Saturday, September 4, 2021

A 76 Year Old Female With Recurrent Syncope, Lightheadedness, Palpitations and Negative Stress Test

Written by Lucas Goss MD, peer reviewed by Meyers, Smith, Bracey

A 76 year old female with a history of arial fibrillation not on anticoagulation, non-obstructive CAD found on coronary CTA 2 years prior, HTN, HLD, recurrent lightheadedness, and syncope status post loop recorder placement, presented for another episode of feeling lightheaded, diaphoretic, and feeling like she “was going to die.” She was discharged just the day prior for her second hospitalization for similar episodes. She was actually at the pharmacy to pick up her medicines the day after discharge when this episode occurred, and pharmacy staff sat her down in a chair while they awaited the ambulance. Her symptoms were mostly gone by the time of arrival.

Vital signs on arrival: BP 143/89, HR 63, RR 18.

During her recent hospitalizations she had a negative CT pulmonary angiogram (CTPA), negative nuclear stress test, normal echo, and her loop recorder did not identify any concerning findings when interrogated. During the first of two prior recent hospitalizations for similar symptoms, her troponin I rose from undetectable to 219 ng/L and trended back down, and the notes seem to attribute this to her blood pressure which was in the 200/110 range. During her second hospitalization (from which she was just discharged yesterday), she had multiple troponins all undetectable, less than 6 ng/L. 

A note on Loop Recorders, thanks to our electrophysiologist: 

They only record if:

1. The HR meets the programmed criteria (eg, pause over 3 seconds, HR<30 bpm, HR>*** etc). It’s unusual to program this “automatic recording trigger as HR of 50 or 40. 

2. The patient triggers recording when they have symptoms. In those scenarios it records a loop of several minutes before and a minute or so after (variable depending on company).

So if the patient did not trigger a recording when she had symptoms, then people usually don’t program automatic recording with HR in 40’s or 50’s otherwise decide memory will be full and there would be a lot of recordings that will be overwritten. 

Smith comment on troponins: the definition of myocardial infarction is 2 of the following:

1. Troponin rise and/or fall with at least one value above the 99th percentile reference range

2. Plus one or more of the following: A. Symptoms of MI; B. ECG evidence of ischemia;  C. Development of pathologic Q waves; D.  Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology; E. • Identification of a coronary thrombus by angiography or autopsy (not for types 2 or 3 MIs).

This patient had 1. and 2A., so she had a myocardial infarction.  

Now one needs to decide which type of Acute MI (usually type 1 or 2).  If type 2 MI, one must find an etiology of supply demand mismatch, or identify coronary dissection or spasm or a few other entities.  Syncope is the result of temporary loss of perfusion to the brain, and there are many etiologies, all of them are bad.  One must find the etiology.  More likely, this is a type 1 MI and the patient needs an angiogram regardless of ECG findings.

Here is her ECG on arrival (symptom free):

Initial ECG#1: (1159) 

ECG from 2 days prior (not "baseline," during prior admission):

Initial interpretation:

Sinus rhythm, normal QRS, no clear signs of ischemia, no signs of hyperkalemia, normal QT.

Meyers note: I read this ECG in real time, compared it to the prior, and did not see any clear signs of ischemia or OMI. In retrospect, I think perhaps the TWI in aVL is slightly more abnormal, and the ST segment and T wave in V3 slightly more "pushed down" than in the ECG from 2 days ago, but it is still not diagnostic to me. 

Case Continued

Labs demonstrated an unremarkable CBC and BMP, however her HS troponin I that was obtained in triage was mildly elevated at 23 ng/L. A repeat was obtained after she was seen by the physician at 1700 and had increased to 138 ng/L. Again, the combination of troponin rise and fall with symptoms is diagnostic of acute MI.


ECG #2: (1707)

There is baseline movement and artifact in critical leads such as II, III, aVF, and aVL where there is likely new STE and enlarging T waves in the inferior leads, with slight reciprocal changes in aVL.

The ECG should be immediately repeated to confirm or deny this suspicion, but it seems that it was not repeated at that time. 

Cardiology was consulted for admission and definitive coronary imaging. They accepted the patient, however while she was awaiting a floor bed, she became hypotensive and bradycardic.


ECG#3: (1834) 


This repeat ECG demonstrates a junctional escape rhythm with a rate of 36, however no definitive signs of OMI. At this time the patient was ill-appearing, lightheaded, and diaphoretic. Her blood pressure was 80/40. She was given 0.5mg of atropine while pads were being placed and shortly after her junctional rhythm resolved with improvement in her blood pressure and symptoms:


ECG#4: (1851)

She is now back in sinus rhythm on repeat ECG. There may be the tiniest hint of STE in lead III, and aVL shows the tiniest bit of reciprocal STD and increase in size of the negative T wave. There is a tiny amount of reciprocal STD in I, and there is a barely-perceptible amount of STD in V2 and V3 compared to prior. These findings are all highly suspicious for inferoposterior OMI.

