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\begin{document}

\title{Injury to the left main coronary artery disease or severe hypokalemia?
Possible duality in the same electrocardiogram: A case report and a
focused review of the literature}



\author[1]{Sergio Vásquez Lozano}%
\author[2]{Cristian Orlando Porras Bueno}%
\author[1]{Gabriel Ruiz Hernández}%
\author[3]{Mabel Olarte Jurado}%
\author[3]{Maria  Blanco Rueda}%
\affil[1]{Fundacion Cardiovascular de Colombia}%
\affil[2]{Pontifical Xavierian University}%
\affil[3]{Autonomous University of Bucaramanga}%


\vspace{-1em}



  
  \date{May 28, 2024}


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\textbf{Introduction}

An obstructive lesion of the left main coronary artery (LMCA) has
typically been described on the electrocardiogram (ECG) as a generalised
ST segment depression (SST) (maximum in V4-V6) associated with inverted
T waves in the same leads and elevation. of the SST in
aVR\textsuperscript{1}. Likewise, elevated SST in aVR is associated with
multivessel coronary artery disease \textsuperscript{1}. The presence of
these findings, together with an adequate clinical correlation, should
alert medical personnel to promptly rule out these conditions and
prevent possible adverse outcomes.

However, these electrocardiographic changes are not 100\% specific for
an obstructive lesion of the LMCA, since elevated SST in AVR could be
observed in multivessel coronary disease (three or more vessels),
occlusion of the proximal segment of the anterior descending artery, and
diffuse subendocardial ischemia \textsuperscript{2}.

Regarding the pathophysiology of hypokalemia, at the level of the
cardiomyocytes, an increase in the resting membrane potential is
generated, and the duration of the action potential and the refractory
period increase. Changes that are potentially arrhythmogenic, such as ST
segment depression, T wave flattening, and prominent U waves, which have
been described as a ``hallmark'' of hypokalemia \textsuperscript{3}.

However, an elevation of the SST in AVR simulating an LMCA lesion is a
rare finding within the electrocardiographic alterations described in
hypokalemia, which include: premature atrial and ventricular complexes,
sinus bradycardia, prolonged QTc, junctional tachycardia, AV block,
ventricular tachyarrhythmias, as well as SST depression, with a decrease
in the amplitude and inversion of the T wave and an increase in the
amplitude of the U wave, usually from V4 to V6 \textsuperscript{4}.
Below, we describe a clinical case of severe hypokalemia simulating on
an ECG an obstructive lesion pattern of the LMCA.

\textbf{Case history/Examination}

An 84-year-old woman with a history of high blood pressure and
cholecystitis on targeted antibiotic therapy in the previous 5 days was
admitted to the emergency department of a hospital specialising in
cardiology and cardiovascular surgery because she had an episode of
syncope while sitting in another hospital without referring other
symptoms to the questioning. Upon admission, his vital signs were within
the normal range, with abdominal pain on palpation in the right upper
quadrant of the abdomen, as well as a positive Murphy's sign and
arrhythmic heart sounds discordant with the pulse, with no other
findings on the examination.

The initial ECG showed a typical atrial flutter with rapid ventricular
response, with a 0.1 mV rise in SST in aVR, as well as a decrease in SST
and inversion of the T wave in Dl, inferior derivatives, and from V2 to
V5 (Figure 1), suggesting a possible obstructive lesion of the LMCA. In
addition, acute myocardial injury was documented with high-sensitivity
troponin T; however, chest pain was not documented, so it was considered
secondary to the ongoing infectious process. Likewise, strikingly,
severe hypokalemia was documented (1.9 meq/L), which, when corrected,
showed the resolution of the initially mentioned electrocardiographic
findings suggestive of a LMCA lesion, also returning to a sinus rhythm
in the ECG (Figure 2).

For its part, the echocardiogram demonstrated preserved biventricular
function, with a left ventricular ejection fraction (LVEF) of 61\%,
without contractility disorders, valvular heart disease, or other
relevant findings (Figure 3). Therefore, it was considered that the
electrocardiographic findings were secondary to hypocalcemia, thus
completing the broad-spectrum antibiotic therapy for his cholecystitis
and presenting a satisfactory clinical and paraclinical evolution during
follow-up.

