Friday, January 8, 2021

Acute chest pain, ST Depression in V2 and V3, relief with Nitroglycerine, "normal" coronaries, and apical ballooning. Is it takotsubo?

This was submitted by Michael Fischer, one of our outstanding 2nd year EM residents at Hennepin Healthcare.

Case

A previously healthy female in her 40s presented 1 hour after abrupt onset 10/10 crushing chest pain that started while brushing her hair that morning. The pain radiated to her bilateral jaw and right shoulder, and did not seem to be exertional or pleuritic in nature.  

 

Here is her pre-hospital ECG: 



What do you think?












Smith: V2 and V3 have some minimal ST depression with downsloping.  This is highly suggestive of posterior MI.



This was read by EMS as non-specific. Aspirin 324mg was given by EMS. Nitroglycerin spray x3 was also given which brought her pain down to 3/10 upon arrival to the ED. She was vitally stable with systolic BP of 140s. No cardiac history, not taking any medications, but does have 1st degree relatives with CAD.  

 

Here is her first ED ECG:


The ST Depression is more pronounced, and has extended to V4







This was interpreted as ST-depression in V2-V4. Additional sublingual nitro was given x2, bringing her pain to 0/10 in her chest, however she still had pain in her jaw.  

 

Given the abrupt onset of pain, aortic pathology was also a concern. Bedside echocardiography revealed grossly intact left ventricular function, non-dilated aortic root. Suprasternal view of the aorta revealed normal caliber aorta with no obvious dissection flap. Upper extremity pulses were equal. D-dimer was sent as further rule out for dissection.  

 

A repeat ECG was obtained with her chest pain resolved after nitroglycerin: 


Almost completely resolved




This was interpreted as resolved anterior ST-depression. 

 

Over the course of the next 30 minutes while labs were pending, her chest pain slowly returned. Her troponin returned at 0.682 ng/mL (upper reference limit of 0.045 ng/mL), D-dimer negative. At this point, interventional cardiology was consulted and recommended medical management with plan for the catheterization lab that afternoon. She remained vitally stable with systolic BP in the 130-140s. She was started on a nitro drip and was heparinized.  

 

Her chest pain continued to wax and wane on the nitro infusion. She additionally received hydromorphone and ondansetron. Interventional cardiology was consulted again regarding her waxing and waning pain, at which time they took the patient to the catheterization lab.  

 

Given her rapid improvement on nitro, it was thought that her symptoms could be due to coronary vasospasm given her overall lack of CAD risk factors. Ruptured plaque and coronary dissection remained leading differentials as well.  

 

Angiogram report: 

Normal coronary arteries.  

Left ventriculogram demonstrated apical ballooning and hypercontractile base consistent with stress-induced cardiomyopathy.  

 

Takotsubo Cardiomyopathy- The Great Imitator! 

As previously discussed in this blog, Takostubo cardiomyopathy may manifest as T-wave inversion or ST elevation that can mimic a STEMI. This patient’s ECG with anterior ST depression is an atypical ECG presentation in takotsubo, and diagnostic of posterior MI, prompting angiography to rule out acute coronary occlusion.  


On chart review, there was no inciting stressor thought to precede her symptoms. She did well and was discharged on an ACE-inhibitor and beta-blocker. 


Smith comment: This ECG is very unusual for takotsubo.  And although it correlates mostly closely with posterior transmural ischemia (posterior STEMI), it would not be unusual for subendocardial ischemia due to LAD spasm or LAD subtotal thrombosis.  Thus, I am not entirely convinced of takotsubo in this case.  


All management was appropriate.  The cath lab certainly needed activation.  The coronaries were clean.  There was apical ballooning on ventriculogram.  


However, the cath report does not mention whether the LAD wraps around to the inferior wall, and there was no intravascular ultrasound (IVUS) to prove absence of ruptured plaque that does not manifest on plain angiogram (which only shows the lumen of the artery and, unlike IVUS, does not show extraluminal plaque).


Moreover, the onset of chest pain was without inciting event, as usually happens with takotsubo, and was relieved with nitroglycerin, which strongly suggests some element of coronary ischemia.


