Journal Pre-proof

ST segment and T wave abnormalities: A narrative review

José Nunes de Alencar Neto, Victor Felipe de Andrade Matos,

Matheus Kiszka Scheffer, Sandro Pinelli Felicioni, Mariana Fuziy
Nogueira De Marchi, Manuel Martínez-Sellés

PII: S0022-0736(24)00147-X
DOI: https://doi.org/10.1016/j.jelectrocard.2024.05.085
Reference: YJELC 53740

To appear in: Journal of Electrocardiology

Please cite this article as: J.N. de Alencar Neto, V.F. de Andrade Matos, M.K. Scheffer,
et al., ST segment and T wave abnormalities: A narrative review, Journal of
Electrocardiology (2023), https://doi.org/10.1016/j.jelectrocard.2024.05.085

This is a PDF file of an article that has undergone enhancements after acceptance, such
as the addition of a cover page and metadata, and formatting for readability, but it is
not yet the definitive version of record. This version will undergo additional copyediting,
typesetting and review before it is published in its final form, but we are providing this
version to give early visibility of the article. Please note that, during the production
process, errors may be discovered which could affect the content, and all legal disclaimers
that apply to the journal pertain.

© 2024 Published by Elsevier Inc.

 Journal Pre-proof

ST segment and T wave Abnormalities: A

narrative review
José Nunes de Alencar Neto1; Victor Felipe de Andrade Matos1; Matheus Kiszka
Scheffer1; Sandro Pinelli Felicioni1; Mariana Fuziy Nogueira De Marchi1; Manuel
Martínez-Sellés2,3

1. Electrocardiography. Instituto Dante Pazzanese de Cardiologia. São

Paulo – Brazil.

of
2. Cardiology Department, Hospital General Universitario Gregorio Marañón,
Instituto de Investigación Sanitaria Gregorio Marañón, CIBERCV. Madrid,

ro
Spain.
3. Universidad Europea. Universidad Complutense. Madrid, Spain.
-p
re
lP

ADDRESS FOR CORRESPONDENCE:

Victor Felipe de Andrade Matos
na

Instituto Dante Pazzanese de Cardiologia

ur

Avenida Dr. Dante Pazzanese No. 500, Vila Mariana

Jo

São Paulo 04012-091

Brazil

Tel: +55 84 999875685

victor.matos@dantepazzanese.org.br

Word count: 6630

 Journal Pre-proof

ABSTRACT
Introduction: The electrocardiogram (ECG) is a valuable tool for interpreting
ventricular repolarization. This article aims to broaden the diagnostic scope
beyond the conventional ischemia-centric approach, integrating an
understanding of pathophisiological influences on ST-T wave changes.

Methods: A review was conducted on the physiological underpinnings of

ventricular repolarization and the pathophisiological processes that can change
ECG patterns. The research encompassed primary repolarization abnormalities
due to uniform variations in ventricular action potential, secondary changes from

of
electrical or mechanical alterations, and non-ischemic conditions influencing ST-
T segments.

ro
Results: Primary T waves are characterized by symmetrical waves with broad
-p
bases and variable QT intervals, indicative of direct myocardial action potential
modifications due to ischemia, electrolyte imbalances, and channelopathies.
re
Secondary T waves are asymmetric and often unassociated with significant QT
interval changes, suggesting depolarization alterations or changes in cardiac
lP

geometry and contractility.

na

Conclusion: We advocate for a unified ECG analysis, recognizing primary and

secondary ST-T changes, and their clinical implications. Our proposed analytical
framework enhances the clinician's ability to discern a wide array of cardiac
ur

conditions, extending diagnostic accuracy beyond myocardial ischemia.

Jo

Keywords: ST-T Wave; ECG; Electrocardiography; Repolarization; Ischemia

 Journal Pre-proof

INTRODUCTION

The electrocardiogram (ECG) is an essential tool in cardiovascular diagnosis,

including the interpretation of ventricular repolarization as depicted by ST-T wave
changes. While these changes have traditionally been predominantly associated
with myocardial ischemia, this narrow focus overlooks a wide range of non-
ischemic conditions that can also influence ST-T segments, potentially leading to
misdiagnosis and oversimplification in clinical practice. This manuscript reviews
repolarization abnormalities through the established framework of primary and

of
secondary repolarization changes[1]. Primary and secondary repolarization
abnormalities are discussed, and this knowledge enables us to systematize

ro
diagnostic hypotheses for repolarization abnormalities in a patient-centered
-p
diagnostic process that transcends the conventional ischemia-centric model.
re

PRIMARY POSITIVE ST-T

lP
na

Primary repolarization abnormalities are defined as those predominantly caused

by uniform changes in the shape or duration of ventricular transmembrane action
ur

potentials[2]. These can include abnormalities induced by ischemia, drugs,

abnormal electrolyte concentrations, or channelopathies[3]. Primary alterations
Jo

in repolarization tend to manifest as a tendency towards symmetry or established

symmetry in the T wave, which may be concordant or discordant with the QRS
but fundamentally broadens its base and extends towards the J point[4].
Depending on the condition, this process can lead to elevation or depression of
the J point if the T wave is positive or negative, respectively.

In addition, primary repolarization changes are often accompanied by changes in

the duration of the corrected QT interval, reflecting changes in the ventricular
action potential. As primary abnormalities directly affect the action potentials of
the ventricular myocardium, changes in their duration are expected. This may
result in a shortening or prolongation of the corrected QT interval. Most of these
abnormalities can be attributed to changes in the slope of phase 3 alone, or to
 Journal Pre-proof

combined changes in phases 2 and 3 of the ventricular action potential[5].

Examples include digitalis effects, which typically result from shortening of phase
2[6], decreased slope of phase 3, and absolute shortening of the ventricular
action potential.

Acute coronary occlusion

In cases of acute coronary occlusion leading to chest pain, myocardial ischemia

triggers hyperkalemia, acidosis, and hypoxia, which in turn reduce adenosine

of
triphosphate (ATP) levels[7]. The ATP depletion activates IKatp channels,

ro
especially pronounced in the epicardium due to its higher ATP sensitivity and
larger transient outward current (Ito). This results in a marked suppression of the
-p
action potential plateau and a significant abbreviation of the action potential dome
(APD) in epicardial cells. A simulation study has elucidated the significant impact
re
of action potential shape on T-wave symmetry[8]: shortening the APD is
lP

correlated with the emergence of taller and more symmetrical T-waves, where
the symmetry ratio (SR) approaches a value close to 1.0. SR is defined as the
na

ratio of the area under the T-wave from its onset (To) to the peak (Tp) divided by
the area from the T-wave peak to the end (Te). Moreover, an increase in
dispersion of repolarization due to simultaneous shortening of the minimum APD
ur

and lengthening of the maximum APD resulted in similar T-wave morphology.

Jo

However, an increase in dispersion of repolarization attributed solely to the

lengthening of the maximum APD (e.g., endocardial APD) has a distinct effect in
that SR remains approximately constant at different magnitudes of dispersion of
repolarization.

