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.