The patient in todays case is a 50 year old male. He has a medical hx notable for hypertension, hyperlipidemia and previous tobacco use disorder. The patient presented due to chest pain that was typical in nature, retrosternal and radiating to the left arm and neck. He denied any exertional chest pain.
The below ECG was recorded. It is unclear if the patient was pain free at this time.
The ECG does not show any definite signs of ischemia. In fact, the ECG was described as normal, and without serial ECGs or prior ECGs for comparison it could be. Initial high sensitivity troponin I returned at 6ng/L (normal <34ng/L) repeat troponin at 3 hours was 13, later peaking at 15 the following day.
Due to the nature of the symptoms (in spite of absence of a single troponin value above the 99th percentile URL), the patient was suspected to have unstable angina and referred for a coronary angiogram the following day. The angiogram did not reveal any obstructive coronary artery disease. The IC stated that "another cause for the patient’s complaint must be sought."
Smith: there was no intravascular ultrasound or optical coherence tomography, both of which could be used to find rupture plaque that does not show up as stensosis on the angiogram. Nor was there a challenge to look for coronary spasm. I think none of these a commonly done in cases in which the troponin is not elevated since the probability of ACS is low.
The patient was discharged only to present with chest pain again within one week. The below ECG was recorded during chest pain. What do you think?
The above ECG demonstrates obvious significant ST changes. How would you proceed in handling this patient? Do you think this patient needs another cath lab activation? What will you say if the IC declines arguing the recent CAG was normal one week prior? What if the IC states that this is myocarditis, will you accept that as a plausible explanation?
The ECG shows ischemic looking ST elevation in the inferior leads (II, III and aVF) and lateral leads (V5-V6). There is ST depression in leads V2-V3 signifying posterior involvement as well.
But this patient had a normal coronary angiogram one week prior! It must be myocarditis then right?
No! Even though this patient had a normal angiogram one week prior that is no guarantee he is not experiencing a type I MI. In fact, with the typical chest pain and the presenting ECG type I MI is the absolutely the most likely cause of the patient's symptoms. This patient needs emergent coronary angiogram. An erroneous assumption of not OMI could be devastating.
- This patient could have a conventional type I MI from plaque rupture despite having no significant stenosis one week prior.
- The patient could be having an embolic coronary artery occlusion.
- The patient could be having SCAD or extension of an aortic dissection to a coronary artery.
- Also on the list of differentials are myocarditis, takotsubo, coronary artery spasm.
Just prior to the angiography the patient became unwell with a heart rate in the 30’s. At the same time massive ST elevation in the inferior leads were noted. Almost instantaneously after intubation of the RCA ostium with the diagnostic catheter the ST elevation rapidly disappeared. Below is a still image obtained of the RCA angiogram. The yellow arrow pointing at the proximal portion of the RCA that shows significant narrowing.
How can this be? Angiography was normal a week prior. A CT angiogram of the aorta was obtained, no dissection was found. Below is an image from the CT scan showing the aortic root and RCA. The cardiac chambers are denoted with the yellow arrow pointing to the proximal segment of the proximal RCA.
This patient was having a type 2 acute MI from coronary artery spasm of the proximal part of the RCA. The angiography still image and the CT angiogram both show severe narrowing of the pRCA. This explains ST-elevation and bradycardia. Most episodes of chest pain were of short duration (minutes). The slight troponin release a week prior, typical symptoms, angiographic, electrocardiographic and radiologic investigations are all consistent with variant angina as a cause of the intermittent ST elevation. Troponin T during the second visit peaked at a modest 83 ng/L. The patient was prescribed calcium channel blocker and extended release nitroglycerin. Long term follow up is not available.
Learning points:
- The ECG does not lie and sometimes patients need a second cath lab activation.
- Listen to the patient, if the symptoms are typical in nature an ECG during pain must be obtained.
- Plaque rupture cannot be ruled out by angiography alone. When there is such "Myocardial Infarction with Non-Obstructive Coronary Arteries" (MINOCA), there are ways to look for plaque rupture beyond standard angiogram (which is only a "lumenogram". The best of these is optical coherence tomography. Intravascular ultrasound is also acceptable.
- Variant angina has typical symptoms that may be of short duration and not related to activity.
See this case and this case for more examples of "Prinzmetal's" variant angina.
- As per Dr. Nossen — the fact that today's patient so recently had a normal cath does not rule out the possibility that recurrence of CP could indeed be due to new acute coronary occlusion.
- Another reason for our interest in today's case — is that this patient was found on his 2nd admission to have coronary artery spasm with massive inferior lead ST elevation and marked bradycardia with positive troponin — all in the absence of underlying coronary disease. This evidence for pure coronary spasm without underlying coronary disease is not a common occurrence.
- To EMPHASIZE: Persistent symptoms in a patient with new worrisome CP is sufficent justification to perform diagnostic cath, even when serial troponins are negative and ECGs are interpreted as unremarkable.
- Given that this patient's history of new CP was worrisome enough that it alone served as the reason for cardiac cath — My threshold for interpreting an ECG as "not normal" was immediately lowered! By this, I mean — even seemingly minimal ECG findings in this clinical context should be interpreted as potentially suspicious.
- Comparison with prior ECGs is extremely important in such cases (Given this patient's past medical history — it is clear that prior tracings had to have been done).
