Friday, April 20, 2018

OMI Can be Diagnosed by "Pseudonormalization of ST Segments"

This post was written by Tarissa Lai, one of our outstanding EM residents at Hennepin County Medical 
Center, with comments by Steve Smith and Dan Lee.

Case

A 30 something y.o. female with HTN, HLD, diabetes, ESRD on dialysis is brought in by EMS with 
sudden onset, left -sided chest pain for the past four hours.


This is her pre-hospital ECG:

 This is her first ECG in the ED:
What do you think?



















I interpreted this as normal sinus rhythm with LVH, but no significantly peaked T waves concerning 
for hyperkalemia. I did not appreciate any significant ST elevation.

However, the prehospital ECG is more worrisome: the T-wave inversion in V5 and V6 is preceded
by ST Elevation. In LVH, T-wave inversion in leads V5 and V6 should be preceded by ST depression, or
at least by an isoelectric ST segment. These look like ischemic ST segments and T-waves.

More Clinical history:
I first met her on an overnight shift while she was sleeping in a hallway bed. She was a difficult 
historian as she kept answering in one word replies before falling back asleep. The patient had gone 
to dialysis that day without any significant change in her regimen. While she was in her bed at home, 
she had sudden onset of left sided chest pain that radiated to her shoulder.  The pain
was pleuritic, without nausea or diaphoresis. The nitro she took in the ambulance did not help. 
Her physical exam was remarkable for a young woman sleeping comfortably in bed, whose chest pain
was easily reproducible with palpation.


Although her comfortable appearance with pleuritic and reproducible chest pain were reassuring, some 
components of her story were concerning, including the sudden left sided chest pain and radiation to 
her shoulder. Given her risk factors (HTN, HLD, ESRD from diabetes) I decided to obtain a broad 
cardiac workup for the patient: serial ECGs, labs, serial troponins, CXR and bedside cardiac ultrasound. 
She also received an additional nitro in the ED after receiving aspirin and nitro via EMS.


This is the patient's old ECG from ~2 months prior:
There is ST elevation that is most notable in V1, V2 and aVR with ST depression that is most obvious 
in the inferior leads and V6. I interpreted these as findings consistent with "secondary" ST-T abnormalities due to
her known LVH.
When comparing the old and new ECGs, there is:
New relative ST depression in V1-V3 and
New relative ST Elevation in: II, III, aVF and in V5 and V6.
When I say "relative," I mean relative to the previous ECG, which is the baseline, chronic, non-ischemic ECG.



Here is the Point of Care Cardiac Ultrasound (POCUS), short axis:

This shows the anterior wall (top) and septum contracting perfectly, but the postero-lateral walls not contracting.


Parasternal Long Axis View


There is a posterolateral wall motion abnormality. This appears to be new, as her last formal 
echocardiogram 2 years ago was relatively normal.

All of this is consistent with an acute postero-lateral MI. [New relative ST elevation in V5 and V6 (lateral
wall), new relative ST depression in V1-V3 (posterior wall) and new relative ST Elevation in II, III, aVF
(inferior wall).

At this time, her initial troponin came back at 103.2 ng/mL (103,000 ng/L, extremely high!!),
and her K was 4.6 mEq/L.

While the patient was known to have mild troponin elevations in the past, this was clearly diagnostic of acute MI.


Given the WMA on her echo, a repeat ECG was obtained with posterior lead placement:
There is now STE in V7, V8 and V9, which is consistent with a posterior MI.
The decreased voltage noted in the first couple ECGs is even more obvious now.
There is now also ST depression in V2 and V3 (previously only relative)
On closer evaluation of her old ECG compared to the ones from today, you can see what might
be called "ST Segment Pseudonormalization." Her previous ST elevation in V1-V3 is now gone,
and the voltage from her LVH is decreasing with each successive ECG. This would make sense in
the setting of an acute posterior MI, which can present with precordial ST depression.

V1-V3 side by side:

NEW OLD  


The patient was emergently taken to the cath lab and found to have severe multi-vessel disease with 
high thrombus burden, and the culprit lesion was a 100% thrombotic occlusion in the proximal
left circumflex.