Interestingly enough, her loop recorder was interrogated again and did not identify this event.

She was admitted to cardiology with plan for non-emergent cath the next day as well as EP evaluation for potential sinus node dysfunction. 

Overnight her troponins rose from 23 to 138 to 390 to 668 to 1,000 to 1,219, then they stopped measuring them at 2am in the morning (we are clearly committed to ignoring them anyway, so why wake us up for them?!).

While awaiting catheterization an EKG was obtained due to worsening symptoms:


ECG#5 (Hospital day 2)

This ECG shows sinus bradycardia with signs of inferoposterior reperfusion. Leads III and aVL are diagnostic of acute MI, but, because of the T-wave inversion, it is probably with an open artery (or collateral circulation). There is some STE in inferior leads leading into T waves with terminal inversion, which is reciprocally mirrored in aVL. There are posterior reperfusion T waves in the precordial leads, much taller than on the most recent ECG. 

Another repeat ECG was obtained a few hours later (just prior to catheterization):

ECG#6 (Hospital Day 2)

This ECG is slightly confusing as to the state of the vessel, as there is newly worsened STD maximal in V2-V4, but ongoing terminal T wave inversion in the inferior leads. I would assume that there is ongoing ischemia until proven otherwise.

Smith note: 3 possibilities: 

1. The artery is open but with TIMI-2 flow, enough to perfuse vessels to the inferior wall, but not to the posterior wall.  

2. TIMI-2 flow can be enough to result in T-wave inversion (apparent reperfusion) even though there is ongoing ischemia. 

3. There is collateral flow that is robust enough to result in T-wave inversion in the inferior, but not the posterior, wall.


Cardiac catheterization findings:

RCA: 100% stenosis from lesion described as “complex, noncalcified, consistent with atherosclerotic disease as well as a filling defect consistent with thrombus” supplying the inferior and posterior walls, which was successfully stented.

LAD: Mild luminal irregularities

Circumflex: Minor luminal irregularities


The patient afterwards underwent dual chamber pacemaker implantation due to sick sinus syndrome, as she continued to revert back into a junctional bradycardia.


What was interesting about this case is that she had multiple presentations for similar progressive symptoms, but had both negative stress test as well as echo within 2 weeks of this presentation. Additionally, after her episode of junctional bradycardia her loop recorder was interrogated and did not identify the event.


Learning Point #1: Recent Negative Stress Tests Do Not Rule Out ACS

Do not rely on a recent negative stress test to rule out acute coronary syndrome or high risk coronary lesions. A stress test has nothing to do with ACUTE coronary syndrome. A stress test is ostensibly designed to help detect symptomatic, chronic, stable coronary disease, in hopes that a patient's chronic stable exertional symptoms may be attributed to that stable coronary disease. Acute coronary syndrome can arise from small unstable atherosclerotic lesions that can rupture and cause OMI. These lesions may not be picked up on stress testing (because they are not yet ruptured and occluding!), as was the case above.  Several studies have demonstrated concerningly high percentages of patients experiencing acute MI with recent negative stress testing.1,2,3, 4 The supposed utility of stress testing is to identify critical, chronic, stenoses causing reduced coronary blood flow which reproduces a patient's stable angina symptoms. Coronary lesions not significant enough to be detected on stress testing can still undergo plaque rupture and thrombosis causing acute MI.

See Chest Pain, "Negative" Stress Tests, POCUS, & ECG Equations -- A Case from Salim Rezaie (R.E.B.E.L. EM)


Learning Point #2

Be able to recognize posterior reperfusion T waves as demonstrated here with large tall upright T waves with associated subtle ST depression.

See Series of Prehospital ECGs Showing Reperfusion

       A woman in her 70s with bradycardia and hypotension


 References on evaluating patients in the ED who had a recent negative stress test:

  1. Walker J et al. Coronary disease in Emergency Department Chest Pain Patients with Recent Negative Stress Testing. West J Emerg Med 2010. PMID: 21079714
  2. Hoilund-Carlsen PF et al. Usefulness of the Exercise Electrocardiogram in Diagnosing Ischemic or Coronary Heart Disease in Patients with Chest Pain. Am J Cardiol 2005. PMID: 15619400
  3. Smith SW et al. Incidence of Myocardial Infarction in Emergency Department Chest Pain Patients with a Recent Negative Stress Imaging Test. Acad Emerg Med 2005.; 12:51 
  4. Engineer RS, Lauer MS, Emerman CL. Chest pain after recent stress test: Is there a warranty? Ann Emerg Med [Internet] 2004;44(4, Supplement):S47. Available from:

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