An elderly woman found down with bradycardia and hypotension

Submitted by Alex Bracey, with edits by Pendell Meyers and Steve Smith

A female in her 70s with PMH of hypertension, coronary artery disease, and a remote history of an aortic valve replacement was brought into the ED after being found down by her son. On arrival she was confused. Her initial ECG is shown below.

What do you think?

- Sinus bradycardia with HR of ~50 BPM (plus artifact that mimics PVCs)

- Peaked T waves particularly visible in leads V1-V3, I, and aVL

- RBBB with QRS duration 152 ms (comparison to prior shows similar RBBB morphology but with QRS duration of 116 ms)

In addition to being bradycardic as seen on this ECG, she was also hypotensive, with systolic blood pressures maintaining around 60 mmHg.

At this point let’s review the most common causes of bradycardia and hypotension:
Drugs: AV nodal blockers, Calcium channel blockers
Ischemia: usually RCA occlusion leading to bradycardia via sinus bradycardia or AV blocks
Electrolytes: Hyperkalemia

With this patient’s history of CAD and HTN it may be inferred that the patient is likely on an AV nodal blocking agent (i.e., calcium channel blockers (CCB) or beta-blockers (BB)). A review of this patient’s chart indeed confirmed that this patient had been prescribed metoprolol succinate (extended release).

Based on the ECG it is likely that you have already surmised the other underlying pathology: hyperkalemia (as demonstrated by bradycardia, peaked T waves and widened QRS).

The astute ED physician and resident correctly identified this ECG as concerning for hyperkalemia and empirically gave insulin/dextrose, calcium gluconate, albuterol, and intravenous fluid. The patient also received push dose epinephrine for hypotension. Following these interventions, the initial potassium returned at 6.5. This is not a particularly high level by itself, but certainly can cause these ECG changes and hemodynamic problems in a synergistic relationship known as BRASH syndrome (Bradycardia, Renal failure, AV nodal blocking agents, Shock, and Hyperkalemia).

Here is the subsequently recorded ECG after therapies:

 - Normal sinus rhythm at a rate of 82

 - Small amount of reduction in T-wave amplitude/peakedness

 - Relative narrowing of QRS interval (136 ms)

The particular combination of bradycardia, renal failure (this patient had a creatinine of 1.64 without a history of renal disease), AV nodal blockade, shock, and hyperkalemia has been coined BRASH syndrome.

The BRASH syndrome was coined on social media, not yet in peer-reviewed literature (like OMI). This interesting article on EmCrit references many cases with all of these findings, but none gave it this name, so you will have a hard time searching PubMed for this syndrome!

Briefly, BRASH occurs when a patient taking AV nodal blockers develops renal failure leading to decreased clearance of both potassium and AV nodal blocking medications, with worsening bradycardia and hypotension resulting from hyperkalemia and increased serum levels of beta blockers. The decreased cardiac output and blood pressure further worsens the renal failure, and so on. Of course, a similar syndrome occurs in patients with pre-existing renal failure, dialysis patients in particular.

The ECG for these patients may manifest with the classic peaked T-waves and/or any of the 4 "B’s of hyperkalemia" in combination or isolation, including Broad (Widened QRS), Brady, Bizarre, Blocks (AV blocks).

Upon further questioning, the patient’s husband recalls that the patient continued taking her supplemental potassium but had recently stopped her torsemide. She was subsequently admitted to the intensive care unit where her hyperkalemia was managed with insulin and diuretics. Her subsequent ECGs remained unchanged.

Teaching Points:

1) Expedient ECG interpretation is paramount in the presentation of bradycardic, hypotensive patients.

2) The combination of bradycardia and hypotension will most commonly be caused by one of three etiologies remembered by the mnemonic "DIE": Drugs (e.g., AV nodal blockers), Ischemia (acute coronary occlusion), and Electrolytes (esp. potassium).

3) In BRASH syndrome, a patient taking an AV nodal blocking medication develops renal failure and hyperkalemia which manifests on the ECG with peaked T-waves and/or any of the 4 B’s of hyperkalemia:  Broad (Widened QRS), Brady, Bizarre, Blocks (AV Blocks).

