Tuesday, September 29, 2015

Monday, September 28, 2015

Unstable Angina: Again, it still exists......

A middle aged male with no coronary risk factors presented with new stuttering chest pressure, worse with exertion and better with rest, with some diaphoresis and SOB.  The pain is constant at presentation.

Here is the first ECG:
There is very subtle ST elevation in lead III, with reciprocal ST depression in aVL.
There is also ST depression in V3 and V4, so this is occlusion or near occlusion of a vessel supplying both inferior and posterior walls.
This is all but diagnostic of acute MI, though does not meet "STEMI" criteria.

Here is the previous ECG:
Normal


The emergency physicians immediately recognized the ECG signs of acute coronary occlusion (though not STEMI) and activated "Pathway B": immediate consultation with our cardiologist for possible cath lab activation.

NTG was given with some relief, then IV NTG was given with complete relief of pain.

A repeat ECG was recorded:
All ST segments have normalized.
This makes the first ECG even more diagnostic of ischemia.

All who were there agreed that this was acute coronary syndrome, but that the artery was open, the patient without symptoms, and that with dual antiplatelet therapy and heparin, the patient could wait until the next day for the cath lab.

Next day, the patient went for angiogram and had a 95 % thrombotic occlusion of the right posterior descending artery off the RCA.

All 4th generation (contemporary) troponins were negative:
 (level of detection 0.010 ng/mL, 99% = 0.030 ng/mL):

0 hours: undetectable
3 hours: undetectable
7 hours: 0.010
21 hours: 0.012
24 hours: 0.010
26 hours: undetectable
29 hours: undetectable.

The apparent slight rise and fall cannot be depended upon since the precision of the assay is not good at such low levels.  the 10% CV (good precision) is at 0.030 ng/mL.  At lower levels, the precision is much less.

If you used the HEART score on this patient, the score would have been 4 points, which suggests a 30 day major adverse events rate > 1%.  Therefore, in this case, even if the clinicians had not recognized the specificity of the ECG findings, further risk stratification (stress testing or CT coronary angiogram) would likely be done.

EDACS score = 19.  (greater than 15 is positive).  But, in addition, with EDACS: if the ECG shows specific findings, the score is positive no matter what the number.  This is not true with HEART score.  

But there are many who are calling for an end to such testing in patients with negative troponins.

That only works when the ECG is adequately interpreted.  

I would add that in anyone in whom you have a high suspicion based on the history, do not trust the risk scores.  This patient had a very high risk story.



Friday, September 25, 2015

Central Nervous System T-waves

A middle-aged woman presented with symptoms of mild ischemic stroke.  There were no chest symptoms.

An ECG was recorded as part of the workup:
Bizarre inverted T-waves in nearly every lead, with greatly prolonged QT interval.
QT = 560 ms. Bazett corrected QT = 727 ms
These are classic for CNS catastrophe, especially hemorrhagic stroke
They are unusual in a small ischemic stroke.

This has been called the "spiked helmet sign," in this case, and in this case.

An Echocardiogram showed apical WMA and both LV and RV thrombi.

The stroke had a very low NIH score and did not receive any reperfusion the therapy for this.

Incredibly, no troponins were ever measured.

A CT Coronary Angiogram showed normal coronary arteries.

She was found to have cancer.

What happened?

There are two at least two possible scenarios:

1. She had stress cardiomyopathy for an unkown reason, developed LV and RV thrombi, which embolized to her brain.

2.  She developed LV and RV thrombi due to cancer.  These then caused the stroke, which caused the stress cardiomyopathy.

I believe the latter is more likely, as T-waves like this are most commonly seen in CNS catastrophes.  A mild stroke is normally not enough to cause this (it is not enough of a CNS catastrophe), but I think this goes to show how intimate the connection between the brain and the heart can be.


3 days later



4th day



Tuesday, September 22, 2015

Is this STEMI? No, it is one of the most common reasons for false cath lab activation.

This was contributed by Brooks Walsh, with a little editing and additions, plus a section of false positive cath lab activations added by me.  Brooks is a fine emergency physician from the Yale residency who has a keen and talented interest in ECGs and bedside cardiac echo.

Case

A middle-aged man was sent to the ED from a primary care clinic, with “ECG changes” and worry for STEMI.

The ECG shows ST elevation (STE) across the precordium, highest in V2 and V3. There are only minimal R waves in those leads [in fact, such tiny R-waves are technically considered Q-waves, and thus the patient has "QS"-waves (deep Q-waves without any R-wave at all], with markedly deep S waves.

The ECG from the office that day, although not available here, was essentially identical to the above ECG. He had been at the clinic for a scheduled appointment. He denied having had any chest pain, SOB, nausea, or other ischemic symptoms at any point in the day. However, records sent from the clinic indicated he had had a STEMI treated with PCI at another hospital 4 months prior.

Besides a new STEMI, what can account for the ST segment elevation?