Diagnostic angiogram:

Post PCI of the circumflex artery. She had an uncrossable lesion in the LAD with an estimated 99% 
occlusion. Arrowheads represent some of the remaining thrombotic lesions.

Troponin peaked around 325 ng/mL (massive). Pertinent results of the formal Transthoracic Echo:
    -Moderately severe concentric left ventricular hypertrophy.
    -Severely decreased left ventricular systolic function with an estimated EF of 22%.
    -Akinesis of the apical septal, apical inferior, and apical segments
    -Hypokinesis of the basal to mid anterolateral and basal to mid inferolateral segments. (Basal
    Inferolateral = Posterior)

    Learning Points:
    1. Pseudonormalization of STE and/or STD, as in this patient with LVH, but also in LBBB and other
    etiologies of chronic ST shift, should raise concern for OMI (Occlusion Myocardial Infarction).
    2. Likewise, ST shift from a previous ECG (relative ST elevation or depression) is equivalent to STE or STD.
    3. Ultrasounds can be very helpful in guiding your diagnostic pathway: location of WMA on US led 
    to obtaining posterior leads.
    4. Clinical presentation is important, but so is history. Have a higher suspicion for true pathology in 
    anyone with significant comorbidities such as ESRD from diabetes, even if they are young and 
    appear “not sick” on presentation.
    5. Refractory Chest pain with a clearly positive troponin, without an alternative explanation, is an indication
    for emergent cath lab activation regardless of ECG or bedside echo findings.



    Comments by Dan

    This case was particularly interesting for several reasons. First, the patient is such a young woman to have an occlusion MI (OMI), the likely difference being her significant risk factors. If she had no risk factors, it is doubtful that she would have developed such extensive coronary artery disease as we see on the angiogram. 

    Because the troponins were so high, the clinicians did not need to rely on other diagnostics, including posterior leads and ultrasound, to confirm OMI and salvage what myocardium could be saved after hours of constant chest pain before the patient presented.  However, this additional information was supportive.

    Note that by current guidelines, this patient had a NSTEMI, but it would hard to argue that her condition would not have worsened if she was left to 'next day cath'.  I took part in her ICU care and she was extubated and stable to transfer to a stepdown unit after a few days. Her repeat ECHO showed an improving EF of 37%. Patients like her are the reason we are advocating for a change in the ACS paradigm from STEMI to OMI

    Her first EKG in isolation has no hard findings that are diagnostic for an acute coronary occlusion. The importance of having a baseline EKG for comparison cannot be understated. The old EKG shows LVH by Sokolow-Lyon and Cornell criteria but much of that voltage is resolved in the new EKG, which is commonly seen in acute occlusion superimposed onto LVH. For some reason (with debatable physiology), coronary occlusion often causes decrease in the high voltage of LVH on the EKG. Thus it is difficult to study occlusions, particularly subtle occlusions, in the context of LVH. Armstrong et al attempted to study it but may have included too many 'obvious' cases - the criteria from that paper would certainly have missed this case.

    There is an interesting finding in this EKG which is the positive notching of the latter portion of the QRS complex, upright in I, II, aVL and downward notching in III, aVF.  

    I believe these represent the equivalent of Q-waves, or infarcted myocardium, of the posterior (inferobasal, lateral) wall. They appear in the latter part of the QRS complex because the posterior/basal wall is the last part of the ventricle to depolarize. The notching is not seen in the precordial leads because as it is traditionally taught, a tall R wave in V1 represents the 'upside down' Q wave in posterior infarction.  Thus, if you have LVH in which baseline precordial voltages are already predominantly negative, a posterior infarction should 'cancel out' some of that voltage and possibly diminish the voltage evidence of LVH on the EKG. Note that this is completely different from 'terminal QRS distortion'

    This paper by Nui et al describes this finding (the "Delayed Activation Wave") in left circumflex occlusions but (I believe mistakenly) compares it to terminal QRS distortion. This finding is not new, and is analogous to Cabrera's and Chapman's sign.  As a Q-wave equivalent, this notching would be expected to persist in subsequent EKGs, as seen in the patient's follow up EKG 6 days later:

    Wednesday, April 18, 2018

    T-wave inversions and dynamic ST elevation


    Written by Pendell Meyers, with edits by Steve Smith

    I received a text message with no clinical information other than the following ECG, with the question "Is this Wellens? No prior ECG available."



