Monday, December 24, 2018

Intermittent increasing exertional chest pain and serial negative troponins

I was shown this ECG at triage, recorded on a patient with a chief complaint of chest pain, where I was working:
What do you think?

My immediate thought, and the diagnosis I wrote into the formal interpretation was: "Ischemic looking ECG, worry for ACS."

Why did I think this?  There is an abnormally inverted T-wave in lead III and some ST depression in V3-V6, and a downsloping ST segment in V2.

I then went to talk to the patient:
This 40-something woman with no medical history or risk factors presented to triage, where I was working, stating that she was having short episodes of substernal CP with exertion, starting 2 weeks ago. The last episode was shortly prior to arrival and she was asymptomatic on arrival.  There had been a total of approximately 6 episodes, never lasting more than 15 minutes.  Most recent was shortly prior to arrival.   She described mid sternal non radiating pressure-like chest pain associated with dyspnea and diaphoresis. Symptoms resolve fairly quickly with rest. Symptoms have never occurred at rest. Prior these symptoms, she was a fairly active person with good exercise tolerance and no exertional symptoms. 

The patient had no more chest pain while in the ED.

3 Troponins each 2 hours apart were all below the level of detection.

A repeat ECG was done 7 hours later.
There is less ST depression
This confirms that the ECG is dynamic

HEART score = 3

Hx: 2
ECG: most would give it a 1, but if you know ECGs, this one is ischemia until proven otherwise.
Age: 0
Risk factors: 0
Troponin: 0

This score shows why careful history and careful ECG interpretation is critical:

First, pain which comes and goes and does not last long is frequently too brief to result in a positive troponin.  Thus, absence of positive troponin is not particularly reassuring.  

I am much more worried about pain that is dynamic than pain that is constant for two reasons: 
1) it is much more typical of angina and 
2) the troponin is very often negative.

Second: The ECG is far from normal and actually looks ischemic.

If I were to modify the HEART score, I would give 3 or 4 for the history alone!  I would give 2 for the ECG.  That would be 5 or 6.
With this history and these 2 ECGs, there is no doubt about ACS, in this case "Unstable Angina" because troponins are all negative.

An angiogram is indicated.

The admitting physician was concerned about "Stable Angina."  However, since this is new and exacerbated by ever decreasing amounts of activity, this is unstable angina

Instead of an angiogram, they ordered a stress echo was done, starting with a rest echo.

Result of stress echo
1. Regional wall motion abnormality--basal to mid inferior akinesis at rest, no change with stress.
2. Regional wall motion abnormality--apical septum, mid anteroseptum, and mid to apical anterior hypokinesis with stress.
3. Left ventricular function normal at rest, no change with stress.
4. Ischemic ECG response with adequate heart rate.
5. The patient did report angina with stress.
6. Exercise capacity was poor (40% predicted for age and gender).

Therefore an Angiogram was done:

ACS - Unstable Angina .
Culprit is 95% stenosis in the distal RCA.
It was stented.

ECG after PCI:
Nearly completely normal now.

Learning Points:

1. The ECG is still essential for diagnosis of ACS.  Even with high sensitivity troponins, much ACS is missed if the ECG is ignored.

2. In patients with normal troponins, intermittent chest pain is far more worrisome than constant chest pain

3. Increasing crescendo angina, even if exertional, is unstable, not stable

Comment by KEN GRAUER, MD (12/24/2018):
Excellent example by Dr. Smith of a less obvious pattern of ischemia — and of the benefit of serial tracings for confirming the findings on the initial ECG. For clarity — I’ve put the first 2 ECGs done on this patient together in Figure-1.
Figure-1: The first 2 ECGs done in this case (See text).
I’ll reinforce the following important points brought out by Dr. Smith:
  • Despite the relatively younger age for this female patient (40yo) and the lack of cardiac risk factors — the clinical history is classic for angina pectoris: The patient describes new-onset brief episodes (≤15 minutes) of mid-sternal chest pain precipitated by exercise, and promptly relieved by rest.
  • As per Dr. Smith — not only has this patient told us that she has angina — but she has told us that she has unstable angina becauseiPrior to the past 2 weeks — she was active with good exercise tolerance and no exertional symptoms; andiiHer episodes are precipitated by progressively less strenuous exercise. Given this history — the burden of proof is on us to rule out (rather than rule in) significant coronary disease!

