Implications of localized ST depression in a vascular territory and

altered precordial T wave balance in ischemic heart disease

Abstract

The incidence of ACS is rising globally. ECG is still one of the best diagnostic modalities for it.
Although some of the ECG changes of ACS are well known among medical practitioners, there are
a handful of ECG changes which don’t get the recognition they deserve. Among those are localized
ST-segment depression in a vascular territory and altered precordial T wave balance. The urgency
of management varies among the various subtypes of ACS, especially in low resource settings. ST
segment depression localized to a vascular territory is a sign of STEMI in the reciprocal lead which
may not always be evident and hence, requires emergent reperfusion therapy. On the other hand,
altered precordial T wave balance (T wave in V1>T wave in V6, T wave in V1> 1.5 mm and
upright T wave in V1) may be predictive of significant CAD.

Keywords

ST depression, electrocardiography, new onset T wave, lead V1, myocardial infarction

Introduction

In patients with myocardial infarction, the ST segment depression localized to a vascular territory in
electrocardiography is a frequent, yet overlooked sign. Although localized ST-segment depression
in anterior precordial leads is widely recognized as a sign of posterior wall ST elevation myocardial
infarction (STEMI), the same is not true for localized ST depression in other vascular territories. In
that case, the ST depression may be mistaken with non-ST elevation myocardial infarction
(NSTEMI) or unstable angina. This may delay emergent reperfusion therapy. Similarly, the loss of
precordial T wave balance is also a valuable sign when it comes to a patient with chest pain. These
signs should be specifically observed as they are easily overlooked if not given due attention.
Welch et al have found that normal and non-specific electrocardiograms (ECGs) were found to
have combined rates of in-hospital mortality and life-threatening adverse events of 19.2 and 27.5%
respectively[1]. The main aim of this article is to provide a detailed overview of the
pathophysiology behind the occurrence of these signs and show how they can be useful in real life
scenarios.

Discussion

A. Localized ST depression in a vascular territory : A subtle sign of transmural infarction

and the need for emergent reperfusion therapy

i. Mechanism of ST segment changes

Ischemia leads to an increase in extracellular potassium cation (K+). This is secondary to K+ efflux
from ATP sensitive K+ channels (KATP) which become activated due to low ATP [2]. This
accumulation of extracellular K+ is considered to be an important mechanism for ST changes in the
setting of ischemia. The role of KATP has been supported by the absence of ST-segment elevation in
mice with homozygous knockout (KO) of the Kir6.2 gene which encodes the pore-forming subunit
of cardiac surface KATP channels [3] and the attenuation of ST-segment elevation in people taking
sulfonylureas [4].

- ST-segment elevation

ST segment is typically at the same voltage as the TP segment. During diastole, accumulated
extracellular K+ at the baseline will produce a resting voltage difference between injured and non-
injured areas of the myocardium. This will result in depression of the resting T-P segment which
will result in apparent "ST elevation" [5]. In addition to this, the action of K ATP channels will cause
earlier repolarization of epicardial tissue compared to myocardial and endocardial tissue because
epicardial cells have a greater response to low ATP due either to a larger number of K ATP channels
or channels that are more sensitive to decreased levels of ATP [6]. Earlier repolarization of the
epicardium and thus resulting increase of transmural voltage gradient during ischemia will be
associated with ST-segment elevation.

- ST segment depression

The pathophysiology of ST depression is still not clear. The most simplistic model is the dipole
hypothesis proposed by Wilson et al. [7]. It states that the ischemic area of the myocardium which
is situated in the sub-endocardial region acts as the positive pole, while the non-ischemic area of
myocardium acts as the negative pole. The ventricular surface and the precordium over the
ischemic region face the negative pole of the dipole which leads to ST depression. This hypothesis
was discarded because of its inability to explain the clinical difficulty in localizing ST depression.
Kilpatrick et al [8] hypothesized that ST depression on ECG was due to the current of injury
flowing from an endocardial ischemic region to the outside of the heart through the great vessels
and atria. This was suggested to be the cause of the non-localizing nature of ST depression. This
hypothesis was challenged by Li et al [9] who reported an increase in the magnitude of ST
depression when the aforementioned paths were interrupted in sheep heart. The most accepted
theory is that proposed by Li et al. [9] He found on sheep heart that the lateral boundary, which is
perpendicular to the endocardium, between ischemic and non-ischemic tissue is sharp and distinct
whereas the boundary parallel to the endocardium is not so distinct due to unknown reasons [9].
The sharpness of demarcation between the healthy and ischemic tissues is directly proportional to
the potential difference and hence the current generated. So, the ST depression on epicardium is
thought to reflect the position of lateral boundary of the ischemic region which is typically shared
between vascular territories. This was suggested to be the reason for the non-localizing nature of ST
depression.

