Tuesday, May 29, 2018

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?






Analysis:

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):  
DIAGNOSTIC - CORONARY
· 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. 


INTERVENTION
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.

Outcome


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)

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Detailed Analysis & Comments by KEN GRAUER, MD:
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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!

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