Thus, we may never know whether this was LAD ACS, LAD spasm, or a very strange sort of takotsubo.


3 comments:

  1. Thank you so very much Mike Fischer, and Steve.
    this case interests me... questions, and certainly not criticisms:
    1. i thought CP with ST depression V2, and or V3 was an indication for stat cath (possible posterior wall OMI till proven otherwise. altho at a recent Amal Mattu toronto cards course, Amal said he'd get posterior leads to look for ST elevation, and act on that. But i think that in a case like this, i'd feel more comfortable with stat cath (tho not sure what our interventionalists would say.)

    2. funny: i also thought IVUS would be nice, but not even sure where they do that in northern california.

    3. above: "D-dimer was sent as further rule out for dissection." although the dimer is interesting i thought it certainly does not rule out dissection, as does not the bedside US.
    (just had a 34 y old chest /abdominal pain BP 270/140, i did a stat bedside US , including over the sternal notch, saw no obvious pathology. but the CT chest/abd/pelvis in the next few minutes showed a dissection stanford type A to the iliacs, which may be a poor reflection on my US expertise perhaps).

    4. wouldn't apical ballooning have inferior wall changes? the site of the ischemia? or not necessarily?

    5. why discharged on ace-inhibitor and beta-blocker, if her coronaries are "clean"; is this the treatment for takotsubo (which means "octopus trap" in japanese)?

    Michael, extraordinary, illustrative and problematic case. thank you for this detailed blog.
    very cool discussion. thank you, steve.

    ReplyDelete
    Replies
    1. 1. i thought CP with ST depression V2, and or V3 was an indication for stat cath (possible posterior wall OMI till proven otherwise. altho at a recent Amal Mattu toronto cards course, Amal said he'd get posterior leads to look for ST elevation, and act on that. But i think that in a case like this, i'd feel more comfortable with stat cath (tho not sure what our interventionalists would say.)

      STD V2/V3 IS INDICATION. THIS CASE ILLUSTRATES THAT SOMETIMES IT MAY BE FALSE POSITIVE (ALTHOUGH THIS ONE IS NOT NECESSARILY A FALSE POSITIVE). WE JUST SUBMITTED AN ABSTRACT SHOWING THAT STD MAX IN V2-V4 IS POSTERIOR MI 85% OF THE TIME. ABSENCE OF STE IN POSTERIOR LEADS SHOULD NOT DISSUADE YOU FROM THE DIAGNOSIS. I THINK AMAL IS WRONG ABOUT THAT AND HE DOES NOT HAVE DATA TO SUPPORT IT.

      2. funny: i also thought IVUS would be nice, but not even sure where they do that in northern california. YES, SHOULD USE IVUS

      3. above: "D-dimer was sent as further rule out for dissection." although the dimer is interesting i thought it certainly does not rule out dissection, as does not the bedside US.
      (just had a 34 y old chest /abdominal pain BP 270/140, i did a stat bedside US , including over the sternal notch, saw no obvious pathology. but the CT chest/abd/pelvis in the next few minutes showed a dissection stanford type A to the iliacs, which may be a poor reflection on my US expertise perhaps). WE DID NOT STATE THAT IT RULED OUT DISSECTION, JUST THAT IT WAS NEGATIVE. IT DOES HAVE SOME USE AND MICHAEL USED IT.

      4. wouldn't apical ballooning have inferior wall changes? the site of the ischemia? or not necessarily? APICAL BALLOONING IS MOTION ABNORMALITY OF ALL WALLS, INCLUDING INFERIOR. IF IT FULLY MANIFESTS ON THE ECG, YOU WOULD SEE ECG CHANGES OF ALL WALLS. THIS IS ONE REASON WHY I THINK TAKOTSUBO IS NOT THE CORRECT DIAGNOSIS

      5. why discharged on ace-inhibitor and beta-blocker, if her coronaries are "clean"; is this the treatment for takotsubo (which means "octopus trap" in japanese)? I DON'T KNOW WHAT THE THINKING WAS, BUT WE OBVIOUSLY DID NOT PRESENT ALL THE MEDICAL HISTORY OR THINKING HERE.

      Delete

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