Comments by KEN GRAUER, MD (6/6/2018):
SUPERB Case !!! I’ll add 2 points: 
  • i) The BEST proof of Artifact, is when you are able to see the underlying rhythm continue undisturbed throughout the tracing. BLUE arrows in Figure-1 show evidence that the QRS continues here throughout the long-lead rhythm strip V5 — which proves that the large deflections “X” and “Y” cannot be real. And a look at simultaneously-recorded leads (within the dotted BLUE rectangle) proves that deflection “Z” is not an extra beat, but rather a distorted ST-T wave. 
  • ii) The T wave peaking seen with hyperkalemia applies not only to T waves that are positive — but also to T waves that are negative. Note how “pointed” the inverted T waves in leads V1, V2, V3 are — and that while still deeply inverted, this “point” smoothens out after correction of hyperkalemia.
Figure-1: Blue arrows show the underlying rhythm continues throughout.

Left Bundle Branch Block, Severe Chest pain, Previous Normal Angio. What is going on?

A middle-aged woman with idiopathic cardiomyopathy and biventricular failure, with previous EF of 15%, presented with sudden onset severe substernal chest pain.  

She had LBBB with a wide QRS, and therefore was a candidate for biventricular pacer for cardiac resynchronization, but when they had inserted her pacemaker, they could not get the LV lead into place (technical difficulties).  Therefore, she had a typical RV pacer.

She had a recent near perfect angiogram, described below.  

Here is her initial ED ECG:
1.  Is it paced?
2. What do you notice compared to the previous, below?
3. Is there any evidence of ischemia here?

Normal LBBB with normal proportional discordance of ST-T's.
Left axis deviation, which is common in LBBB

1.  It is not paced.  It is simply left bundle branch block (LBBB)

2.  The initial ECG has an inferior axis.  This suggests the limb leads are reversed because, whereas the previous has a large monophasic R-wave in aVL, with a negative QRS in III, the initial ECG has the opposite.

3. This initial ECG has no evidence of ischemia.

Previous normal angiogram, done to assess reason for cardiomyopathy:

Minimal coronary artery disease

Impression and recommendations:
No epicardial coronary artery disease noted to explain advancing systolic
heart failure or abnormal TTE

Suspect non-ischemic cause of cardiomyopathy

The LMCA is relatively a small caliber vessel.
No significant coronary artery disease noted.

The LAD extends to the apex.
The LAD is a medium caliber vessel.
There is a medium caliber, branching first diagonal branch with tubular 20% stenosis
stenosis in the ostial-proximal vessel segment.
There is mild plaque in the mid LAD beyond D1.
D2 is absent.
D3 is a small caliber vessel.

Large caliber vessel.
OM1 is absent (due to presence of Ramus)
OM2 is a large caliber branching vessel that supplies a majority of the
inferior and inferolateral wall to the apex.
There is a small caliber OM3.
No significant coronary artery disease noted.

Large caliber vessel.
RCA has Normal take off.
The rPDA is a medium caliber vessel (with slightly early take off) that
reaches the cardiac apex.
The RPAV is a medium caliber vessel that supplies two small rPLA branches.
No significant coronary artery disease noted.

There is a medium caliber Ramus intermediate with mild ostial plaque.

With a previous angiogram that is so nearly normal, new ACS is very unlikely.  See this post from last week about completely normal angiograms:

Chest pain, Ventricular Paced Rhythm, and a Completely Normal Angiogram 3 Months Prior.

Case continued:

The pain continued, severe, and a 2nd ECG was recorded at 24 minutes:
What do you see now?

The upright R-wave in aVL is restored.  Leads have been changed.

There is now a significant ST change in III and aVL, with new ST elevation in III that meets the modified Sgarbossa criteria: there is 2 mm of discordant ST elevation in lead III, which is 33% of the preceding S-wave, measured at 6 mm.  This exceeds the 20-25% criterion and even in just one lead is diagnostic of acute coronary occlusion.  This is especially true in that there is a change.