    What do you think?


















    I responded that this ECG represented benign T-wave inversion (BTWI), not Wellens. I asked for more history.

    It turns out this was a 25 year old male with no past medical history presenting after he was found "passed out" or laying down on the floor of the nursing home facility where he works. He was reported to be intermittently answering questions and seeming "not himself." Family reported that he had 2 similar episodes in the past 3 months, which the patient describes as similar to "bad trips," including increased fatigue, confusion, and vague hallucinations. He had been evaluated last month at an outside hospital by a psychiatrist. He denied any substance use on the day of presentation. There was no history of exertional syncope or sudden death in the family.

    Apparently a single troponin was ordered on the basis of the perceived ECG findings, which was negative. Three serial ECGs were performed which were all identical (though BTWI is not necessarily always perfectly constant).

    He was discharged.

    Two days later he presented again with a similar story. Here is his ECG on arrival from the second visit:
    This ECG shows sinus rhythm around 65 bpm. The QRS complex has moderately high voltage but otherwise normal morphology. There is STE in V1-V3 of 1.0, 1.5, and 1.5 millimeters, which is completely normal. There are prominent J-waves in leads V4-V6, as well as leads II, III, and aVF. Lead V3 shows the first and third complexes with terminal T-wave inversions, but the second complex does not appear to have this terminal T-wave inversion - whether this is due to a brief episode of baseline wandering / lead manipulation, or beat to beat variation is unknown, but I believe it is more likely brief baseline movement. The terminal T-wave inversion is no longer present in V4 as it was in the first presentation. Overall the second ECG is better characterized as "benign early repolarization" or simply "benign ST elevation" than by BTWI.



    Another single troponin was normal. He was discharged with outpatient psychiatry and primary care.


    How do I recognize this as BTWI? 

    Most importantly because it matches the examples of BTWI I have seen on this blog, and does not match Wellens syndrome. The T-wave inversion in lead V3 of the initial ECG just does not look like reperfusion. Lead V4 of the initial ECG has the complete morphologic package of BTWI, including high voltage (large R wave), smaller S-wave, prominent J-wave followed by minimal STE and then characteristic terminal T-wave inversion. The history obviously helps as well, as this was a young African-American patient with symptoms of near-zero pretest probability of ACS. Some cases will not be so easy clinically.

    Also important, "Wellens' syndrome" requires clinical factors in addition to ECG findings, including chest pain which resolved prior to recording of the ECG. Wellens' syndrome is not diagnosed during ongoing pain, as this would not be consistent with reperfusion (which should produce resolution of pain). On the ECG Wellens' syndrome also requires that there are preserved R-waves in the precordial leads.

    Below I have reproduced a list of findings of BTWI from a series of other blog posts on this topic on this site, and we will go through each one with respect to the first presentation ECG:



    1. There is a relatively short QT interval (QTc less than 425)
    YES. Computerized QTc in this case was 424 msec.

    2. The leads with T-wave inversion often have very distinct J-waves
    YES. J-waves are present in V4-6, as well as II, III, aVF.

    3. The T-wave inversion is usually in leads V3-V6 (in contrast to Wellens' syndrome, in which they are V2-V4)
    Here the TWI is in leads V3-4 only. So this doesn't really distinguish. Also, Wellens' syndrome is simply one particular example of reperfusion (in this case, of the anterior wall). Reperfusion can obviously happen in any coronary distribution, and the same pattern of findings will happen in any affected wall.

    4. The T-wave inversion does not evolve and is generally stable over time (in contrast to Wellens', which always evolves)
    There is certainly no evolution consistent with continued reperfusion from OMI (occlusion MI), as there would be in the case of Wellens' syndrome. The changes from presentation 1 to 2 are clear, but these are potentially explainable by lead placement or simply the normal variation of ECG findings in normal healthy patients from day to day or hour to hour (we don't really know the answer to this, except to say that we have a large amount of personal experience showing many cases of benign ECG patterns which show changes with repeat ECGs). We have shown many times on this blog that essentially no normal ECG is 100% guaranteed to be completely stable over time. See this case. And this case. And this case. And this very recent case with supporting references:

    Huge Precordial ST Elevation in an ED Patient



    The opposite, however, is fairly reliable: if the patient has OMI or reperfusion from OMI, the ECG abnormalities will evolve along the expected progression (depending upon continued occlusion and infarction or reperfusion). Therefore, lack of serial ECG changes in the appropriate time frame can be interpreted as evidence against ischemia, but presence of changes is not necessarily indicative of ischemia (it might be, but it might not because there is a significant amount of variation based on lead placement, day to day, etc). Those who have studied cases of OMI versus benign ECG patterns from this blog can usually tell the difference.