\textbf{Differential diagnosis, investigations and treatment}

In relation to the differential diagnosis of electrocardiographic
alterations caused by severe hypokalemia, certain pathologies with
similar electrocardiographic findings have been
described\textsuperscript{5}. These include:

\begin{itemize}
\tightlist
\item
  Myocardial ischemia: T-wave inversion and ST-segment depression, which
  are characteristic of hypokalemia, may also be indicative of
  myocardial ischemia.
\item
  Hypocalcemia: QT interval prolongation, which may occur in
  hypokalemia, may also be a sign of hypocalcemia.
\item
  Hypomagnesemia: Like hypokalemia, hypomagnesemia can cause arrhythmias
  and QT interval prolongation.
\item
  Use of certain medications: Some medications, such as antiarrhythmics,
  tricyclic antidepressants, and antipsychotics, can cause
  electrocardiographic alterations similar to those of hypokalemia.
\end{itemize}

After performing an exhaustive interrogatory and a complete laboratory
test, these conditions were ruled out in our case. Consequently, it is
crucial to keep in mind that, in addition to the ECG, the differential
diagnosis should always be supported by a thorough clinical evaluation
that includes the patient's medical history, physical examination, and
laboratory results.

\textbf{Outcome and follow up}

During the hospitalisation, her electrocardiographic findings resolved
after replenishing her potassium levels to normal values, and her
clinical and paraclinical condition also improved after completing
antibiotic therapy for her cholecystitis. During the 3-month follow-up,
he denied having syncope or other symptoms.

\textbf{Discussion}

After performing a review of the available medical literature in the
major clinical databases (PubMed, Google Scholar, and Scielo), we found
just one case report of hypokalemia simulating a pattern of obstruction
of the left main coronary artery \textsuperscript{3}.

In this case, described by Burgos et al., a 42-year-old female patient
with a medical history of gestational hypertension and acute
gastroenteritis consulted the emergency department due to palpitations.
Her initial electrocardiogram presented sinus tachycardia, with
elevation of the ST segment of 0.2 mV in aVR and V1 and diffuse
depression of the ST segment in more than 7 leads. These findings are
similar to those found in our case, however differing equally, given
that in our case a typical atrial flutter with rapid ventricular
response was documented.

Furthermore, as in our case, hypokalemia was also documented, but
moderate (2.8 meq/L), and an echocardiogram was within normal
parameters, which ruled out left ventricular dysfunction, segmental
contractility disorders, or valvular heart disease, among others.
However, unlike our case, the case described by Burgos et al. did not
present myocardial injury, which allowed them to further doubt a
possible occlusion of the trunk of the left coronary artery.

Finally, it should be noted that despite the differences in age,
clinical presentation, the presence of acute myocardial injury, and the
additional finding of typical atrial flutter in our case, in both cases
the pattern of occlusion of the trunk of the left coronary artery was
resolved by correcting the hypokalemia. Table 1 of the article presents
and contrasts the main characteristics of the two cases mentioned.

Regarding the pathophysiology of the electrocardiographic alterations
seen in hypokalemia, modified potassium ion balance in the cardiac cells
causes repolarization abnormalities in hypokalemia. Potassium channels
normally open during the repolarization phase of a cardiac action
potential, allowing potassium ions to leave the cell. The cell becomes
hyperpolarized as a result, going back to its resting
state\textsuperscript{3,6}. This ionic balance can be disrupted by low
potassium levels in the blood plasma in hypokalemia, leading to aberrant
repolarization, as evidenced by alterations in the T-wave and ST-segment
on the ECG \textsuperscript{3,6}. Furthermore, certain sodium and
calcium channels may become more active in hypokalemia, which may
further modify repolarization and possibly cause
arrhythmias\textsuperscript{3,6}.

Respect the electrocardiographic findings described in hypokalemia;
these include premature atrial and ventricular complexes, sinus
bradycardia, prolonged QTc, junctional tachycardia, atrioventricular
blocks, ventricular tachyarrhythmias, as well as segment ST depression,
with a decrease in the amplitude and inversion of the T wave and an
increase in the amplitude of the U wave, usually from V4 to
V6\textsuperscript{4,7,8}. However, ST segment elevation in aVR with
generalized descending of the same in more than 7 leads simulating an
occlusion of the left main coronary artery has not been specifically
described.

However, the LMCA occlusion pattern does include it, although its
specificity increases, in the presence of elevated SST in V1 (less than
in aVR), in aVL, in Dl and aVL, or from V2 to V6, regarding the pattern
of LMCA occlusion that has been described, which corresponds to an
elevation of the AVR segment with a decrease in the diffuse SST in more
than 7 leads \textsuperscript{9}. The above, according to the cohort
study carried out by Chun Wei Liu et al., where these findings were
found \textsuperscript{9}. Likewise, the previously described
electrocardiographic findings were also absent, as in the case of Burgos
et al.