Comment: Patients with previous severe systolic failure are at extreme risk when they have a new coronary occlusion.  They should get the benefit of the doubt, if there is any doubt, and go to the cath lab.  It is incumbent upon the providers to prove absence of coronary occlusion.  A previous normal angiogram should not be depended upon.

The occlusion was diagnosed by the resident, who wanted to activate the cath lab, but the faculty was not convinced.

Another ECG was recorded at 46 minutes:
Now the axis is reversed, again!
And now there is excessively discordant ST elevation in aVL, with excessively discordant ST depression in lead III.
So is this an inferior MI?  Or high lateral MI?
It doesn't matter!  Activate the cath lab!

Cardiology was consulted but alas, for whatever reason, the cath lab was not activated (perhaps because of the previously near normal angiogram), and another ECG was recorded at 92 minutes:
Increasing disproportionate ST deviation

105 minutes

122 minutes
Axis changed again
Ischemia not changed

The cath lab was finally activated.


Acute Lateral ST elevation MI with LBBB.
Culprit is 100% occlusion of the LCX OM2
Lesion reduced to 0%
Very suspicious for extracoronary source of thrombus in OM2: Paroxysmal atrial fib vs. LV
thrombus.  AICD interrogation will be helpful incase of P Afib!

No significant CAD in LAD or RCA.

Coronary angiogram with OM2 occlusion treated with PTCA - clot displaced to distal vessel. Imaging suggests possible embolic etiology rather than plaque rupture. 

Post cath:
ST deviation is resolved.

Troponin I peaked at 88 ng/mL
Echo showed EF now less than 10%
Probable new regional wall motion abnormality of inferolateral wall.

Pt did not have much improvement in her symptoms after cath.  


Absence of atherosclerosis on angiogram raised concern about embolic etiology but no AF on device interrogation and TTE without e/o LV thrombus. Would like to obtain TEE to better evaluate for presence of thrombus.

A transesophageal echo (TEE) was done and a thrombus was found in left atrial appendage.  This is the apparent source of embolism and occlusion!

Learning Points:

1. The Smith Modified Sgarbossa criteria are perhaps 75-80% sensitive (similar to STEMI criteria in normal conduction).

2. However, they are 99% specific.

3.  There are reasons other than atherosclerosis for acute coronary occlusion.

4.  Thus, do not let a previous normal angiogram become an obstacle to ECG interpretation.

5. Lead placement may confuse the location of the MI, but it should not prevent you from making the diagnosis and activating the cath lab.