    5. The leads with T-wave inversion (left precordial) usually have some ST elevation
    In the first presentation ECG there is minimal STE. In the second presentation there is slightly more.

    6. Right precordial leads often have ST elevation typical of classic early repolarization
    In the first presentation, no. In the second presentation, yes.

    7. The T-wave inversion in leads V4-V6 is preceded by minimal S-waves
    YES, seen in V4 of the first presentation ECG.

    8. The T-wave inversion in leads V4-V6 is preceded by high R-wave amplitude
    YES, again seen in V4 of the first presentation ECG.

    9. II, III, and aVF also frequently have T-wave inversion
    YES, the first presentation ECG does have flat/minimally inverted T-waves in the inferior leads.


    Learning Points:

    Benign T-wave Inversion is recognizable and (with experience) reliably differentiated from anterior reperfusion (Wellens).

    Almost all the patterns of normal variant ECGs may show some changes upon serial ECGs. This may be due to lead placement and/or actual primary morphologic change of unknown etiology and significance. These changes can be distinguished from ischemic progression changes.

    If you record serial ECGs and there is no evolution over an appropriate time frame, then the lack of evolution is a fairly strong piece of evidence against ischemic ECG changes. The presence of dynamic changes on repeat ECGs, however, may be either progression of ischemia or meaningless, normal variation in a patient's baseline - with the experience provided by this blog these are usually not difficult to differentiate.



    References

    1. Kambara et al. Early repol is not stable over time.  https://www.sciencedirect.com/science/article/pii/0002914976901429

    2. Mahaveer C. Mehta, MD.  Abnash C. Jain, MD.  Early Repolarization on Scalar Electrocardiogram. The American Journal of the Medical Sciences. June 1995; 309(6):305–311.


    ABSTRACT

    Sixty thousand electrocardiograms were analyzed for 5 years. Six hundred (1%) revealed early repolarization (ER). Features of ER were compared with race-, age-, and sex-matched controls (93.5% were Caucasians, 77% were males, 78.3% were younger than 50 years, and only 3.5% were older than 70). Those with ER had elevated, concave, ST segments in all electrocardiograms (1—5 mv), which were located most commonly in precordial leads (73%), with reciprocal ST depression (50%) in aVR, and notch and slur on R wave (56%). Other results included sinus bradycardia in 22%, shorter and depressed PR interval in 38%, slightly asymmetrical T waves in 96.7%, and U waves in 50%. Sixty patients exercised normalized ST segment and shortened QT interval (83%). In another 60 patients, serial studies for 10 years showed disappearance of ER in 18%, and was seen intermittently in the rest of the patients. The authors conclude that in these patients with ER: 1) male preponderance was found; 2) incidence in Caucasians was as common as in blacks; 3) patients often were younger than 50 years; 4) sinus bradycardia was the most common arrhythmia; 5) the PR interval was short and depressed; 6) the T wave was slightly asymmetrical; 7) exercise normalized ST segment; 8) incidence and degree of ST elevation reduced as age advanced; 9) possible mechanisms of ER are vagotonia, sympathetic stimulation, early repolarization of sub-epicardium, and difference in monophasic action potential observed on the endocardium and epicardium.

    3. Here is a good review of early repolarization by Mehta:

    Tuesday, April 17, 2018

    Potato Poisoning (Not due to Solanine in greens!). With Positive Modified Sgarbossa Criteria.

    A dialysis patient presented with progressive weakness over 3 days.  He denied chest pain or shortness of breath.  He also had a history of cardiomyopathy, DM, and HTN.