As per Dr. Smith — ECG #1 = the initial ECG done in the EDis clearly abnormal (Figure-1). In the interest of fine-tuning our assessment of this initial ECG — I note the following findings:
  • Slight ST segment depression in several leads.
  • ST segment flattening (straightening) in multiple leads — which I have highlighted by the short, straight RED lines in Figure-1.
  • Isolated shallow T wave inversion in lead III is by itself not necessarily abnormal — but it is abnormal in the context of subtle abnormalities in each of the 3 inferior leads. Thus, there is ST straightening and slight downsloping in leads II and aVF — and some ST coving in lead III that leads into the inverted T wave in this lead.
  • NOTE: By way of comparison — the ST-T wave in lead aVL within the dotted BLUE rectangle is normal. The portion of the ST segment that is straight is much shorter for this complex in aVL — and, transition from the ST segment to the beginning of the T wave is much more gradual with a smooth upsloping (BLUE arrow). It should be obvious that the ST-T waves in all leads with RED lines look very different (with a longer straight ST segment and a more abrupt beginning of the T wave).
What do these ECG Findings Mean?
I describe the above findings in ECG #1 as, nonspecific ST-wave abnormalities”. The reason they are called “nonspecific” — is that numerous conditions (many of which are non-cardiac, such as hyperventilation; temperature extremes; “sick patient”; fear or pain; electrolyte disorders, etc.) may produce similar ECG findings as those seen in ECG #1.
  • However, in the context of a classic history for angina (as is the case for this patient! ) — these ECG findings should be interpreted as ischemic until proven otherwise!
ECG #2 obtained 7 hours lateris also clearly abnormal:
  • As per Dr. Smith — there is less ST depression in ECG #2 compared to ECG #1.
  • Lead-to-Lead Comparison of ECG #1 and ECG #2 reveals another very important finding. Note that despite no more than minimal change in R wave progression and QRS morphology in the chest leads — T wave amplitude in leads V2-thru-V6 has clearly increased in ECG #2. This confirms that there have been dynamic ST-wave changes in this 2nd ECG done 7 hours later after complete resolution of chest pain.
  • Note that the nonspecific ST-T wave straightening persists in many leads in ECG #2.
KEY Points:
  • While true that an abnormal troponin might expedite diagnosis — the fact that serial troponins were all negative in this case is not at all unexpected. This patient has anginal chest pain — but not myocardial infarction.
  • The Stress Echo did not have to be done. Although this test turned out to be markedly abnormal — a definitive diagnosis was already evident (and was already made by Dr. Smith). The fact that this patient provided a classic history for unstable angina + an abnormal initial ECG + dynamic ST-T wave changes on the 2nd ECG after resolution of chest pain — is definitive for a diagnosis of acute coronary disease until proven otherwise by a negative cath.
  • PEARL: If the results of a clinical test you are about to order will not change your management — then you probably do not need to order that test! False negative results can be seen with Stress Echo. Cardiac cath will be needed regardless. I understand that the admitting physician “wanted to be sure” — but the reality is, that all Stress Echo did in this case was to delay coronary catheterization while increasing the cost of care.
  • It is important to get good at recognizing subtle ECG findings such as nonspecific ST-T wave straightening (flattening), as highlighted by the RED lines in ECG #1. Many clinicians (including some cardiologists) call such ST-T waves “normal”. This case illustrates how under the right clinical circumstances, such subtle ECG findings may be diagnostic. With practice — it becomes easy to instantly recognize this nonspecific ST-T wave straightening. You can then correlate this finding to the clinical scenario to determine if there is relevance to the case at hand.
  • Finally — this case also illustrates how lead-to-lead comparison of serial tracings, correlated to the clinical history can make a definitive diagnosis that may obviate the need for “other tests” prior to cardiac catheterization.


  1. Interesting case but I’m not sure how the first 2 statements in the stress echo report - detailing the LV wall motion abnormalities at rest and with stress - are consistent with the 3rd statement, that LV function was normal at rest and with stress!

    1. I know. Agree. I just copied it exactly. I think it is a typo.

  2. >>downsloping ST segment in V2
    Also downsloping ST in II with biphasic -/+ T wave.