In this context, during myocardial ischemia, the T wave becomes more

symmetrical, with a decreasing symmetry ratio tending to ≤ 1.0, manifesting itself
on ECG as a T wave of increased duration, long base, and tall amplitude (Figure
1). This pattern is known as hyperacute T wave and is the first
electrocardiographic manifestation of an acute coronary occlusion, aligning with
Birnbaum and Sclarovsky grades of ischemic changes[9]. During acute
myocardial ischemia, the considerable transmembrane potential gradient across
 Journal Pre-proof

the ventricular wall (Vm) progresses to the characteristic ST-segment elevation

observed on ECG[10].

Electrolyte disorders

As hyperkalemia accelerates phase 3 of ventricular repolarization, it reduces the

APD and forms a peaked and symmetrical tented T wave, best visualized from
V2-V4 and limb leads II-III[11,12]. The narrow base of the tented T wave is a key
distinguishing feature compared to the hyperacute T wave broad base. Higher

of
serum levels may also induce ST segment elevation[13].

ro
Elevated extracellular potassium concentration ([K+]o) notably impacts cardiac
-p
repolarization by enhancing the conductance of IKr, a phenomenon that is directly
proportional to the square root of [K+]o[14]. When [K+]o is increased to 6 mmol/L,
re
the augmentation in IKr conductance leads to a reduction in the APD, particularly
in the epicardial cells, where the APD is considerably decreased. This reduction
lP

results in a shortened QT interval on the electrocardiogram, reflecting the

accelerated repolarization phase[15]. Moreover, the resultant dispersion of
na

repolarization causes the T-wave amplitude to become more pronounced[16].

ur

Inflammation
Jo

Although the pericardial sac itself lacks electrical activity, pericardium

inflammation can disrupt the epicardium AP. In pericarditis, T wave tends towards
symmetry and ST-segment elevation may appear in most leads and tends not to
exceed 5 mm in amplitude, possibly due to subendocardial zone sparing. ST
segment depression may occur in aVR and V1 due to their distant and opposite
position relative to the normal heart axis. Unlike acute coronary occlusion, whose
ECG changes align with the occluded arterial territory, pericarditis, due to its
broad inflammatory nature, diffusely alters the electrocardiographic tracing
without presenting a reciprocal wall[17].
 Journal Pre-proof

Myocarditis can also exhibit primary repolarization abnormalities, mimicking

acute myocardial infarction with ST-segment elevation in a significant proportion
of patients[18,19]. Alternatively, myocarditis may present secondary
repolarization abnormalities such as T wave inversion[20].

Genetic channelopathies

of
Long QT Syndrome (LQTS) is an inherited disorder characterized by prolonged
QT intervals on the ECG and a heightened risk of developing polymorphic

ro
ventricular tachycardia and sudden cardiac death. This condition extends the
-p
APD and the QT interval[21].

Research has also shown that the Tp-e interval, the duration from the peak to the
re
end of the T wave, is frequently prolonged in LQTS patients[22]. Moreover,
lP

studies suggest that the Tpeak-to-end (Tp-e)/QT ratio may be a more reliable
indicator of torsades de pointes risk than the QTc interval or QT dispersion,
particularly in acquired forms of LQTS[23]. A Tp-e/QT ratio exceeding 0.28 has
na

been strongly associated with the risk of torsades de pointes[24,25]. T-wave

analysis is crucial for identifying concealed Long QT Syndrome (LQTS), where
ur

the QT interval may appear normal. Key measures such as the Tpeak-to-end
Jo

interval, T-wave left slope, and T-wave's center of gravity (notably in the last 25%
of the T-wave) significantly aid diagnosis. Particularly in lead V6, these
parameters can distinguish between LQTS patients and healthy controls,
effectively identifying 83.33% of concealed LQTS cases[26].

There is also experimental and early evidence that this marker is also correlated
with increased risk in early repolarization[27,28] and short QT syndromes[25].
Figure 2 exemplifies some primary positive ST-T ECGs.
 Journal Pre-proof

Direct cardioversion

The pathophysiology of ST segment elevation with symmetric T wave following

direct current cardioversion is not fully understood. The initial descriptions of this
phenomenon came from studies that linked it to atrial and ventricular
tachyarrhythmias[29,30]. The rapid electrical activity in tachyarrhythmias makes
the balance of ionic currents more susceptible to disturbance, explaining these
findings. To enhance this discussion, we must consider the impact of
cardioversion to myocardium. The electrical energy delivered may transiently

of
disrupt ionic channels and affect repolarization process, leading to the formation
of primary symmetric positive T wave.

ro
-p
PRIMARY NEGATIVE ST-T
re
lP

Inverted primary T wave pattern and ST segment depression are associated with
coronary and non-coronary cardiac conditions and may be permanent or
na

temporary. When transient, the resolution time varies from days to years,
depending on the underlying cause. There is no universally accepted cutpoints
for the terms used in this section, but, for clarity, we will define T wave inversion
ur

as mild (< 5 mm), deep (5-10 mm) or giant (>10 mm). Figure 3 exemplifies primary
Jo

negative ST-T ECGs.

Coronary syndromes

Myocardial edema resulting from subacute or chronic ischemia is typically

associated with severe obstruction in the anterior descending artery in its
proximal portion[31,32]. A prototype of this phemomenum, Wellens' pattern can
manifest both as a biphasic or as a deep inverted T wave in anterior wall[33].
 Journal Pre-proof

The biphasic morphology reflects the moment when ST elevation is resolving due
to spontaneous coronary recanalization, but myocardial edema is significant
enough to invert T wave. This pattern has been described in various reports as
"pseudo-Wellens"[34–38]. This term is probably inappropriate as it implies that
the biphasic T wave has only one diagnosis and that differential diagnoses are
rare. This may prevent a broad clinical assessment necessary for the accurate
diagnosis and management of cardiac events. In addition, this article stresses
that no single alteration is entirely specific to any syndrome. For example,
Wellens' pattern is a differential diagnosis for virtually all negative primary T
waves described in this section.

of
In acute ischemia, the dynamics of T wave changes are complex and often

ro
misunderstood. A common misconception is that acute ongoing ischemia directly
causes negative T waves. However, the negativity of T wave is a consequence
-p
of associated ST depression in the same leads[4]. It usually occurs when ongoing
ischemia is resolving or has subsided and can persist for a prolonged period. This
re
persistence can be a residual marker of past ischemic episodes, such as Wellens'
lP

pattern or after a Prinzmetal anginal event. Interestingly, negative T waves might

also represent a reciprocal inversion of a diametrically opposite hyperacute T
na

wave. Therefore, using the term "subepicardial ischemia" to evaluate a negative

T wave is discouraged[3].
ur

In acute coronary occlusion, ST segment depression may indicate some potential

diagnoses: acute lateral (formerly "posterior") wall myocardial infarction with total
Jo

coronary occlusion; reciprocal ST segment depression from a ST segment

elevation in a diametrically opposite ventricular wall during acute coronary
occlusion, or true subendocardial ischemia/current of injury from offer and
demand imbalance[39].