Comments by KEN GRAUER, MD (6/5/2018):
Superb blog post by Dr. Smith with numerous teaching points! I’ll aim my Comments on augmenting several key concepts that were addressed.
  • Among the reasons for delay in optimal treatment of this patient was failure to recognize lead misplacement. Most experienced clinicians are comfortable recognizing the most common form of lead misplacement — which is mix-up of the LA-RA electrodes. This technical mishap is often obvious due to global negativity of the P, QRS and T wave in lead I (which should otherwise never happen) — and global positivity in lead aVR. Other types of lead misplacement may be far subtler. This is the case here!
  • The 1st ECG done in the ED manifests LA-LLead Reversal. The BEST summary I have seen on recognition of the various types of lead reversal is found in Life-In-The-Fast-Lane. It is comforting that no crib sheets of key findings are needed — because all you need do is Google, “LITFL Lead Reversal” — and a link to this invaluable post immediately comes up!
As per LITFL — the findings of LA-LL Lead Reversal are:
  • Lead III becomes inverted (from its previous appearance).
  • Leads I and II switch places.
  • Leads aVL and aVF switch places.
  • Lead aVR remains unchanged.
  • PEARL: The KEY to rapid recognition of probable LA-LL Lead Reversal — is that the P wave is unexpectedly larger in lead I than it is in lead II (whereas it is usually the other way around).
For clarity — I’ve put the first 3 ECGs shown in this blog into a single figure (Figure-1). Sinus rhythm with LBBB morphology in the chest leads is present in all 3 tracings. As per Dr. Smith — there is a dramatic change in the limb lead QRS axis between the Initial ECG done in the ED (Top tracing in Figure-1) — compared to the Prior (Baseline) ECG (Middle tracing).
  • What is unusual about the relative size of the P waves in leads I and II in the Initial ED ECG?
Figure-1: A simultaneous look at the first 3 tracings in this case.
ANSWER: The P wave in lead I is much larger than the P wave in lead II in this Initial ECG (Top tracing in Figure-1). In contrast — the P wave in lead II is larger (as it should be) in the Prior (Baseline) ECG. Other findings consistent with LA-LL Lead Reversal are seen when comparing the Initial ED ECG with the Baseline ECG:
  • The appearance of leads I and II is essentially switched.
  • The appearance of leads aVL and aVF is essentially switched.
  • Polarity of the P wave, QRS complex, and ST segment in lead III is inverted.
  • Lead aVR is unchanged.
The 3rd (Bottom) tracing in Figure-1 was the 2nd ECG obtained in the ED, 24 minutes after the Initial ECG.
  • Comparing this 2nd ECG in the ED with the Baseline ECG — suggests there is subtle-but-real qualitative change in the ST-T waves in each of the inferior leads. These ST-T waves now look hyperacute. The magic “mirror-image” opposite picture is seen for the ST-T waves in leads III and aVL. In a patient with new chest pain — these changes are highly suggestive of acute coronary occlusion.
Return to the Initial ECG (Top tracing in Figure-1). Considering that we now know there was LA-LL Lead Reversal in this Initial ECG — I think the same hyperacute changes we noted in the 2nd ECG done in the ED were probably already present in this Initial ECG.
  • If you “invert” the P wave, QRS complex and ST-T wave in lead III of the Initial ECG … — Isn’t the picture you get very similar to what we see in lead III in the 2nd ED ECG?
  • If we consider that aVL in the Initial ECG was actually lead aVF — Don’t we see some of the subtle ST elevation that we now see in aVF of the 2nd ECG?
  • And, if we consider that aVF in the Initial ECG was actually lead aVL — Wouldn’t we have that magic “mirror-image” opposite picture for inverted lead III and lead aVL?
BOTTOM LINE: Great case by Dr. Smith, with numerous important teaching points on all aspects of this case. Add to those the PEARL of remembering that marked axis change with unexpected large size of the P wave in lead I (compared to lead II) may be a “tip-off” to LA-LL Lead Reversal.

Chest pain, Ventricular Paced Rhythm, and a Completely Normal Angiogram 3 Months Prior.

One of our graduates, Rochelle Zarzar, who is now an education fellow, sent me this from one of the hospitals she works at now:

An elderly woman presented with chest pain.  She had been nauseous the night before and did not feel well, then awoke 2 hours prior with chest pain.

She had had a completely normal angiogram 3 months prior.

Here is that angiogram report:
The left main coronary artery is normal.
Left anterior descending is a type 3 vessel and is normal.
Left circumflex is nondominant and normal.

The right coronary artery is dominant and normal.

The nurses immediately recorded an ECG.  This was 2 hours after the onset of CP:
What do you think?


There is a ventricular paced rhythm.  It is unusual in that the QRS is mostly positive in leads V1 and V2.  This suggests that it is a biventricular pacer that is timed to pace both ventricles simultaneously (only one spike).  There is concordant ST depression of at least 1 mm in V3 (+ Sgarbossa), and proportionally excessively discordant ST elevation in I and aVL, with reciprocal concordant ST depression in III and aVF (+ Smith modified Sgarbossa).  

So this is clearly an acute coronary occlusion (Occlusion MI, or OMI).

Remember: all you need for the diagnosis of OMI is for the Smith Modified Sgarbossa to be (+) in just one lead.  

Here it is positive in 3 leads.

They later found the old ECG:
Paced, with (as expected) all appropriately discordant ST segments
The change confirms the ECG diagnosis, which in any case should not be in question.

