A 20-something male drank heavily of ethanol and used cocaine, then was involved in a stressful verbal altercation, at which time he developed chest pain.
911 was called and the medics recorded this ECG (unfortunately, leads V4-V6 are missing)
He arrived in the ED and had this ECG recorded:
The ECG shows Brugada morphology in V1 and V2, and the typical normal variant ST elevation in lead V3.
Brugada morphology can be caused by baseline Brugada morphology, including Brugada syndrome, or by hyperkalemia or Sodium channel blockade.
Cocaine not only has effects on dopamine neurotransmission, but is also a sodium channel blocker, as are all "-caine" local anesthetics. Cocaine is well known to result in Brugada morphology.
See this post and associated case reports:
The patient was admitted and ruled out for acute MI by serial troponins.
Below are subsequent ECGs, showing resolution of the Brugada morphology as the cocaine metabolizes. Cocaine metabolism is rapid. After approximately 3-4 hours, the cocaine and its effect are gone. Testing for cocaine is for the inactive metabolite Benzoylecgonine, and this inactive metabolite is present for days. So a positive screening test for "cocaine" does not imply persistent intoxication.
Here are the serial ECGs:
Time 1 hour:
Time 4 hours:
Time 10 hours:
The vast majority of cocaine chest pain is NOT due to myocardial ischemia or infarction, and most is in young males with normal variant ST Elevation or LVH, so it often looks scary on the ECG.
As there was no personal history of syncope or family history of sudden death, the patient was discharged with cardiology followup.
911 was called and the medics recorded this ECG (unfortunately, leads V4-V6 are missing)
 |
| Due to marked ST Elevation, the computer read was ***STEMI*** What do you think? |
He arrived in the ED and had this ECG recorded:
 |
| Very similar to the prehospital ECG. The Mortara (Veritas algorithm) Interpretation was:
MARKED ST ELEVATION, CONSIDER SEPTAL INJURY
***ACUTE MI***What do you think? |
The ECG shows Brugada morphology in V1 and V2, and the typical normal variant ST elevation in lead V3.
Brugada morphology can be caused by baseline Brugada morphology, including Brugada syndrome, or by hyperkalemia or Sodium channel blockade.
Cocaine not only has effects on dopamine neurotransmission, but is also a sodium channel blocker, as are all "-caine" local anesthetics. Cocaine is well known to result in Brugada morphology.
See this post and associated case reports:
Cardiac arrest, severe acidosis, and a bizarre ECG
The patient was admitted and ruled out for acute MI by serial troponins.
Below are subsequent ECGs, showing resolution of the Brugada morphology as the cocaine metabolizes. Cocaine metabolism is rapid. After approximately 3-4 hours, the cocaine and its effect are gone. Testing for cocaine is for the inactive metabolite Benzoylecgonine, and this inactive metabolite is present for days. So a positive screening test for "cocaine" does not imply persistent intoxication.
Here are the serial ECGs:
Time 1 hour:
 |
| Cocaine Brugada Effect is still present |
Time 4 hours:
 |
| Minimal effect is still present |
Time 10 hours:
 |
| The ECG only shows some slight abnormalities in V1 and V2, with minimal residual saddleback morphology in lead V2. |
The vast majority of cocaine chest pain is NOT due to myocardial ischemia or infarction, and most is in young males with normal variant ST Elevation or LVH, so it often looks scary on the ECG.
As there was no personal history of syncope or family history of sudden death, the patient was discharged with cardiology followup.
Interesting case that is very important to recognize. This is “Brugada Phenocopy” — which relates to Brugada-1 or -2 patterns that may be induced by other conditions, rather than being a true Brugada “Syndrome”. The list of “other conditions” that may temporarily produce a Brugada ECG pattern is large and includes (among others) — certain DRUGS (ie, calcium channel blockers, beta-blockers; antianginals; psychotropics; alcohol, cocaine, and others) — Acute febrile illness — variations in autonomic tone — hypothermia — electrolyte imbalance — ischemia/infarction — bradycardia — following cardioversion or defibrillation. The clinical significance of a temporarily-induced Brugada pattern is uncertain, and depends on the individual patient and clinical circumstances. Often, the ECG pattern resolves completely with resolution of the precipitating problem without the potentially worrisome accompaniments of a true Brugada Syndrome. That appears to be the case here, in which this patient presented with cocaine overdose that resolved to the point that the patient was able to be discharged with follow-up. THANKS to Dr. Smith for presenting this insightful case that: i) should not be misdiagnosed as acute septal stemi; and ii) should instead be recognized as probable Brugada Phenotype, with first priority aimed at addressing the precipitating cause (ie, Cocaine use).
ReplyDeletethanks, Ken!
DeleteVery interesting case. It is interesting to notice the transformations from Brugada pattern type-1 (coved type) to Brugada pattern type-2 (saddleback type).
ReplyDeleteRecently I discovered the following link on various etiology (rapidly increasing) of Brugada phenocopy:
http://www.brugadaphenocopy.com/about-brugada-phenocopy.html
Thanks for presenting this case.
Very interesting case with Dr. Smith's and Prof. Ken Grauer's informative interpretation. I just have a query that if this Brugada Phenocopy can lead to the life-threatening ventricular arrythmias as true Brugada syndrome does and Do we need a preventive treatment for these lethal ventrucular arrythmias? Thank you!
ReplyDeleteIn this case, it only requires monitoring and waiting for metabolism of the cocaine. every situation is different.
DeleteThank you, sir!
Delete