Digitalis

At therapeutic levels, digitalis induces characteristic electrocardiographic

changes that include PR interval prolongation through vagal effect, ST segment
 Journal Pre-proof

depression, T wave inversion, and QT interval shortening. The changes in

monophasic action potential result from toxic digitalis-induced extracellular
potassium accumulation due to inhibition of Na+/K+ exchange mechanism. This
elevation increases membrane potassium conductance, accelerating
repolarization and depressing the action potential plateau phase[40,41].

Channelopathies

Brugada Syndrome (BrS) type 1 diagnosis hinges on an ECG displaying a ST-

of
segment elevation ≥2 mm in right precordial leads V1 and/or V2, either

ro
spontaneously or post-sodium channel blocker infusion[42]. Correct diagnosis
mandates ruling out other causes of similar ECG patterns, often referred to as
-p
Brugada phenocopies[43]. Although the QT interval usually appears normal, it
re
may be subtly prolonged in right precordial leads[44]. BrS demonstrates a distinct
tendency towards T wave symmetry, notably through an increased Tp-e interval
lP

and amplified Tp-e/QT ratio particularly evident in leads showing a coved ST

elevation configuration[45]. There is a significant correlation between historical
na

arrhythmic events, a QTc ≥460 ms in lead V2, Tp-e interval, and Tp-e
dispersion[46,47].
ur

LQTS may also manifest with distinct T-wave morphologies. Genotype-specific

research has delineated characteristic T-wave patterns across the three most
Jo

prevalent LQTS subtypes: LQT1 typically presents with broad-based T-waves,

LQT2 with low-amplitude bifid T-waves, and LQT3 with late-onset peaked or
biphasic T-waves. Remarkably, the emergence of giant T-waves, occasionally
referred to as T-U waves due to their magnitude, has been linked to imminent
episodes of torsades de pointes[48,49].
 Journal Pre-proof

Cerebral T waves and spiked helmet sign

Takotsubo cardiomyopathy can manifest through a reversible negative, deep and

symmetrical T wave, along with QT interval prolongation or even with ST-segment
elevation that mimics an acute coronary occlusion[50,51].

Subarachnoid hemorrhage and other acute cerebral events can precipitate

cardiac disorders through autonomic stimulation and catecholamine surges. This
adrenergic discharge leads to cardiomyocytolysis and myocardial edema,
causing repolarization abnormalities similar to those in takotsubo syndrome[52]

of
and a pattern of deep and negative T wave, named cerebral T wave. Additional

ro
ECG changes may include large, flattened or notched T waves, ST segment
elevation or depression and prominent U waves, reflecting the profound impact
-p
of neurological injury on cardiac electrophysiology[52,53]. Prolongation of the QT
interval is frequently observed and is associated with an increased risk of
re
arrhythmias within the first 48 hours following the event[54,55].
lP

The spiked helmet sign, an electrocardiographic pattern associated with severe

systemic stress, reflects the sympathetic discharge associated with critical
na

illnesses (Figure 4)[56,57]. It elevates the baseline preceding and following the
QRS and creates a distinctive dome and spike appearance reminiscent of a
ur

German military helmet[58]. Often accompanied by QTc prolongation and ST

segment elevation, this pattern can be mistaken for ACO. However, the baseline
Jo

shift beginning before the QRS complex argues against ischemia.

The insular cortex plays a crucial role in autonomic nervous system signaling. In
ischemic strokes in this territory, rarely a cerebral T wave may arise. In the
context, the presence of cerebral T waves and ventricular dysfunction can be
seen as a continuum of manifestations of autonomic dysfunction[59].

The electrical memory is a rare phenomenon due to changes in endocardium-

epicardium transmural gradient, where arises an inverted T wave in the precordial
leads[60]. It may appear after the resolution of transient tachycardia or right
ventricular pacing[61].
 Journal Pre-proof

SECONDARY ST-T ABNORMALITIES

Secondary repolarization abnormalities can be defined as those indicating

alterations secondary to electrical alterations of cardiac depolarization. According
to some authors, these secondary T waves are fundamentally asymmetric, with
their first half rising more slowly than the second, marking their most distinctive
characteristic[62,63].

Alterations in electromechanical coupling, heart geometry, and autonomic

of
influences, might generate secondary repolarization changes. Cardiac

ro
contraction and relaxation are produced during the ST-T phase[64,65] and, as a
consequence, are influenced significantly by mechanoelectrical coupling. As the
-p
heart contracts and changes its shape, these mechanical alterations have a direct
re
effect on the electrical activity of the heart, particularly on repolarization[66].
Mathematical models have been developed to assess the impact of geometrical
lP

changes on ECG. These models consistently show that incorporating motion into
the heart leads to noticeable changes in the STT-interval, while the QRS complex
na

remains largely unaffected[67–70] (Figure 5). Notably, T-wave amplitude tends to

be lower in a dynamic heart compared to a static one[71].
ur

An illustrative example of a secondary repolarization abnormality is the strain

pattern observed in patients with left ventricular hypertrophy, where electrical
Jo

(depolarization) and mechanical (coupling or geometry) changes occur

simultaneously. A prototype maybe the typical "left ventricular strain pattern,"
where the T wave is inverted, and the ST segment is depressed in leads where
the QRS area is positive, typically in the left precordial leads and limb leads I and
II[72]. The evolution of this pattern often parallels the progression of left
ventricular hypertrophy and dilatation, especially in conditions like aortic valve
disease.

In Hypertrophic Cardiomyopathy, the abnormal distribution of ventricular mass

and myocardial fibrosis classically causes negative asymmetrical T wave and
signs of left ventricular overload with strain. Apical hypertrophic cardiomyopathy,
 Journal Pre-proof

the Yamaguchi Syndrome, is a rare variant characterized by myocardial

hypertrophy predominantly at the left ventricular apex. About half apical
hypertrophic cardiomyopathy cases manifests as a giant T wave inversion in
precordial leads, with a wavelength exceeding 10 mm[60,73].

Resting electrocardiographic changes with negative, deep, and symmetrical T

wave in asymptomatic individuals should also prompt investigation for other
genetic conditions, such as arrhythmogenic cardiomyopathy and non-compacted
cardiomyopathies[60].

Abnormal repolarization may be secondary to depolarization changes. It can lead

of
to an asymmetric T wave with discordant QRS polarity. Left ventricular
hypertrophy with strain, bundle branch blocks, and pre-excitation syndrome were

ro
the main causes of secondary T waves. -p
Literature reports indicate ST segment depressions or T wave inversions
unrelated to ischemia, and sometimes linked to cardiogenic and non-cardiogenic
re
pulmonary edema[74]. We believe that these phenomena can be explained by
lP

alterations in the ventricular pressure curves of the patient, which can affect the
ST-T segment as secondary alterations.
na

Post-infarction ventricular aneurysm can present as ST segment elevation in

leads with pathological Q waves also exemplifying this phenomenon[75–77].
ur

Furthermore, alterations in cardiac contractility or geometry due to pulmonary

embolism may also cause ST segment elevations[78].
Jo

Figure 6 exemplifies secondary ST-T abnormalities.