Rochelle made the diagnosis immediately:
"When they handed me that EKG, all I knew about her was the EKG itself and that she had chest pain, so I immediately called cardiology and activated the cath lab.  When I spoke to cardiology, they acknowledged the ECG changes but still doubted that it was a STEMI since she had a clean cath just 3 months ago.

"They told me to deactivate the cath lab and to check the troponin.  

"Troponin I later returned at 3.0 ng/mL."  

"I also had done a bedside echo in the meantime and I saw a new anterior/lateral wall motion abnormality and a new decrease in her EF (last echo in March showed EF of 55-60%)."  

"I called them back, they agreed that given the elevated troponin, that she should go to the cath lab."  

"Still, they did not want me to order heparin or ticagrelor since they were not convinced and thought maybe this could all be a stress cardiomyopathy." 

Here is the emergent cath report (I am uncertain as to the door to balloon time, or the exact delay to cath):  
· Right dominant coronary artery system
· The left main artery is severely diseased. There was subtotal occlusion with large thrombus in the distal segment of the left main with involvement of the ostia of the LAD, ramus, and LCX.  

Note: "Ramus" refers to "ramus intermedius", which is a variant of anatomy in which there is a large branch between the circumflex and the LAD, usually replacing the first diagonal of the LAD.

The ostium of the large branch off the ramus intermedius also was involved. The distal segments (minimal disease) and RCA (minimal disease) were similar to angiogram performed 3 months prior. 

Thrombectomy and Angiojet were performed into the LAD, ramus, and LCX. Flow was improved but not to TIMI 3. Stand alone PTCA was then performed for each of these segments but also could not restore flow completely. Therefore, stenting with a 3.0 x 20 mm Promus Premier drug eluting stent from the left main coronary artery into the LAD was successfully performed. The flow into the ramus and LCX remained poor, and thus kissing balloon inflations were performed in each of these branches. Additional stenting not performed due to the acuity of presentation and multiple side branch involvement.


The patient's subsequent course was complicated by cardiogenic shock, but she ultimately had a favorable outcome.

Embolism was suspected as the etiology; however, at the time she sent me this, the exact etiology had not been found.

Previous Normal Angiogram

There is little literature on the evaluation of apparent ACS, STEMI, OMI in patients with a previous normal angiogram.  The few studies I found are so small they are barely worth mentioning, except to say that it was rare to have new CAD soon after a totally normal angiogram.

1. Angiograms are "lumenograms."  You cannot see the plaque that is extraluminal, and pathology studies show that the vast majority of plaque is extraluminal.  Therefore, small amounts of luminal narrowing correlate with potentially very large occult plaque that could only be seen with intravascular ultrasound (IVUS) or with CT or MRI.

2. "Normal" was, in the past, used for coronaries with small nonobstructive (e.g., less than 50% stenosis) lesions.
--20-50% lesions progress and are known to fissure/ulcerate
--Over 50% (70%?) may be flow-limiting and correlate with stable angina.  Using fractional flow reserve can identify those who benefit from PCI.

3.  Most Acute MI occurs in plaque that is non-obstructive!  This is in spite of the fact that any given obstructive plaque is more likely to fissure and ulcerate and cause MI than any given non-obstructive plaque.  How is that possible?  Because the prevalence of minor plaque is so high!!  Many people walk around every day with nonobstructive plaque, and often multiple lesions in multiple arteries.  So even if a small percent of these plaques rupture, they result in a lot of acute MI over a population.

4. In the present age, "normal" should only be used for angiograms without any plaque at all.

5. "Non-obstructive" angiogram is often the terminology used when there is plaque, but it is not causing flow limitation (less than 50-70% narrowing).

6.  If the patient had a truly normal angiogram, then at 5 years from angiogram, new coronary disease is unlikely.  But this is based on very small studies.

7.  There are other causes of angina, myocardial infarction, and coronary occlusion [Spasm, "Syndrome X" (coronary endothelial dysfunction of small vessels), emboli, and others].  So, just because there was a truly normal angiogram does not rule out acute coronary occlusion (Occlusion MI, or OMI)

Normal Coronaries in Suspected Acute Coronary Syndrome:

The paragraphs below discuss the situation of patients with apparent MI who then go for an angiogram and it is found to be normal.  