The T waves are dramatically biphasic, with a steep descent, suggesting a Wellen’s pattern. The poor R wave progression, however, rules out Wellen’s syndrome, which requires R-wave preservation. Additionally, the patient denies any recent symptoms. (A true Wellen’s syndrome is observed after ischemic symptoms have resolved.)

The deep S waves and ST elevation could be the result of left ventricular hypertrophy.  Although R-waves may be absent in LVH, LVH has high voltage R-waves in V4-V6.  So this is NOT LVH.

Persistent STE after prior MI (also known as "left ventricular aneurysm morphology")

This is an ECG entity that is most accurately termed “persistent STE after prior MI,” but is more commonly (and somewhat less accurately) called left ventricular aneurysm. This is usually seen after large anterior MIs (1), especially in those patients who had delayed reperfusion therapy, or none. Typically, these patients show deep QS complexes in V1 – V3, or perhaps minimal r-waves with a deep S wave. STE will usually be mild, less than 3mm, and most prominent in leads V1-V3.

The correlation with anatomic aneurysm is imprecise – patients with persistent STE might not have a true anatomic aneurysm on echocardiography, and instead may only manifest systolic dyskinesis. (2) Conversely, many patients with dyskinesis or aneurysm do not have persistent STE. (3)

From Arvan and Varat, reference 2

The problem with persistent STE is that patients may be inappropriately administered or denied reperfusion therapy if they present with new ischemic-type symptoms. How can we be sure that he isn’t having a new STEMI on top of his old STEMI?

Differentiating persistent STE from “acute on chronic STE”

The first method involves analyzing the height of the T waves relative to the amplitude of the QRS complexes (i.e. height of R + depth of S).

Dr. Stephen Smith has derived and validated two calculations that can help differentiate new MI versus persistent STE. (4, 5)
The second is the best and easiest to use.

It is important to know that this rule only applies to cases in which the differential diagnosis is anterior STEMI vs. anterior LV aneurysm.  This is the case when there are deep well-formed Q-waves (usually QS-waves).

Two other words of caution:

1. In patients with prolonged chest pain (> 6 hours), the T-waves become less hyperacute and these were the only cases of false negatives.

2. Acute STEMI can be superimposed on LV aneurysm.  In this case, the T-wave becomes hyperacute again, so the formula works even though there is an underlying LV aneurysm.

Apply the rule to this case:

In this case, I overestimated the height of the T wave in V4, but the formula still supports persistent STE over STEMI.
The lead with the highest ratio is V4 at 0.25, which is substantially below 0.36


Second, a bedside echo demonstrated an aneurysmal, akinetic apex, with a thin wall.  Acute STEMI usually has an akinetic wall, but it will not be thin-walled.

This is consistent with an old LAD-distribution MI. While akinesis can also be seen in either persistent STE or acute MI, the dyskinesis and thinned wall strongly supports persistent STE.

It is also dilated.  It takes time for the heart to dilate after MI; it is not present at the time of acute STEMI.

Here is a still image of the latter part of the video:
​Red line indicates thin, dyskinetic apex and distal septum

A note of caution: Focused echocardiography (unlike comprehensive echo) should not be used to guide reperfusion decisions in patients with concerning symptoms, where the likelihood of acute coronary occlusion is high. This patient was entirely symptom-free, and the echo was simply supportive of clinical judgment, and was used in the context of old ECGs and cath reports.


Old ECG when patient did have a STEMI:

Lastly, the records were obtained from the hospital where PCI was performed many months ago, including a full sequence of ECGs. The patient had developed chest pain early in the morning, and called 911. An ECG was obtained by EMS.
Mild ST-segment elevation in V1 and V2, but there is also characteristic ST-depression, followed by a peaked T-wave, in V3 and V4. This is a de Winter pattern, suggesting proximal LAD occlusion.




In the ED, the ECG evolved to that of a classic anterior STEMI.
There are marked ST elevations in the precordium. The loss of anterior S waves, and elevated J point, has been described as grade 3 ischemia, and predicts a poor response to reperfusion therapy. 

The patient was transferred for reperfusion. The ECGs obtained post-PCI, unfortunately, shows persistent STE.
Not only does this predict a larger infarct, but also strongly predicts chronic microvascular damage.(6) This damage might explain why persistent STE is better correlated with myocardial dysfunction (e.g. dyskinesis) than with true aneurysm. Indeed, his pre-discharge echo showed an EF of 20% - 30%, and dyskinesis of the distal septum and apex.
Such persistent STE is called the "No-Reflow" phenomenon.  There is such severe downstream clogging of arterioles with platelet-fibrin aggregates, that, in spite of large vessel reperfusion, there is no true reperfusion.  This can be assessed on angiography as "blush" or TIMI myocardial perfusion grading.

The outcome of cases is predicted better by the ECG than by angiography, with persistent STE portending a bad outcome even with an open artery!

Case progression

In our ED, he had negative serial troponins. After the old records were obtained he was discharged home.