UNIFIED THEORIES OF REPOLARIZATION FOR

CLINICAL ECG ANALYSIS

We recommend a unified analysis of ECG repolarization alterations based on the

detailed examination in this paper and understanding that the ST-T segment may
be primary or secondary (Figure 7). This analysis is based on the following
 Journal Pre-proof

assumption: primary T waves are accompanied by certain landmark features that

do not necessarily need to be present; however, each factor adds to the likelihood
of being primary. These features include symmetrical T waves (Symmetry Ratio
tending to 1.0 or increased Tp-Te/QT ratios), broad base, and wide amplitude,
coupled with shortening or lengthening of the QT interval. ECGs exhibiting these
characteristics should draw clinical attention to conditions that cause direct
alterations in the action potential of cardiac cells, such as ischemia,
hyperkalemia, pericarditis, cerebral T waves, and other conditions (Table 1). The
clinical investigation should begin with an attempt to align patient clinical and
epidemiological data with these hypotheses.

of
On the other hand, T-wave alterations that are not accompanied by these

ro
landmark features should be considered secondary. Secondary T waves—which
are typically asymmetric, do not have a broad base, nor significantly alter the QT
-p
interval—should prompt clinicians to consider the possibility of depolarization
alterations (analysis of QRS may indicate the presence of conditions such as
re
bundle branch block or ventricular overload, for example), as well as changes in
lP

electromechanical coupling, contractility, and cardiac geometry (Table 2).

Given the intricacies of the action potentials and their manifestations on the
na

electrocardiogram, it becomes clear that the ST segment and T wave should not
be viewed in isolation but rather as integral components of a continuous
ur

repolarization process[79]. The interplay of ionic currents and cellular dynamics

that shape these ECG components reflects the underlying physiological state and
Jo

can provide deep insights into cardiac function. Thus, readers are encouraged to
interpret the ST segment and T wave as part of the broader continuum of action
potential and repolarization. Analysis of the ST segment should be conducted
with the same interpretation framework: STE can be either primary or secondary,
and analysis of the T wave will assist in this differentiation.

CONCLUSION
 Journal Pre-proof

Primary and secondary ST-T abnormalities extend beyond myocardial ischemia,

and include different conditions, including channelopathies, structural heart
changes, electrolyte imbalances, and direct myocardial injury.

of
ro
-p
re
lP
na
ur
Jo
 Journal Pre-proof

REFERENCES

[1] Surawicz B, Knilans TK. Chou’s Electrocardiography in Clinical Practice: Adult

and Pediatric. Saunders/Elsevier; 2008.
[2] Abildskov JA, Burgess MJ, Millar K, Wyatt R, Baule G. The primary T wave--a
new electrocardiographic waveform. Am Heart J 1971;81:242–9.
https://doi.org/10.1016/0002-8703(71)90135-9.
[3] Rautaharju PM, Surawicz B, Gettes LS. AHA/ACCF/HRS Recommendations for
the Standardization and Interpretation of the Electrocardiogram. Circulation
2009;119:e241–50. https://doi.org/10.1161/CIRCULATIONAHA.108.191096.
[4] de Luna AB, Zareba W, Fiol M, Nikus K, Birnbaum Y, Baranowski R, et al.
Negative T Wave in Ischemic Heart Disease: A Consensus Article. Ann Noninvasive
Electrocardiol Off J Int Soc Holter Noninvasive Electrocardiol Inc 2014;19:426–41.
https://doi.org/10.1111/anec.12193.
[5] Macfarlane PW, Van Oosterom A, Palhm O, Kligfield P, Janse M. Comprehensive

of
electrocardiography. Second Edi. Springer; 2011.
[6] Cheng TO. Digitalis Administration: An Underappreciated but Common Cause of

ro
Short QT Interval. Circulation 2004;109:e152–e152.
https://doi.org/10.1161/01.CIR.0000118177.56908.5B.
[7] Shaw RM, Rudy Y. Electrophysiologic effects of acute myocardial ischemia: a
-p
theoretical study of altered cell excitability and action potential duration. Cardiovasc Res
1997;35:256–72. https://doi.org/10.1016/s0008-6363(97)00093-x.
re
[8] Arteyeva NV, Komarov IA, Azarov JE. Action potential morphology affects T-
wave symmetry (simulation study). J Electrocardiol 2023;81:237–43.
https://doi.org/10.1016/j.jelectrocard.2023.10.004.
lP

[9] Birnbaum Y, Sclarovsky S. The grades of ischemia on the presenting

electrocardiogram of patients with ST elevation acute myocardial infarction. J
Electrocardiol 2001;34:17–26. https://doi.org/10.1054/jelc.2001.28819.
na

[10] Kleber AG. Resting membrane potential, extracellular potassium activity, and
intracellular sodium activity during acute global ischemia in isolated perfused guinea pig
hearts. Circ Res 1983;52:442–50.
ur

[11] Fisch C, Knoebel SB, Feigenbaum H, Greenspan K. Potassium and the

monophasic action potential, electrocardiogram, conduction and arrhythmias. Prog
Cardiovasc Dis 1966;8:387–418. https://doi.org/10.1016/s0033-0620(66)80029-4.
Jo

[12] Levine HD, Vazifdar JP, Lown B, Merrill JP. Tent-shaped T waves of normal
amplitude in potassium intoxication. Am Heart J 1952;43:437–50.
https://doi.org/10.1016/0002-8703(52)90086-0.
[13] Levine HD, Wanzer SH, Merrill JP. Dialyzable Currents of Injury in Potassium
Intoxication Resembling Acute Myocardial Infarction or Pericarditis. Circulation
1956;13:29–36. https://doi.org/10.1161/01.CIR.13.1.29.
[14] Zeng J, Laurita KR, Rosenbaum DS, Rudy Y. Two components of the delayed
rectifier K+ current in ventricular myocytes of the guinea pig type. Theoretical
formulation and their role in repolarization. Circ Res 1995;77:140–52.
https://doi.org/10.1161/01.res.77.1.140.
[15] Viswanathan PC, Shaw RM, Rudy Y. Effects of IKr and IKs heterogeneity on
action potential duration and its rate dependence: a simulation study. Circulation
1999;99:2466–74. https://doi.org/10.1161/01.cir.99.18.2466.
[16] Gima K, Rudy Y. Ionic Current Basis of Electrocardiographic Waveforms A
Model Study. Circ Res 2002;90:889–96.
[17] Spodick DH. Diagnostic Electrocardiographic Sequences in Acute Pericarditis.
 Journal Pre-proof

Circulation 1973;48:575–80. https://doi.org/10.1161/01.CIR.48.3.575.