These do NOT discuss the issue of a PREVIOUS normal angiogram in apparent ACS, as above.

Problem: In patients with apparent STEMI (ECG, troponin, echo) but who do not have occlusion on the ECG, and do not have visible thrombus or visible culprit, can there be unseen ruptured plaque that caused thrombus which then lysed?  Or are all these cases due to such entities as spasm, takotsubo, etc.

I called Tim Henry, Chair of Cardiology at Cedars Sinai in LA, and also the founder of the Level 1 STEMI program at Minneapolis Heart Institute (which has managed 7000 STEMI patients since its inception), and co-author of my EKG book.  He says that it would be very rare, but possible, to have a STEMI caused by thrombus from ruptured plaque that does not show a culprit lesion.  

Literature I found

The 4 articles below, about 8% of cases referred for primary angioplasty of STEMI have completely normal coronaries.  Many of these are false positive ECGs, but some are MI with due to spontaneous reperfusion.  If there is spontaneous reperfusion, the ECG will always show typical evolution or resolution.  

This case has an unequivocal ECG; it is clearly STEMI.  In cases in which the ECG is not unequivocal, absence of change over time proves it is not a STEMI.

By the way:
1) Non STEMI but with ST elevation due to non-AMI etiologies (early repol, LVH, etc.) is never documented in these studies.  
2) Furthermore, the mere presence of non-obstructive coronary disease, unless one sees a culprit lesion, does not prove that the symptoms were due to AMI.  
3) Troponin elevation is nonspecific.  Troponin is elevated in acute or chronic myocardial injury that is not MI, and also in type 2 MI).  The previous includes such entities as pulmonary embolism, myocarditis, stress cardiomyopathy, dilated cardiomyopathy, hypertensive cardiomyopathy, and more.  

Coronaries can now be evaluated with other means, such as intravascular ultrasound (IVUS).  Even when there is stenosis, most atherosclerosis is extraluminal.  It can be seen with IVUS, but not with a "lumenogram," which is what an angiogram is.  These atherosclerotic plaques can cause intralumenal thrombosis with STEMI.  If the clot lyses completely, the ischemia resolves and the angiogram may be normal.  This is what Tim Henry says would be rare.

Bibliography, with edited abstracts

There were 821 cath lab activations and 86% were treated by mechanical revascularization. In 76 patients (8.5%), no coronary artery stenosis was documented. Observations documented angiographically included coronary spasms (6.6%) and muscle bridges (5.3%). During a mean follow-up of 11.2±6.4 months, one patient developed an acute myocardial infarction requiring coronary intervention. All other patients were free of any cardiac event.

Article 2, full text

Of 898 patients who had cath lab activations for primary PCI, normal coronary angiograms were obtained for 26 patients (2.6%). Among these, the diagnosis at discharge was a small myocardial infarction in seven patients (0.7%), acute (peri)myocarditis in five patients, dilated cardiomyopathy in four patients, hypertension with left ventricular hypertrophy in three patients, pulmonary embolism in two patients and misinterpretation of the electrocardiogram (ie, no cardiac disease) in five patients. Seven patients with small infarctions underwent angiography within 30 min to 90 min of complete relief of the signs of acute ischemia, and thus, angiograms during pain were not taken.   None of the 898 patients catheterized during ongoing symptoms of ischemia had a normal coronary angiogram. Spontaneous coronary spasm as the only cause (without underlying coronary atherosclerosis) for the evolving infarction was not seen. Thus, the causes of the seven small infarcts in patients with normal angiograms remain uncertain.

