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 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 state3,6. 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 3,6. Furthermore, certain sodium and
calcium channels may become more active in hypokalemia, which may
further modify repolarization and possibly cause arrhythmias3,6.
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 V64,7,8. 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 9. The above, according to the cohort
study carried out by Chun Wei Liu et al., where these findings were
found 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 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.