[18] Wang K, Asinger RW, Marriott HJL. ST-segment elevation in conditions other
than acute myocardial infarction. N Engl J Med 2003;349:2128–35.
https://doi.org/10.1056/NEJMra022580.
[19] Karjalainen J, Heikkilä J. Incidence of three presentations of acute myocarditis in
young men in military service. A 20-year experience. Eur Heart J 1999;20:1120–5.
https://doi.org/10.1053/euhj.1998.1444.
[20] Di Bella G, Florian A, Oreto L, Napolitano C, Todaro MC, Donato R, et al.
Electrocardiographic findings and myocardial damage in acute myocarditis detected by
cardiac magnetic resonance. Clin Res Cardiol Off J Ger Card Soc 2012;101:617–24.
https://doi.org/10.1007/s00392-012-0433-5.
[21] Krahn AD, Laksman Z, Sy RW, Postema PG, Ackerman MJ, Wilde AAM, et al.
Congenital Long QT Syndrome. JACC Clin Electrophysiol 2022;8:687–706.
https://doi.org/10.1016/j.jacep.2022.02.017.
[22] Lubinski A, Lewicka-Nowak E, Kempa M, Baczynska AM, Romanowska I,

of
Swiatecka G. New insight into repolarization abnormalities in patients with congenital
long QT syndrome: the increased transmural dispersion of repolarization. Pacing Clin

ro
Electrophysiol PACE 1998;21:172–5. https://doi.org/10.1111/j.1540-
8159.1998.tb01083.x.
[23] Topilski I, Rogowski O, Rosso R, Justo D, Copperman Y, Glikson M, et al. The
-p
morphology of the QT interval predicts torsade de pointes during acquired
bradyarrhythmias. J Am Coll Cardiol 2007;49:320–8.
re
https://doi.org/10.1016/j.jacc.2006.08.058.
[24] Yamaguchi M, Shimizu M, Ino H, Terai H, Uchiyama K, Oe K, et al. T wave
peak-to-end interval and QT dispersion in acquired long QT syndrome: a new index for
lP

arrhythmogenicity. Clin Sci Lond Engl 1979 2003;105:671–6.

https://doi.org/10.1042/CS20030010.
[25] Gupta P, Patel C, Patel H, Narayanaswamy S, Malhotra B, Green JT, et al. T(p-
na

e)/QT ratio as an index of arrhythmogenesis. J Electrocardiol 2008;41:567–74.

https://doi.org/10.1016/j.jelectrocard.2008.07.016.
[26] Sugrue A, Noseworthy PA, Kremen V, Bos JM, Qiang B, Rohatgi RK, et al.
ur

Identification of Concealed and Manifest Long QT Syndrome Using a Novel T Wave

Analysis Program. Circ Arrhythm Electrophysiol 2016;9:e003830.
https://doi.org/10.1161/CIRCEP.115.003830.
Jo

[27] Yoon N, Hong SN, Cho JG, Jeong HK, Lee KH, Park HW. Experimental
verification of the value of the Tpeak–Tend interval in ventricular arrhythmia inducibility
in an early repolarization syndrome model. J Cardiovasc Electrophysiol 2019;30:2098–
105. https://doi.org/10.1111/jce.14123.
[28] Antzelevitch C. Tpeak-tend interval as a marker of arrhythmic risk in early
repolarization syndrome. J Cardiovasc Electrophysiol 2019;30:2106–7.
https://doi.org/10.1111/jce.14118.
[29] Van Gelder IC, Crijns HJ, Van Der Laarse A, Van Gilst WH, Lie KI. Incidence
and clinical significance of ST segment elevation after electrical cardioversion of atrial
fibrillation and atrial flutter. Am Heart J 1991;121:51–6. https://doi.org/10.1016/0002-
8703(91)90954-G.
[30] Kok LC, Mitchell MA, Haines DE, Mounsey JP, DiMarco JP. Transient ST
elevation after transthoracic cardioversion in patients with hemodynamically unstable
ventricular tachyarrhythmia. Am J Cardiol 2000;85:878–81, A9.
[31] de Zwaan C, Bar FW, Wellens HJ. Characteristic electrocardiographic pattern
indicating a critical stenosis high in left anterior descending coronary artery in patients
 Journal Pre-proof

admitted because of impending myocardial infarction. Am Heart J 1982;103:730–6.

[32] Cardona A, Zareba KM, Nagaraja HN, Schaal SF, Simonetti OP, Ambrosio G, et
al. T-wave abnormality as electrocardiographic signature of myocardial edema in non-
ST-elevation acute coronary syndromes. J Am Heart Assoc 2018.
https://doi.org/10.1161/JAHA.117.007118.
[33] Migliore F, Zorzi A, Marra MP, Basso C, Corbetti F, De Lazzari M, et al.
Myocardial edema underlies dynamic T-wave inversion (Wellens’ ECG pattern) in
patients with reversible left ventricular dysfunction. Heart Rhythm 2011;8:1629–34.
https://doi.org/10.1016/j.hrthm.2011.04.035.
[34] Effoe VS, O’Neal W, Santos R, Rubinsztain L, Zafari AM. Pseudo-Wellens
syndrome, acute pancreatitis, and an anomalous coronary artery: a case report. J Med
Case Reports 2019;13:387–387. https://doi.org/10.1186/s13256-019-2315-1.
[35] Inayat F, Riaz I, Ali NS, Figueredo VM. Pseudo-Wellens’ syndrome secondary to
concurrent cannabis and phencyclidine intoxication. BMJ Case Rep
2018;2018:bcr2018225755, bcr-2018–225755. https://doi.org/10.1136/bcr-2018-

of
225755.
[36] Ju TR, Yeo I, Pontone G, Bhatt R. Pseudo-Wellens syndrome from sepsis-induced

ro
cardiomyopathy: a case report and review of the literature. J Med Case Reports
2021;15:151. https://doi.org/10.1186/s13256-021-02756-y.
[37] Ola O, Tak T. Pseudo-Wellens Syndrome in a Patient with Hypertension and Left
-p
Ventricular Hypertrophy. Am J Case Rep 2019;20:1231–4.
https://doi.org/10.12659/AJCR.916623.
re
[38] Sedhai YR, Basnyat S, Bhattacharya PT. Pseudo-Wellens’ syndrome in
pulmonary embolism. BMJ Case Rep 2018;11:e227464. https://doi.org/10.1136/bcr-
2018-227464.
lP

[39] Pollehn T, Brady WJ, Perron AD, Morris F. The electrocardiographic differential
diagnosis of ST segment depression. Emerg Med J 2002;19:129–35.
https://doi.org/10.1136/emj.19.2.129.
na

[40] Rosen MR. Cellular electrophysiology of digitalis toxicity. J Am Coll Cardiol

1985;5:22A-34A. https://doi.org/10.1016/S0735-1097(85)80460-5.
[41] Rosen MR, Gelband H, Merker C, Hoffman BF. Mechanisms of digitalis toxicity.
ur

Effects of ouabain on phase four of canine Purkinje fiber transmembrane potentials.

