, notably the CARE guideline, during the conduct of this report.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.