ii. Clinical implication

Localized ST depression is usually a marker of STEMI on reciprocal leads which may not always
be evident. This is especially true in high lateral leads where the low voltages lead to ST elevation
not meeting the arbitrarily defined criteria for ST elevation.

iii. Example

ECG of a 72-year-old male with after 5.5 h of sudden onset, constant and substernal chest pressure
is presented in Fig. 1. It shows ST depression in leads III and aVF. Initial troponin was 0.82 ng/mL.
Unfortunately, the findings were not recognized. Cardiac catheterization was performed only the
following day which showed that the obtuse marginal artery had 90% stenosis with Thrombolysis in
Myocardial Infarction (TIMI) I-II flow. Post catheterization ECG showed a new Q-wave with T
wave inversion in aVL (Fig. 2). The peak troponin I was 8.6 ng/mL and a new wall motion
abnormality was detected in echocardiography. This was, in fact, a missed completed high lateral
MI.
 B. New onset upright T wave in lead V1: A sign of significant CAD

i. Mechanism of formation of T wave

T wave is generated due to ventricular repolarization which proceeds from epicardium to

endocardium [10]. This is counter-intuitive as the epicardium is last to depolarize. But due to the
shorter duration of the action potential in epicardial cells, it is the first to repolarize. Unlike
depolarization which occurs due to conduction, repolarization occurs through synchronization. This
is responsible for the longer duration of T wave compared to the QRS complex [11]. The normal
direction of the T wave in the precordial leads generally follows the direction of the QRS complex,
but in the anterior leads (V2-V4) an upright T wave can be observed even in the presence of
predominantly negative QRS complex [10]. The T wave is normally inverted in lead V1. The
electric vectors of the heart are such that if positive T wave is present in lead V1(which is relatively
uncommon) they are usually smaller in amplitude than the T wave in lead V6. This is called normal
precordial T wave balance. As the T wave is normally inverted in lead V1, presence of upright T
wave in V1 may be abnormal. This finding has been named new upright T wave in V1 (NUTV1)
and must be compared with previous ECGs. NUTV1 is also seen in left ventricular hypertrophy,
left bundle branch block and lead displacement.

ii. Clinical Implications

The absence of the normal precordial T wave balance is one of the subtle signs of significant
coronary artery disease (coronary artery stenosis >50%) in ECG. Studies have shown that loss of
precordial T wave balance (T1>T6), [12-14],T wave in V1>1.5 mm [15] and upright T wave in V1
[16] are associated with significant coronary artery disease. The reason for this is unclear and needs
further research. Thesummary of the findings of the above studies is presented in Table 1.

Conclusion

ST segment depression localized to a vascular territory is a sign of STEMI in the reciprocal lead
which may not always be evident and hence, requires emergent reperfusion therapy. Similarly,
altered precordial T wave balance (T1>T6, T wave in V1>1.5 mm and upright T wave in V1) may
be predictive of significant CAD.
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 Figures:

Figure 1: The ECG of 72-year-old male showing ST depression in leads III and aVF and less
than 1 mm of ST elevation in aVL.

Figure 2: Post catheterization ECG of the same patient showing a new Q-wave with T wave
inversion in aVL.
Tables

Table 1: Summary of various related studies on the significance of upright T wave in V1 and
TV1>TV6

Study Findings
Ref. [15] Upright T wave in V1 > 1.5 mm had OR=2.38(1.78 - 3.12) for
coronary artery stenosis of greater than 50%.
Ref. [12] TV1 > TV6 sign has sensitivity, specificity and false positivity of
72.9% 84.4% and 15.6% respectively for significant CAD.
Ref [16] Upright TV1 was an independent predictor of significant CAD
(OR 4.249, 95% CI 1.594–11.328).
Ref [13] Upright T wave in V1 was present in 184 of 218 patients who had
>75% occlusion of coronary arteries more frequently on Left
circumflex artery.
Ref [14] TV1 > TV6 had the sensitivity of 16.1%, the specificity of 95.6%,
and accuracy of 94.2% for significant coronary artery stenosis.