Circulation 1973;47:681–9. https://doi.org/10.1161/01.cir.47.4.681.
[42] Brugada J, Campuzano O, Arbelo E, Sarquella-Brugada G, Brugada R. Present
Jo

Status of Brugada Syndrome: JACC State-of-the-Art Review. J Am Coll Cardiol 2018.

https://doi.org/10.1016/j.jacc.2018.06.037.
[43] de Oliveira Neto NR, de Oliveira WS, Mastrocola F, Sacilotto L. Brugada
phenocopy: Mechanisms, diagnosis, and implications. J Electrocardiol 2019;55:45–50.
https://doi.org/10.1016/j.jelectrocard.2019.04.017.
[44] Pitzalis MV, Anaclerio M, Iacoviello M, Forleo C, Guida P, Troccoli R, et al. QT-
interval prolongation inright precordial leads: an additional electrocardiographic hallmark
of Brugada syndrome. J Am Coll Cardiol 2003;42:1632–7.
https://doi.org/10.1016/j.jacc.2003.07.005.
[45] Antzelevitch C. Brugada Syndrome. Pacing Clin Electrophysiol 2006;29:1130–
59. https://doi.org/10.1111/j.1540-8159.2006.00507.x.
[46] Castro Hevia J, Antzelevitch C, Tornés Bárzaga F, Dorantes Sánchez M, Dorticós
Balea F, Zayas Molina R, et al. Tpeak-Tend and Tpeak-Tend dispersion as risk factors
for ventricular tachycardia/ventricular fibrillation in patients with the Brugada syndrome.
J Am Coll Cardiol 2006;47:1828–34. https://doi.org/10.1016/j.jacc.2005.12.049.
[47] Tse G, Gong M, Wong WT, Georgopoulos S, Letsas KP, Vassiliou VS, et al. The
 Journal Pre-proof

Tpeak - Tend interval as an electrocardiographic risk marker of arrhythmic and mortality

outcomes: A systematic review and meta-analysis. Heart Rhythm 2017;14:1131–7.
https://doi.org/10.1016/j.hrthm.2017.05.031.
[48] Zhang L, Timothy KW, Vincent GM, Lehmann MH, Fox J, Giuli LC, et al.
Spectrum of ST-T-wave patterns and repolarization parameters in congenital long-QT
syndrome: ECG findings identify genotypes. Circulation 2000;102:2849–55.
[49] Goldenberg I, Zareba W, Moss AJ. Long QT syndrome. Curr Probl Cardiol
2008;33:629–94.
[50] Andrade AA, Stainback RF. Takotsubo cardiomyopathy. Tex Heart Inst J
2014;41:299–303. https://doi.org/10.14503/THIJ-14-4108.
[51] Ghadri J-R, Wittstein IS, Prasad A, Sharkey S, Dote K, Akashi YJ, et al.
International Expert Consensus Document on Takotsubo Syndrome (Part I): Clinical
Characteristics, Diagnostic Criteria, and Pathophysiology. Eur Heart J 2018;39:2032–46.
https://doi.org/10.1093/eurheartj/ehy076.
[52] Chatterjee S. ECG Changes in Subarachnoid Haemorrhage: A Synopsis. Neth

of
Heart J Mon J Neth Soc Cardiol Neth Heart Found 2011;19:31–4.
https://doi.org/10.1007/s12471-010-0049-1.

ro
[53] Arruda WO, Lacerda Jr. FS de. Electrocardiographic findings in acute
cerebrovascular hemorrhage a prospective study of 70 patients. Arq Neuropsiquiatr
1992;50:269–74. https://doi.org/10.1590/S0004-282X1992000300002.
-p
[54] Di Pasquale G, Pinelli G, Andreoli A, Manini G, Grazi P, Tognetti F. Holter
detection of cardiac arrhythmias in intracranial subarachnoid hemorrhage. Am J Cardiol
re
1987;59:596–600. https://doi.org/10.1016/0002-9149(87)91176-3.
[55] Rudehill A, Olsson GL, Sundqvist K, Gordon E. ECG abnormalities in patients
with subarachnoid haemorrhage and intracranial tumours. J Neurol Neurosurg Psychiatry
lP

1987;50:1375–81. https://doi.org/10.1136/jnnp.50.10.1375.
[56] Littmann L, Monroe MH. The “Spiked Helmet” Sign: A New
Electrocardiographic Marker of Critical Illness and High Risk of Death. Mayo Clin Proc
na

2011;86:1245–6. https://doi.org/10.4065/mcp.2011.0647.
[57] Samadov F, Gasimov E, Aliyev F, Isayev E. The “Spiked Helmet” sign - A
potential relationship to Takotsubo cardiomyopathy. Am J Emerg Med 2018;36:345.e5-
ur

345.e7. https://doi.org/10.1016/j.ajem.2017.11.041.
[58] Laundon RK, Littmann L. Spiked helmet pattern ST elevation in subarachnoid
hemorrhage. J Electrocardiol 2019;52:96–8.
Jo

https://doi.org/10.1016/j.jelectrocard.2018.11.016.
[59] Stone J, Mor-Avi V, Ardelt A, Lang RM. Frequency of Inverted
Electrocardiographic T Waves (Cerebral T Waves) in Patients With Acute Strokes and
Their Relation to Left Ventricular Wall Motion Abnormalities. Am J Cardiol
2018;121:120–4. https://doi.org/10.1016/j.amjcard.2017.09.025.
[60] Said SA, Bloo R, de Nooijer R, Slootweg A. Cardiac and non-cardiac causes of
T-wave inversion in the precordial leads in adult subjects: A Dutch case series and review
of the literature. World J Cardiol 2015;7:86–100. https://doi.org/10.4330/wjc.v7.i2.86.
[61] Persistent T-wave changes after alteration of the ventricular activation sequence.
New insights into cellular mechanisms of “cardiac memory”. | Circulation n.d.
https://www.ahajournals.org/doi/10.1161/01.cir.88.4.1811?url_ver=Z39.88-
2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed (accessed January
15, 2024).
[62] Bayés De Luna A. Clinical Electrocardiography. Oxford: Wiley-Blackwell; 2012.
https://doi.org/10.1002/9781118392041.
[63] Massie E, Walsh TJ. Clinical vectorcardiography and electrocardiography. Acad
 Journal Pre-proof

Med 1961;36:197.
[64] Wiggers CJ. Modern aspects of the circulation in health and disease. Lea &
Febiger; 1923.
[65] Pollock JD, Makaryus AN. Physiology, Cardiac Cycle. StatPearls, Treasure Island
(FL): StatPearls Publishing; 2023.
[66] Meijborg VMF, Belterman CNW, de Bakker JMT, Coronel R, Conrath CE.
Mechano-electric coupling, heterogeneity in repolarization and the electrocardiographic
T-wave. Prog Biophys Mol Biol 2017;130:356–64.
https://doi.org/10.1016/j.pbiomolbio.2017.05.003.
[67] B. Appleton, Qing Wei, S. Crozier, Feng Liu, S. Wilson, Ling Xia, et al. An
Electrical Heart Model Incorporating Real Geometry and Motion. 2005 IEEE Eng. Med.
Biol. 27th Annu. Conf., 2006, p. 345–8. https://doi.org/10.1109/IEMBS.2005.1616415.
[68] M. Jiang, L. Xia $^*$, G. Shou, Q. Wei, F. Liu, S. Crozier. Effect of Cardiac
Motion on Solution of the Electrocardiography Inverse Problem. IEEE Trans Biomed
Eng 2009;56:923–31. https://doi.org/10.1109/TBME.2008.2005967.