Images were reproduced under the "Fair Use" in Copyright Law, which allows such reproduction for non-profit educational purposes.

Does LV Aneurysm Morphology Result in False Cath Lab Activation?

Before the publication of these studies by Smith and Klein, anterior LVA was very difficult to differentiate from anterior STEMI on the ECG, and was perhaps the most commonly misinterpreted etiology of false positive STE in patients presenting to the emergency department with ischemic symptoms [7, 8, 9, 10, 11, 12, 13]. 

Brady et al. showed eleven ECGs to 450 emergency physicians (EPs).  The ECG of LVA was misdiagnosed as acute STEMI by 72% of EPs, a higher misclassification rate than any other ECG.  The misclassification would have led to inappropriate thrombolytic therapy by 28% of EPs [7].  In a second study by the same authors, there were 202 ECGs with STE and 12 ECGs were misdiagnosed – five ECGs showed LVA, two of which were diagnosed as STEMI [8].  All would have been identified by the rule. Miller et al. studied 100 patients admitted to a cardiac care unit for suspicion of MI. Of these patients, 31 had STE on the ECG; 21 of 21 without prior infarction and 5 of 10 with prior infarction had AMI.   All 5 false positive ECGs with STE were in the location of the previous Q-wave infarct (LVA), and the STE did not represent acute injury [11].  In a large, more recent study, Larson et al. showed that 20 out of 123 false catheterization laboratory activations were due to LVA [12].  


In all of these studies, and also in Rokos et al. [13] every ECG that was shown as a false positive cath lab activation, would have been unequivocally identified as LV aneurysm by the Smith-Klein rules!


References

1.      Tibrewala AV, Asch F, Shah S, Fuisz A, Lindsay Jr J. Association of Size of Myocardial Scar and Persistence of ST-Segment Elevation After Healing of Anterior Wall Myocardial Infarction. Am J Cardiol. 2007;99(8):1106-1108. doi:10.1016/j.amjcard.2006.11.058.

2.         Arvan S, Varat MA. Persistent ST-segment elevation and left ventricular wall abnormalities: A 2-dimensional echocardiographic study. Am J Cardiol. 1984;53(11):1542-1546. doi:10.1016/0002-9149(84)90576-9.

3.         Madias JE. Discordance of diagnosis of ventricular aneurysm made by the electrocardiogram and myocardial imaging: “ST-segment counterpoise” as a hypothetical mechanism. J Electrocardiol. 2006;39(3):340-341. doi:10.1016/j.jelectrocard.2006.02.009.

4.        Smith SW.  T/QRS Amplitude Best Distinguishes Acute Anterior MI from Anterior Left Ventricular Aneurysm.  American Journal of Emergency Medicine 2005; 23(3):279-287.

5.        Klein LR.  Shroff G.  Beeman W.  Smith SW.  Electrocardiographic Criteria to Differentiate Acute Anterior ST Elevation Myocardial Infarction from Left Ventricular Aneurysm.   The American Journal of Emergency Medicine 2015; 33(6):786-790.


6.         Napodano M, Tarantini G, Ramondo A, et al. Myocardial abnormalities underlying persistent ST-segment elevation after anterior myocardial infarction: J Cardiovasc Med. 2009;10(1):44-50. doi:10.2459/JCM.0b013e32831967b2.


7.         Brady WJ, Perron AD, Chan T. Electrocardiographic ST segment elevation: correct identification of AMI and non-AMI syndromes by emergency physicians. Acad Emerg Med 2001;8:349 - 60.

8.         Brady WJ, Perron A, Ullman E. Errors in emergency physician interpretation of ST-segment elevation in emergency department chest pain patients. Acad Emerg Med 2000;7:1256 - 60.

9.          Engel J, Brady WJ, Mattu A, Perron AD. Electrocardiographic ST elevation: left ventricular aneurysm. Am J Emerg Med. 2002 May;20(3):238-42.

10.        Deshpande A, Birnbaum Y. ST-segment elevation: Distinguishing ST elevation myocardial infarction ST elevation secondary to nonischemic etiologies. World J Cardiol. 2014 Oct 26;6(10):1067-79.

11.        Miller DH, Kligfield P, Schreiber TL, Borer JS. Relationship of prior myocardial infarction to false-positive electrocardiographic diagnosis of acute injury in patients with chest pain. Arch Intern Med 1987;147: 257- 61.

12.         Larson DM, Menseen KM, Sharkey SW, Duval S et al. “False-positive” cardiac catheterization laboratory activation among patients with suspected ST-segment elevation myocardial infarction. JAMA. 2007 Dec 19; 298 (23):2754-60.

13.         Rokos IC, French WJ, Mattu A, Nichol G, et al. Appropriate cardiac cath lab activation: optimizing electrocardiograph interpretation and clinical decision making for acute ST-elevation myocardial infarction. Am Heart J. 2010 Dec; 160(6):995-1003.

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