- As noted by Dr. Nossen — it was unclear if the patient did or did not have CP at the time ECG #1 was recorded. As we have emphasized in numerous cases — correlation between the presence and relative severity of CP at the time an ECG is done is critical (albeit all-too-often-neglected) information for optimal ECG interpretation (ie, "Pseudo-normalization of ECG findings may be seen if CP has resolved by the time the ECG is recorded).
- Serial ECGs (recorded in close succession) are an essential component of evaluation when looking for "dynamic" ECG changes that may occur if the initial ECG was recorded during the period of pseudo-normalization.
- The T wave in lead III looked "bulkier"-than-expected given small size of the R wave in III (within the BLUE rectangle in this lead).
- The T wave in lead aVL is usually not inverted when the R wave is all positive (as it is within the BLUE rectangle in this lead).
- Given these findings in leads III and aVL — the ST segment straightening in lead I is not "normal".
- There is more than the usual amount of ST elevation in lead V1 (BLUE arrow in this lead) — and the taller-than-expected T wave in this lead suggested "T wave imbalance" given the greater T wave size than seen in lead V6 (See My Comment in the June 1, 2022 post in Dr. Smith's ECG Blog).
- There is "early transition" — with an R wave already greater than the S wave by lead V2 (which while clearly a nonspecific finding — taller-than-expected anterior R waves can be a sign of posterior infarction).
- While the amount of upsloping J-point ST elevation in lead V2 is not abnormal (BLUE arrow in this lead) — I wondered WHY this J-point elevation was abruptly lost by lead V3? (slanted RED line in this lead).
- BOTTOM Line: I fully acknowledge that all of the above findings are exceedingly subtle and nonspecific. BUT, taken together in this patient with a history of worrisome new CP — careful correlation with the presence and severity of CP symptoms in association with serial ECGs over the ensuing minutes would be needed to know if the above described findings might be real.
NOTE: I believe that ECG #2 obtained days later during CP supported my suspicion about the subtle findings I describe above for ECG #1 — because during coronary spasm (ie, at the time ECG #2 was recorded): i) Lead III now manifests marked ST elevation; ii) Lead aVL now manifests marked reciprocal ST depression; and, iii) The J-point ST depression in leads V1,V2 now clearly indicate posterior involvement; and, iv) There is a marked contrast in ECG #2 between the ST depression in leads V1,V2 and the beginning of marked ST elevation with lead V3 — just as there was that inexplicable loss of J-point elevation between leads V2 and V3 in ECG #1.
-USE.png) |
| Figure 1: I've labeled the initial ECG in today's case. |
- We are told this patient developed more severe bradycardia a bit later on during his evaluation, with a heart rate in the 30s (no tracing available).
- We see 8 consecutive beats in ECG #2 (albeit there is no long lead rhythm strip).
- What is the likely mechanism of the rhythm in ECG #2?
-USE.png) |
| Figure 2: I've labeled the 2nd ECG in today's case. |
- There is sinus bradycardia with marked sinus arrhythmia.
- There is marked baseline artifact — which makes identification of atrial activity challenging. That said — Beat #6 occurs unexpectedly early. However, rather than being a PAC — I believe the RED arrows that are seen in lead V1 suggest a marked sinus arrhythmia.
- My caliper measurement of the PR interval preceding beats #5 and 6 in lead V1 — suggests that the PR interval increases. However, unlike Mobitz I 2nd-degree AV block — P waves are not regular, and there is no dropped QRS after beat #6.
- All 8 beats in ECG #2 appear to be conducted (ie, preceded by a PR interval that is constant for all beats except #6).
- There is 1st-degree AV block (ie, PR interval clearly >0.20 second).
- IMPRESSION: The finding of sinus bradycardia with 1st-degree AV block + marked sinus arrhythmia + the change in PR interval from beat #5-to-beat #6 — suggests a form of vagotonic block (See My Comment in the October 9, 2020 post in Dr. Smith's ECG Blog).
- PEARL: Increased vagal tone is highly likely to be the cause of the abnormal rhythm in ECG #2. Given CP, increased troponin and inferior lead ST elevation — this is the ideal situation for which atropine in modest dose may be optimally effective (ie, during the early hours of acute inferior MI when vagal tone is most likely to be increased and responsive to judicious atropine).
- Especially later on during evaluation of this patient when heart rate continued to drop (ultimately attaining a rate in the 30s) — readiness to administer atropine might prove lifesaving.
- I thought acute myocarditis to be unlikely given the lack of a viral infection — and the anatomic localization of ECG findings (suggestive of acute infero-postero-lateral MI on ECG #2).
- I thought the complete lack of QTc prolongation and anatomic localization of ECG findings made Takotsubo cardiomyopathy unlikely.
- This left MINOCA as the most likely cause of this patient's symptoms. Although important to always consider the possibility of an acute OMI that spontaneously reperfused, such that thrombus is no longer evident by the time cath is performed — today's patient turned out to have coronary artery spasm in the absence of underlying obstructive coronary disease.
- Uncontrolled coronary spasm may be associated with serious arrhythmias, including cardiac arrest (Looi et al — Postgrad Med, 2012; Tan et al — Eur Heart J Case Rep, 2018; Chevalier et al — JACC, 1998; Rodriguez-Manero — EP Europace, 2018). As a result — an ICD may need to be considered in selected cases.
- Use ß-blockers with caution (as they may aggravate coronary spasm).
- Today's patient was noted to be "a previous tobacco user". Given the potential triggering effect of smoking on coronary spasm — absolute abstinence from smoking is essential!
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