of
[69] Wei Q, Liu F, Appleton B, Xia L, Liu N, Wilson S, et al. Effect of cardiac motion
on body surface electrocardiographic potentials: an MRI-based simulation study. Phys

ro
Med Biol 2006;51:3405. https://doi.org/10.1088/0031-9155/51/14/009.
[70] Xia L, Huo M, Wei Q, Liu F, Crozier S. Electrodynamic heart model construction
and ECG simulation. Methods Inf Med 2006;45:564–73.
-p
[71] D. U. J. Keller, O. Jarrousse, T. Fritz, S. Ley, O. Dossel, G. Seemann. Impact of
Physiological Ventricular Deformation on the Morphology of the T-Wave: A Hybrid,
re
Static-Dynamic Approach. IEEE Trans Biomed Eng 2011;58:2109–19.
https://doi.org/10.1109/TBME.2011.2147785.
[72] Hamby RI, Hoffman I, Glassman E. The T loop in right ventricular hypertrophy.
lP

Dis Chest 1969;55:105–9. https://doi.org/10.1378/chest.55.2.105.

[73] Eriksson MJ, Sonnenberg B, Woo A, Rakowski P, Parker TG, Wigle ED, et al.
Long-term outcome in patients with apical hypertrophic cardiomyopathy. J Am Coll
na

Cardiol 2002;39:638–45. https://doi.org/10.1016/s0735-1097(01)01778-8.

[74] Mansour AM, Abdullah O, Allaham H, Danila C, Balla S. Giant Negative T
Waves and QT Prolongation in Non-cardiogenic Pulmonary Edema: A Case Report and
ur

Review of Literature. Cureus 2018;10:e3423. https://doi.org/10.7759/cureus.3423.

[75] Engel J, Brady WJ, Mattu A, Perron AD. Electrocardiographic ST segment
elevation: left ventricular aneurysm. Am J Emerg Med 2002;20:238–42.
Jo

https://doi.org/10.1053/ajem.2002.32634.
[76] Ford RV, Levine HD. The electrocardiographic clue to ventricular aneurysm. Ann
Intern Med 1951;34:998–1016. https://doi.org/10.7326/0003-4819-34-4-998.
[77] Ola O, Dumancas C, Mene-Afejuku TO, Akinlonu A, Al-Juboori M, Visco F, et
al. Left Ventricular Aneurysm May Not Manifest as Persistent ST Elevation on
Electrocardiogram. Am J Case Rep 2017;18:410–3.
https://doi.org/10.12659/AJCR.902884.
[78] Siddiqa A, Haider A, Jog A, Yue B, Krim NR. Pulmonary Embolism Presenting
as ST-Elevation Myocardial Infarction: A Diagnostic Trap. Am J Case Rep
2020;21:e927923-1-e927923-6. https://doi.org/10.12659/AJCR.927923.
[79] Harumi K, Burgess MJ, Abildskov JA. A Theoretic Model of the T Wave.
Circulation 1966;34:657–68. https://doi.org/10.1161/01.CIR.34.4.657.
 Journal Pre-proof

TABLES
Table 1.

Pattern Primary/Secondary, Comments

Positive/Negative

Male pattern Primary or secondary, Seen in approximately 90% of

positive or negative healthy young men; Elevation
of 1–3 mm; Most marked in V2

Normal variants Primary or secondary, Symmetric or Asymmetric.

of
positive or negative Observed in children, black
race, hyperventilation, women

ro
(right precordial leads), etc

Acute myocardial Primary positive

-p Hyperacute symmetric or
infarction tendency to symmetric T wave
re
as a temporal and
morphological predecessor of
lP

ST segment elevation
na

Acute pericarditis Primary positive ST segment elevation in III > II;

Elevation seldom > 5 mm;
ur

Spodick sign; PR-segment

depression
Jo

Hyperkalemia Primary positive Widened QRS and tall,

peaked, short-based tented T
waves; Low-amplitude or
absent P waves

Cardioversion Primary positive Striking ST-segment elevation

with tendency to symmetric T
wave, often >10 mm, but
lasting only a minute or two
immediately after direct-
current shock
 Journal Pre-proof

Prinzmetal’s angina Primary positive Same as ST-segment

elevation in infarction, but
transient

Pericarditis Primary positive STE followd by a T wave that

tends to symmetry, Spodick
sign

Sub-acute or Primary biphasic or Biphasic (early phase)

chronic ischemia negative Symmetric inverted T waves
(late phases)

of
Brugada syndrome Primary negative Elevated J point in V1 and V2,

ro
typically downsloping to a
-p symmetric or tending to
symmetric inverted T wave
re
Digitalis effect Primary negative Downsloping ST depression
with T wave symmetrically
lP

inverted, short QT interval

Alcoholism Primary negative Tends to symmetry. May be

na

transient or permanent

Athletes Primary negative With or without STE; must rule

ur

out hypertrophic
Jo

cardiomyopathy

Hypokalemia Primary flattened T wave can be flattened, ST

segment depression more
evident

Transient changes Primary negative Few seconds for

related to hyperventilation or hours/days
hyperventilation for glucose or alcohol intake

Stroke Primary giant negative Symmetric. May be very deep

 Journal Pre-proof

Central nervous Primary giant negative Known as cerebral T waves.

system May be giant (≥10 mm)
abnormalities and
Takotsubo

Spiked helmet sign Primary giant negative Symmetric, very deep or giant
and followed by a very long QT
interval

Table legend: Physiological and pathological causes of primary repolarization

morphologies.

of
ro
-p
re
lP
na
ur
Jo
 Journal Pre-proof

Table 2.

Pattern Primary/Secondary, Comments

Positive/Negative

Left ventricular Secondary, positive or Other features of left

hypertrophy negative ventricular hypertrophy such
as high voltages or subtle
duration increase in QRS
followed by an asymmetric
ST elevation and T wave in

of
leads where QRS is
negative, such as V1-V3

Bundle-branch block
ro
Secondary, positive or Asymmetric T wave. ST-
negative
-p segment deviation
discordant from the QRS
re

Ventricular aneurysm Secondary, positive or Asymmetric ST elevation and

lP

negative T wave in leads where there

is a q wave or fragmented
na

QRS

Early repolarization Secondary positive Most marked in V4, with

ur

notching at J point; Tall,

upright T waves
Jo

Myocarditis Secondary, positive or Asymmetric

(perimyocarditis) negative

Cardiomyopathies Secondary, positive or Includes hypertrophic

negative cardiomyopathy, Chagas
disease, dilated non
ischemic cardiomyopathy,
arrhythmogenic right
ventricular cardiomyopathy,
 Journal Pre-proof

noncompaction
cardiomyopathy, etc

Secondary to Secondary, positive or Various conditions causing

electrical negative ST depression and T wave
depolarization or inversion often in lateral
ventricular geometry leads (I, aVL, V5, V6)
abnormalities

Cor pulmonale and Secondary, positive or Symmetric or Asymmetric.