    Here is his emergent ECG:
    It is slow and regular.  There are no P-waves. 
    So it is junctional rhythm or a right bundle escape, mimicking LBBB

     (Or it is sinus with a hidden P-wave).At first glance, it appears to have Left Bundle Branch Block (LBBB), with rS in right precordial leads and wide monophasic R-wave in I, aVL, V5 and V6.
    The ST segment in V2 is excessively proportionally discordant, at 5 mm divided by S-wave of 20 mm = 25%.

    Third criterion positive in modified Sgarbossa!
    Is this LAD occlusion in the presence of LBBB?

    Notice
    As in yesterday's case of RBBB: 
    Is this just right bundle branch block?The QRS is too long
    The computer measurement of 218 ms is correct.
    Moreover, the T-waves are very peaked.

    A previous ECG was found and was normal.
    Thus, this ECG is diagnostic of hyperkalemia.
    There may be an underlying sinus pacemaker, but it is impossible to tell because the atrium does not depolarize and thus no P-wave is visible

    Remember that hyperkalemia causes PseudoSTEMI STE in V1 and V2.
    See this case: 

    "Steve, what do you think of this ECG in this Cardiac Arrest Patient?"


    In this case today, that pseudoSTEMI pattern is added to a pseudo-LBBB to result in a modified Sgarbossa false positive morphology!

    LBBB and QRS duration

    In this study of consecutive patients with LBBB who were hospitalized and had an echocardiogram, 13% had a QRS duration greater than 170 ms, and only 1% had a duration greater than 190 ms.

    Clinical Course

    The clinicians recognized this as hyperkalemia.  The lab result was too high to measure (greater than 9.4 mEq/L).


    The patient received albuterol x 6, calcium gluconate x 5 g, D50 (50 ml) x 2, 5 units regular insulin, 40 mg furosemide, and 50 mL of Na bicarb.

    It turns out he had been told several days earlier that his K was low and so he had eaten several baked potatoes.  Baked potatoes have about 926 mg of K (boiled potatoes have 296 milligrams, and an average banana has 426 mg).  KCl is 74 mg per mEq, so the number of milliequivalents is far less, but a dialysis patient eating many baked potatoes is sufficient to substantially raise the K.


    After dialysis, this was the followup ECG:
    Normal, except V1 and V2 are recorded too high on the chest (fully negative P-wave in V1, negative P-wave in V2) and there is slight ST depression.

    Monday, April 16, 2018

    Is this just right bundle branch block?

    This ECG was texted to me with the text:

    "There is a history of RBBB but we do not have an image to compare this with.  I interpret as RBBB with atrial fib.  Anything else?"
    What was my response?




















    The QRS duration is long: the computer measured it at 212 ms.  I measured it at approximately 180 ms.  Either way, it is is too long for simple RBBB.

    My response:  "It is a pretty wide RBBB.  So think about high potassium."
    The minimal ST segment shifts seen throughout are within normal limits, so there is no ischemia here.

    The response was: K = 6.3 mEq/L.

    The patient was treated for hyperkalemia.  Unfortunately, no post-treatment ECG was recorded.



    QRS duration in RBBB and LBBB

    RBBB by definition has a long QRS (at least 120 ms).  But very few are greater than 190 ms.  Literature on this is somewhat hard to find, but in this study of patients with RBBB and Acute MI, only 2% of patients with pre-existing RBBB had a QRS duration greater than 200 ms.  This study only reported durations in 10 ms intervals up to 150 ms, but one might extrapolate from it that approximately 10% of patients with baseline RBBB have a QRS duration greater than 160 ms.  194 ms would be quite unusual.

    The point of this is that if you see BBB with a very long QRS, you must suspect hyperkalemia.  Then of course the peaked T-waves should tip you off.   Unless a patient has severe hypercalcemia (this should be evident by a short QT on the ECG as seen at the bottom of this post), or severe hyperphosphatemia (which is very unusual), treatment with calcium is harmless if you read an ECG falsely positive for hyperkalemia.

    So don't wait for the laboratory K or you might be resuscitating a cardiac arrest (see the case with ECGs #3 and #4 of this post).

    How about LBBB?

    In this study of consecutive patients with LBBB who were hospitalized and had an echocardiogram, 13% had a QRS duration greater than 170 ms, and only 1% had a duration greater than 190 ms. 



    See this case.