Finally, it has been described that a mirror image of leads V5 and V6 is
recorded by the lead aVR. Therefore, lead aVR will nearly always have
ST-segment elevation if there is ST-segment depression in the lateral
precordial leads \textsuperscript{2}, which could explain this finding
in the Burgos et al. case and in our case. Consequently, we can conclude
that in patients with an ECG suggestive of an obstructive lesion of the
LMCA, severe hypokalemia should be ruled out as a differential
diagnosis, mainly when there is no elevation of the ST segment in V1,
nor aVL, nor concomitant chest pain among others.

\textbf{Author contribution statement}

Porras Bueno Cristian Orlando: conceptualization, data curation, formal
analysis, funding acquisition, investigation, methodology, project
administration, resources, supervision, validation, visualisation,
writing (original draft), writing review, and editing.

V\selectlanguage{ngerman}ásquez Lozano Sergio Humberto: conceptualization, data curation, formal
analysis, investigation, writing (original draft), review, and editing.

Ruiz Hernández Gabriel Fernando: conceptualization, data curation,
formal analysis, investigation, writing (original draft), review, and
editing.

Olarte Jurado Mabel Lucero: conceptualization, data curation, formal
analysis, investigation, writing (original draft), review, and editing.

Maria Paula Blanco Rueda: conceptualization, data curation, formal
analysis, investigation, writing (original draft), review, and editing.

\textbf{Acknowledgments}

To the Autonomous University of Bucaramanga (UNAB) and the Pontifical
Xavierian University for promoting publication and research\textbf{.}

\textbf{References}

\textbf{1.} \emph{Prieto-Solís JA, Benito N, Martín-Durán R. Diagnóstico
electrocardiográfico de la obstrucción del tronco coronario izquierdo
mediante el análisis vectorial del segmento ST y el complejo QRS. Rev
Espanola Cardiol. 2008;61(2):137-145. doi:10.1157/13116201}

\textbf{2.} \emph{Nikus KC, Eskola MJ. Electrocardiogram patterns in
acute left main coronary artery occlusion. J Electrocardiol.
2008;41(6):626-629. doi:10.1016/j.jelectrocard.2008.06.020}

\textbf{3.} \emph{Burgos LM, Domínguez M, Battioni L, Costabel JP, Trivi
M. Cambios electrocardiográficos asociados a hipopotasemia: Alteraciones
del segmento ST imitando isquemia miocárdica de múltiples territorios.
Rev Chil Cardiol.
2017;36(3):244-248.doi:10.4067/s0718-85602017000300244}

\textbf{4.} \emph{Thu Kyaw M, Maung ZM. Hypokalemia-Induced Arrhythmia:
A Case Series and Literature Review. Cureus. 2022.
doi:10.7759/cureus.22940}

\textbf{5.} \emph{Sethuraman, C., Mohd, S. F., Govindaraju, S., Tiau, W.
J., Farouk, N. D. M., \& Hassan, H. H. C. (2020). Severe Hypokalemia ECG
Changes Mimicking Those of Acute Coronary Syndrome (ACS) in Patient with
Underlying Ischaemic Heart Disease: A Case Review. Open Journal of
Emergency Medicine, 08(02), 53--58.
https://doi.org/10.4236/ojem.2020.82006}

\textbf{6.} \emph{Duque, M., Aristizábal-Colorado, D., Weir, D.,
Gaviria, M. C., \& Uribe, W. (2020). La repolarización auricular y sus
implicaciones clínicas. Revista Colombiana de Cardiología, 27(1),
36--40. https://doi.org/10.1016/j.rccar.2019.05.006}

\textbf{7.} Teymouri N, Mesbah S, Navabian SMH, et al. ECG frequency
changes in potassium disorders: a narrative review. Am J Cardiovasc Dis.
2022;12(3):112-124. Published 2022 Jun 15.

\textbf{8.} Khan U, Afzal U, Kask L, et al. ''Ion-Flux'': The natural
course of ECG changes in severe hypokalemia. Curr Probl Cardiol.
2024;49(1 Pt C):102158. doi:10.1016/j.cpcardiol.2023.102158

\textbf{9.} \emph{Liu C, Yang F, Hu Y et al. Combining
electrocardiographic criteria for predicting acute total left main
coronary artery occlusion. Front Cardiovasc Med. 2022;9.
doi:10.3389/fcvm.2022.936687}

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