pulmonary embolism negative. May be giant Occasionally very deep

of
Secondary to apical Secondary, giant T wave inversion may be

ro
hypertrophy in negative giant (≥ 10 mm)
Yamaguchi syndrome -p
Table legend: Causes of secondary repolarization abnormalities.
re
lP
na
ur
Jo
 Journal Pre-proof

FIGURES
Figure 1.

of
ro
-p
re
lP
na
ur
Jo

Figure legend: Depiction and electrocardiographic correlates of AP alterations in

acute myocardial ischemia. The top three panels represent AP changes across
different cardiac layers: endocardium, M cells, and epicardium, contrasting
control conditions (black lines) with ischemic conditions (red lines), highlighting
the suppression of the AP plateau and abbreviation of APD during ischemia. The
bottom panel shows the corresponding ECG tracings with annotations for T-wave
onset (To), peak (Tp), and end (Te). This figure illustrates the morphological
changes in the T-wave, becoming taller and more symmetrical as a result of
ischemia-induced alterations in AP, signifying hyperacute T waves with a
symmetry ratio tending to 1.0, denoting a decreased area from Tp to Te in relation
to the area from To to Tp.
 Journal Pre-proof

Figure 2.

of
ro
-p
re
lP
na
ur
Jo

Figure legend: Electrocardiographic Patterns of Primary Positive ST-T

Alterations. A. Acute coronary occlusion displaying primary positive and
symmetrical ST-T segment elevation across leads I, aVL, V1-V6, indicative of
transmural ischemia. B. Symmetrical primary T wave with a broad base seen in
leads II, III, and aVF, characterizing the hyperacute T wave during chest pain. C.
 Journal Pre-proof

Symmetrical and peaked primary T wave in a patient with hyperkalemia,

prominently visualized in V2-V4 and limb leads II and III. D. ST-segment elevation
and primary T wave in a patient with pericarditis, with concurrent Spodick's sign
as evidenced by TP segment depression. E. ST-segment elevation at the J point
in V1 and V2 followed by a symmetrical negative T wave, characteristic of a
Brugada Syndrome pattern.

of
ro
-p
re
lP
na
ur
Jo
 Journal Pre-proof

Figure 3.

of
ro
-p
re
lP
na
ur
Jo

FIgure legend: Electrocardiographic Depictions of Primary Negative ST-T

Alterations. A. Wellens' pattern with biphasic ST-T alteration, suggestive of critical
stenosis in the proximal left anterior descending artery. B. Wellens' pattern with
 Journal Pre-proof

deeply inverted T waves. C. "Spiked helmet sign" observed in a patient with acute
massive pulmonary embolism and severe hypoxia, reflecting systemic stress and
autonomic imbalance. D. Primary ST-T alterations due to digitalis effect,
manifesting as scooped ST-segment depression with negative T waves. This
figure delineates various electrocardiographic scenarios presenting primary
negative ST-T changes, each offering a snapshot into the underlying
pathophysiological processes.

of
ro
-p
re
lP
na
ur
Jo
 Journal Pre-proof

Figure 4.

of
ro
-p
re
lP

Figure legend: Spiked helmet sign.

na
ur
Jo
 Journal Pre-proof

Figure 5.

of
ro
-p
FIgure legend: Simultaneous tracings of left ventricular (LV) pressure and
re
electrocardiogram (ECG) lead III measurements under two different conditions.
The upper tracing (red) represents LV pressure during increased preload (P20),
lP

whereas the middle tracing (blue) represents LV pressure at baseline (P0). The
lower tracings compare ECG lead III at increased preload (red) vs. baseline
na

(blue), demonstrating the influence of ventricular pressure changes on the ST-T

segment of the ECG. This graphical representation illustrates the concept of
ur

mechanoelectrical coupling (MEC) and how variations in cardiac mechanical

function can lead to alterations in the electrical patterns of the heart. Reproduced
Jo

with permission from author and from Elsevier.

 Journal Pre-proof

Figure 6.

of
ro
-p
re
lP
na
ur
Jo

Figure legend: Electrocardiographic Demonstrations of Secondary ST-T

Abnormalities. A. Left bundle branch block (LBBB) characterized by broad,
notched QRS complexes with ST-T wave changes opposite to the main QRS
direction, typically manifesting in the lateral leads. B. Left ventricular hypertrophy
(LVH) showing increased QRS amplitude and strain pattern with ST depression
and asymmetrical T wave inversion in the left-sided leads. C. Right bundle branch
 Journal Pre-proof

block (RBBB) with delayed R wave peak times in right precordial leads and
secondary repolarization abnormalities consistent with a typical RBBB pattern. D.
Ventricular pre-excitation presenting as a shortened PR interval and delta wave
associated with widened QRS complexes and secondary ST-T changes. E. Left
ventricular aneurysm post-myocardial infarction exhibiting persistent ST-segment
elevation in leads with pathologic Q waves, suggestive of aneurysmal wall motion
abnormalities.

of
ro
-p
re
lP
na
ur
Jo
 Journal Pre-proof

Figure 7.

of
ro
-p
re
lP
na
ur
Jo

Figure legend: Decision-making flowchart for the classification of ST-T wave

abnormalities in ECG analysis. The chart delineates a stepwise approach to
differentiate primary from secondary repolarization changes, guiding the clinician
away from the pitfalls of mislabeling abnormalities as ischemic without sufficient
basis. It emphasizes the significance of T wave morphology assessment,
highlighting characteristic features of primary abnormalities (symmetry, broad
base, variation in QT duration) and the distinct nature of secondary abnormalities
(asymmetry, no broad base, stable QT interval). This systematic framework aids
in correlating ECG findings with specific cardiac conditions and directs the
subsequent clinical investigation.
 Journal Pre-proof

of
ro
-p
re
lP
na
ur
Jo
 Journal Pre-proof

CREDIT Author Statement

José Nunes de Alencar, MD: Conceptualization, Methodology, Investigation,

Writing - Original Draft, Writing - Review & Editing, Supervision. Victor Felipe de
Andrade Matos: Investigation, Writing – Original Draft, Writing – Review &
Editing. Matheus Kiszka Scheffer, MD: Investigation. Sandro Pinelli Felicioni, MD,
PhD: Investigation. Mariana Fuziy Nogueira De Marchi, MD: Investigation. Manuel
Martínez-Sellés2,3: Investigation, Writing - Original Draft, Writing - Review & Editing.

of
ro
-p
re
lP
na
ur
Jo
 Journal Pre-proof

CONFLICTS OF INTEREST: no

of
ro
-p
re
lP
na
ur
Jo
 Journal Pre-proof

Graphical abstract

of
ro
-p
re
lP
na
ur
Jo
 Journal Pre-proof

Highlights

 Primary repolarization changes typically manifests with symmetry.

 Secondary repolarization changes often exhibit noticeable asymmetry.
 Ischemia is only one aspect of ECG interpretation, not the sole focus.
 A broader review of ECGs, including multiple factors, is recommended.

of
ro
-p
re
lP
na
ur
Jo