Characteristics of 690 consecutive patients with presumed STEMI referred for primary PCI.  87 (13%) had angiographically normal coronary arteries and were compared with patients with angiographically shown culprit lesions (control group; n = 594). Nine patients with significant coronary disease, but no identifiable culprit lesion, were excluded. Electrocardiograms (ECGs) from both groups were reviewed by 2 cardiologists blinded to angiographic findings.  On expert review of ECGs, 55% of patients in the normal coronaries group had ST-elevation criteria for STEMI (vs 93% in the control group, but the ECG was considered consistent with a diagnosis of STEMI by both observers in only 33% (vs 92% in the control group)   Left branch bundle block independently correlated with normal coronary arteries on multivariate analysis (odds ratio for STEMI 0.016).   The discharge diagnosis in the normal coronaries group was predominantly pericarditis (n = 72; 83%), but these were not adjudicated by the authors (Comment: I frankly don't believe it.  Many of these were probably normal variant ECGs).  Other diagnoses were myocarditis in 3 patients (3%), Takotsubo cardiomyopathy in 2 patients (2%), presumed coronary spasm secondary to intravenous drug abuse in 2 patients (2%), cryptogenic AMI in 1 patient (1%), dilated cardiomyopathy in 1 patient (1%), massive pulmonary embolus in 1 patient (1%), cholelithiasis in 1 patient (1%), and pneumonia in 1 patient (1%).

The most likely alternative diagnosis suggested by both observers for the non-AMI ECGs in the normal coronaries group was normal variant ST changes (25% observer 1 and 26% observer 2) and early repolarization abnormality (25% observer 1 and 14% observer 2). 

The medical records of 941 patients undergoing coronary arteriography for presumed ACS within 48h of onset were critically reviewed. In 70 patients (7.4%, 35 males) no CAD was documented. Alternative substrates of acute myocardial ischemia included coronary artery anomalies (7 patients, 10%), coronary spasm (10 patients, 14.3%), spontaneous coronary dissection (2 patients, 2.8%), paradoxical embolism through a patent foramen ovale (4 patients, 5.7%), embolism from left atrium or calcified aortic valve (4 patients, 5.7%), imbalance between oxygen demand and supply (20 patients, 28.5%), mitral valve prolapse (11 patients, 15.7%). No alternative substrates were found in 12 patients (17.1%). Absence of CAD is an uncommon finding in patients undergoing coronary artery angiography for ACS.

Article 5.

Angina with Normal Coronary Arteries (JAMA 2005)

Detailed Analysis & Comments by KEN GRAUER, MD:
Excellent presentation by Dr. Rochelle Zarzar! The interesting feature of this case is documentation of a completely normal angiogram 3 months prior. This situation apparently dissuaded cardiology from the belief that the initial ECG here represented an OMI ( = Occlusion-related acute MI). Presumably, cardiology had an opportunity to view this initial ECG. We are not told if they were also sent a copy of the prior ECG on this patient. Realizing that “hindsight is 100% in the retrospectoscope” — in the interest of academic edification — I’ll go on record saying that cardiology made a big mistake. Sgarbossa and modified Smith-Sgarbossa criteria are indeed helpful — but they are primarily based on relative measurements. By far the most specific indicator of acute infarction in association with QRS widening from underlying LBBB and/or ventricular pacing — is the finding of ST segment elevation that “shouldn’t be there”. Regardless of the fact that the initial ECG in this case is paced — there just should NOT be the shape of ST elevation that we see in not only one, but 2 leads! ( = leads I and aVL) — nor should their be “mirror-image” reciprocal ST depression. There is often a “magic” reciprocal relationship between the ST-T wave in lead III and lead aVL whenever there is acute evolving infarction. This is “mirror-image” reciprocal relationship IS clearly present in this initial ECG, with confirmation that this is indeed REAL by the finding of reciprocal ST depression in the other 2 inferior leads. In an elderly patient who presents with new chest pain — the finding of these 5 abnormal limb lead ST-T wave changes is diagnostic of acute coronary occlusion, without need to first check serum troponin … The 2nd mistake made by cardiology in this case was either not to request the ECG done 3 months earlier (at the time of that normal cath) — or if they did request it, not to realize that despite slight variation in QRS morphology in the earlier paced tracing, and despite nonspecific ST-T wave abnormalities in a number of leads in this earlier tracing — there simply was NO “ST elevation where there should not have been” in the prior tracing. And, there is now ... GREAT case, and compliments to Dr. Zarzar for her excellent presentation!