    Is This a Simple Right Bundle Branch Block?


    Here is a case of RBBB with a K of 7.9 and QRS duration of 194 ms.


    This was recorded next day at a K of 3.3:
    The QRS duration is 149 ms, much more appropriate for simple RBBB









    Saturday, April 14, 2018

    Besides the Nonspecific T-wave Inversion in aVL, What Else is Abnormal on this ECG?

    This case was sent by Laszlo Farkas, a paramedic from Hungary.  He discussed it with Janos Borbas MD and Robert Sepp MD from University of Szeged 2nd Department of Internal Medicine and Cardiology Clinic. 

    The case inspired me to resurrect a case that I published 10 years ago with the same ECG finding (2nd case below).

    What is the finding?

    What does it signify?

    Case

    An elderly male presented with chest pain.  Here is the first ED ECG:
    Hint: the finding is NOT the T-wave inversion in aVL


    This ECG that I published 10 years ago in Critical Decisions in Emergency and Acute Care Electrocardiography has the same finding:
    What is the finding?

























    The finding is an inverted U-wave, as demonstrated with arrows here:
    Inverted U-waves in a patient with chest pain are reported to be highly specific, but insensitive, for ischemia/infarction.






    Here is the ECG from Laszlo's case again:
    See the inverted U-waves in V3, V4, V5



    In Laszlo's case, he recognized it and recorded another ECG 35 minutes later:
    Now the U-waves are not the issue.
    There is obvious STEMI.


    This is after reperfusion and stenting of an occluded LAD:
    Terminal T-wave inversion, consistent with reperfusion.




    And then 13 minutes later:
    Resolution of much of the ST Elevation (but not all).
    Now U-waves are upright in V2-V550-70% reduction in STE is good evidence of tissue reperfusion
    (there can be reperfusion of the artery without reperfusion of the myocardium, called "No Reflow", and the ECG is the best predictor of reflow, correlating closely with angiographic "myocardial perfusion grade," or "blush")




    Here is case 2:

    This shows the initial ECG shown again, the comparison ECG from previous, and the reperfusion ECG after stenting of LAD that had severe subtotal thrombotic occlusion with TIMI-2 flow:


    This 89 year old had an episode of unresponsiveness. 


    Previous ECG:



    First ECG with arrows (again)
    Slight STD in inferior and lateral leads, some STE in aVL, and profound negative U-waves in V3-V5. 


    After Reperfusion of LAD:
    Reperfusion T-waves (Wellens' waves)




    Short Summary of the U-wave

    [Adapted from one of my chapters (in the ACS section, which I edited) in Critical Decisions in Emergency and Acute Care Electrocardiography.  There are some contributions by Farkas Laszlo.]

    Note: The research on this topic is not of the most robust quality as the finding is unusual, it is not a common finding, and there is not a lot of angiographic ECG research on this.

    A U-wave is a low amplitude, usually positive monophasic deflection after the T-wave, usually with the same vector as the T-wave.  It is co-incident with Phase 4 of the action potential.  The exact etiology of the U wave remains unclear.  Hypotheses include repolorization of the Purkinje fibers and Mechanical Rebound of the myocardium at the end of systole.  It is normally less than 2 mm in height AND less than 25% of the T-wave in height. U wave duration is about 170+-30 ms.  It is usually positive in II, isoelectric in aVL and aVR and may be, less commonly, inverted in III and aVF.  It should be upright in precordial leads.  When inverted in the precordial leads, it implies structural or ischemic heart disease.  It is normally less than 2 mm in height AND less than 25% of the T-wave in height.

    What are the implications of negative U-waves?

    A negative U-wave, other than in lead aVR, III, or aVF, implies ischemic heart disease. It has been described during variant (vasospastic) angina attacks and during stress testing, under which circumstances it has shown high specificity (though low sensitivity) for the presence of a significant LAD stenosis.  It may also be seen with uncontrolled hypertension, under which circumstances the U wave is usually negative-positive (biphasic), whereas in acute ischemia it is more likely to be positive-negative.  In a patient with acute chest pain, a negative U-wave in the precordial leads represents a significant LAD lesion until proven otherwise.  Interestingly, patients with an anterior wall MI and negative U-waves in the precordial leads have been reported to have smaller infarcts, less STE, better collateral circulation, and a larger amount of stunned but viable myocardium, but the numbers are small.  Similarly, a prominent negative U-wave in all inferior leads in the presence of chest pain may be due to inferior ischemia. This negative U-wave may indeed, as with terminal T-wave inversion, signify spontaneous reperfusion.