  3. Your teaching points are exactly what I teach my residents. I must be reading your mind or vice versa. Here is my summary from

    1.) If chest pain has resolved and lasted <30 minutes the EKG, troponin and repeat troponin may all be completely useless.  In this case I would double the points for history.  If it is concerning, give four points instead of two.   

    2.) If the AVERAGE risk for all comers in the low risk group (scores of 0-3) is in the 1% range after a repeat troponin, and those with scores of 2 or 3 have a higher risk than those with scores of 0 or 1, then it follows that those with a score of zero or 1 likely have a risk <1%, but those with a score of 2 or 3 likely have a risk >1%.

  4. Steve and Ken...

    Thanks for a great case illustrating the necessity of inspecting ECGs with a very critical eye. The ischemic changes were very obvious to me immediately because I automatically look for them. I am also often amazed at how many clinicians - even cardiologists (as Ken pointed out) - overlook flattening of the ST segments which is usually accompanied by symmetrical T waves (as is the case in this ECG). Granted, females can sometimes exhibit symmetrical T waves as a normal variant, but in my experience I've really only seen this in younger women - usually in their 20's. And I appreciate the fact that neither of you referred to this ECG as "inferior" ischemia. I still see journal articles referring to "inferior" or "anterior" subendocardial ischemia when all anyone can really say is simply (subendocardial) ischemia.

  5. What about Upright T waves in ECG#1 in V1.. aren't they abnormal in V1?

    1. In our study of early repol, 46% of patients without any ischemia had an upright T-wave in V1, vs. 73% for LAD occlusion. The T-wave in V1 was taller than the T-wave in V6 in 15%, vs. 39% for LAD occlusion.
      So an upright T-wave in V1 is normal.

  6. Thanks for the case Dr smith! I have a question for you. How could RCA be the culprit artery? I am confused. Based on the hypokinetic wall segments, LAD should have been the culprit artery,

    1. Thank you George for your comment and astute observation! I will pass your question on to Dr. Smith directly — but I’ll venture some thoughts on this myself: — i) Seems like there is at least 1 TYPO in the Stress Echo Report (See above 12/24/2018 question by David Richley). Sounds like Dr. Smith was not there … Perhaps there was more than a single error in the Stree Echo report? — ii) — The ONLY info I see given regarding cath results are that the “culprit” was a 95% stenosis in the distal RCA … — but there is NO mentiion of what the rest of the cath showed! Was there multi-vessel disease, perhaps severe? Were there collateral vessels? Granted, a 40-something yo woman with no prior history on no risk factors (as it says in the history) would be less likely to have multivessel disease — but it IS important to know what the rest of the cath report showed in order to properly address your excellent question! If you look at Figure-1 in My Comment above — T wave amplitude in leads V2-thru-V6 is increased, which to me suggested more than simple reperfusion (ie, perhaps anterior ischemia … ?). So I’d definitely want to know more details on what the cath showed (especially given suggestion of mid-to-apical anterior hypokinesis with stress on Stress Echo). ALL of THAT SAID — location of the “culprit” artery in this case to me takes secondary significance to the fact that there are DYNAMIC ST-T wave changes in this patient with chest pain that mandate cath for definitive diagnosis (and hopefully treatment) regardless of what the “culprit artery” happens to be — :)

    2. Not sure now. But RCA can affect the apex if there is a small LAD and the RCA wraps anteriorly around the apex. The ECG is indeed abnormal at the apex (leads V5 and V6).

  7. If there is st segment elevation then can be call it is unstable angina?

    1. “Unstable angina” is a clinical diagnosis — which I definite in the first 2 bullets that I put under my Figure-1. This diagnosis can be supported by ECG changes — but the history is KEY. That said, this case shows subtle-but-real evolving (ie, “dynamic”) ST-T wave changes IN ASSOCIATION WITH the history of changing (worsening) anginal symptoms — and that makes this picture much more concerning. There does not necessarily have to be ST segment elevation for there to be “unstable” angina — :)

    2. Yes, there can be ST Elevation Unstable Angina. MI is defined by the clinical syndrome PLUS a rise and/or fall of troponin with at least one value > 99th % upper ref limit


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