    A Negative U wave may also be found in patients with valvular heart disease, congenital heart disease, hyperthyroidism, and cardiomyopathies.

    What are the implications of an increased amplitude positive U-wave in the precordial leads?

    Prominent U waves (exceed 1 mm) can be seen in hypokalemia, early repolarization, bradycardia, hypothermia, left ventricular enlargement, atrioventricular block, congenital long qt syndrome, left circumflex myocardial infarction.

    Usually, U wave has the same polarity as the T wave. According to earlier findings discordance between T and U and concordant negative T and U wave can also predict hypertension or myocardial ischaemia. 

    In the appropriate clinical context, an increase in U-wave amplitude in the precordial leads may raise suspicion of posterior ischemia (due to an RCA or LCX lesion).  This could be considered the mirror image of a negative U-wave.

    Here is a very nice full text article on the U-wave:

    References
    1. Yamaguchi H, Ishimura T, Nishiyama S, et al. Hypertrophic nonobstructive cardiomyopathy with giant negative T waves (apical hypertrophy): ventriculographic and echocardiographic features in 30 patients. Am J Cardiol 1979; 44:401-12.
    2. Miwa K, Murakami T, Kambara H, Kawai C. U wave inversion during attacks of variant angina. Br Heart J 1983; 50:378-82.
    3. Gerson MC, Phillips JF, Morris SN, McHenry PL. Exercise-induced U-wave inversion as a marker of stenosis of the left anterior descending coronary artery. Circulation 1979; 60:1014-20.
    4. Gerson MC, McHenry PL. Resting U wave inversion as a marker of stenosis of the left anterior descending coronary artery. Am J Med 1980; 69:545-50.
    5. Kishida H, Cole JS, Surawicz B. Negative U wave: a highly specific but poorly understood sign of heart disease. Am J Cardiol 1982; 49:2030-6.
    6.Miwa K, Miyagi Y, Fujita M, Fujiki A, Sasayama S. Transient terminal U wave inversion as a more specific marker for myocardial ischemia. Am Heart J 1993; 125:981-6.
    7. Tamura A, Nagase K, Mikuriya Y, Nasu M. Relation between negative U waves in precordial leads on the admission electrocardiogram and time course of left ventricular wall motion in anterior wall acute myocardial infarction. Am J Cardiol 1999; 84:332-4, A8.
    8. Miyakoda H, Endo A, Kato M, et al. Exercise-induced U-wave changes in patients with coronary artery disease--correlation with tomographic thallium-201 myocardial imaging. Jpn Circ J 1996; 60:641-51.
    9. Chikamori T, Takata J, Seo H, et al. Diagnostic significance of an exercise-induced prominent U wave in acute myocardial infarction. Am J Cardiol 1996; 78:1277-81.
    10. Girish MP, Gupta MD, Mukhopadhyay S, Yusuf J, Sunil Roy TN, Trehan V. U wave: an important noninvasive electrocardiographic diagnostic marker. Indian Pacing Electrophysiol J. 2005 Jan 1;5(1):63-5. PMID: 16943944
    11.  Sovari AA, Farokhi F, Kocheril AG. Inverted U wave, a specific electrocardiographic sign of cardiac ischemia. Am J Emerg Med. 2007 Feb;25(2):235-7.
    12.  Pérez Riera AR, Ferreira C, Filho CF, Ferreira M, Meneghini A, Uchida AH, Schapachnik E, Dubner S, Zhang L. The enigmatic sixth wave of the electrocardiogram: the U wave. Cardiol J. 2008;15(5):408-21. Review. PMID: 18810715
    13. Borbás J, Hategan L, Környei L, Katona M, Csányi B, Tringer Annamária, Forster T, Sepp R. Qualitative and quantitative assessement of ECG characteristics in patients with Andersen-Tawil syndrome. Scientific Congress of Hungarian Society of Cardiology - Cardiologia Hungarica, 2016.

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