60 year old with vomiting, diarrhea, and syncope: is this Wellens? Is this type 2 MI?

 Written by Jesse McLaren, with edits/comments by Smith and Grauer

 

A 60 year-old patient with diabetes and ESRD presented with 24 hours of vomiting, diarrhea, weakness and then a syncopal episode. Vitals: RR 18, sat 98%, HR 103, BP 124/71 and temp 38.0. Here’s their ECG: is this Wellens?

 

 

There’s borderline sinus tach, normal conduction, normal axis, and low voltages in the limb leads. The anterior leads have loss of R waves, mild convex ST segments and primary T wave inversion. In the context of QS waves, T wave inversion indicates old or subacute infarct, or reperfusion after significant infarction. Below is the old ECG:

 

 

This confirms the anterior changes are new--but is this from type 1 or type 2 OMI? The patient was diagnosed and treated for sepsis and DKA, and the only interpretation of the first ECG by the emergency physician was that it didn't meet STEMI criteria.

Smith: 

1) Some type 1 MI only present with atypical symptoms, especially in diabetics. Such atypical symptoms include vomiting, but not diarrhea.  

2)  Type 2 MI requires a supply demand mismatch.  Low supply: hypotension, hypoxia, anemia, dyshemoglobinemias.  High demand: tachycardia, hypertension, dilated LV (wall stretch).  This patient has no evidence of supply demand mismatch.

3) The ECG suggests a nearly completed LAD infarct due to the QS-waves in V2 and V3.

 

The first troponin returned at 68,000 ng/L, which was attributed to type 2 MI (though this is not a simple dichotomy, as Dr. Grauer explains in his comments below.) The patient was referred to cardiology, who found an anteroseptal wall hypokinesis on bedside echo. The patient had a prior stress echo with preserved EF but inducible ischemia in the LAD territory. As they noted, "Not for urgent cath in context of septic/DKA picture clouding assessment for type 1 MI, but definitely requires cath and medical treatment for ACS." So they initiated on dual antiplatelets and heparin with a plan for angiogram the next day after treatment for sepsis/DKA.

Smith: the extremely elevated troponin also in consistent with a subacute and completed (transmural) or nearly completed infarct.

 

Unfortunately, 12 hours after arrival, the patient had a VF arrest. Here’s their post-cardioversion ECG.

 

 

Anterior STEMI(+)OMI, so cath lab activated: the LAD had a 100% occlusion but this was chronic, with collaterals from an intact RCA and circumflex that had a 90% stenosis.

Smith: The anterior wall has clearly been supplied through collaterals from the RCA and circ since there is a chronic LAD occlusion.  The circ has a tight stenosis, but is open.  Thus the anterior wall is susceptible to supply demand mismatch, but (as above) we don't have any evidence of that.  Just because the RCA and circ are open now does not mean they were open 20 hours ago.  And the angiogram frequently does not identify a culprit.  So I suspect that one or both of these were occluded within the past 24 hours, resulting in a large anterior infarct.

There was an unsuccessful attempt to stent the chronic occlusion. Peak troponin was 95,000, EF was reduced to 45% with anterior wall motion abnormality, and below is the discharge ECG showing shallow anterior T wave inversion:

 

 

 

As this post explains, Wellens syndrome describes

1.     patient: anginal symptoms which have resolved

2.     ECG: primary reperfusion T wave inversion in LAD distribution but intact R waves, indicating reperfusion before significant infarction

3.     Troponin: mildly elevated

4.     Angiogram: critical lesion in LAD which is now open, or reperfused by collaterals, but is at high risk of-reocclusion

 

But in this case

1.     patient presented with sepsis vs anginal equivalent: sepsis can cause diffuse ST depression and reciprocal ST elevation in aVR (which is not a “STEMI equivalent” but a sign of diffuse subendocardial ischemia), but should not cause focal ECG changes that mimic OMI

2.     ECG showed primary T wave inversion in LAD distribution, but also loss of R waves indicating significant infarction

3.     Troponin was massively elevated

4.   Angiogram showed chronic total occlusion (CTO) of LAD and limited collateral circulation, which was compromised

As the EXPLORE trial explained, "Concurrent CTO lesions are found in 10% to 15% of patients with STEMI...Because of the procedural complexity and below-average success rate, PCI is attempted only in 10% of all CTO lesions, commonly in an elective setting...In patients with STEMI and concurrent CTO, we did not find an additional benefit for CTO PCI in terms of LVEF or LVEDV. However, a subgroup analysis suggests that patients with CTO in the LAD may benefit from early additional CTO PCI." (Henriques et al. Percutaneous Intervention for Concurrent Chronic Total Occlusions in Patients with STEMI: the EXPLORE trial. JACC 2016)

For patients with CTO, collateral circulation is crucial. As another study found: "In CTO lesions, the antegrade blood flow is completely interrupted, leaving the myocardium entirely dependent on collateral flow...If the collateral to the collateral-dependent myocardium of the CTO area originates directly or distally from the IRA, the myocardium could be endangered in case of blockage during STEMI. This could result in an increase in infarct size and a decrease in LVEF leading to a higher mortality. In our cohort there was a trend for higher mortality in patients with well-developed retrograde collaterals to the CTO, originating from the IRA, which were blocked during STEMI."(Elias et al. Impact of collateral circulation on survival in ST-segment elevation myocardial infarction patients undergoing primary percutaneous coronary intervention with a concomitant chronic total occlusion. JACC 2017)

While this describes collateral circulation compromised by acute thrombus (type 1 MI), it can also be compromised by supply-demand mismatch (type 2 MI). See this post on type 2 posterior OMI secondary to pneumonia and severe anemia: "An emergency formal echo showed an inferolateral wall motion abnormality.  In the record, an old angiogram reported a chronically occluded obtuse marginal (OM).  The previous echo was normal, but a stress echo had shown induced inferolateral hypokinesis.  Thus, there was prior proof that this area was vulnerable to stress; the territory of this artery was reliant on collateral circulation for oxygen delivery."

 

Take home

    1. Wellens syndrome describes LAD type 1 OMI with spontaneous reperfusion, but

         loss R waves, especially QS-waves, imply there has already been a large infarct

    2. spontaneous reperfusion can occur from the artery opening or recruitment of

        collaterals, i.e. reperfusion can occur with arteries that remain occluded (acutely or

         chronically) if there is sufficient collateral circulation - which is tenuous

    3. Patients with CTO rely on collaterals, which can be compromised by type 1 MI

     (thrombus) or type 2 MI (supply/demand mismatch): treatment is directed at

     restoring supply/demand mismatch, reperfusing acutely occluded coronary arteries

     +/- revascularizing CTO

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MY Comment, by KEN GRAUER, MD (8/19/2022):

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Today's case by Dr. McLaren prompts consideration of the relationship between Acute Infection and Myocardial Infarction. A recent article by Musher et al with this exact title reviews a series of fascinating features of this relationship (Musher et al — N Engl J Med 380:171-176, 2019 — with Free-Access summary of KEY Points by Hayek in ACC: Latest in Cardiology, 2019).

• Today's case by Dr. McLaren recounts the hospital admission of a patient with sepsis and DKA — with a complicated course including VFib arrest, massively elevated troponin and ultimately an anterior STEMI.
• Among the points brought out by the above NEJM Review — is the fact that the association between acute infections and acute MI has only been appreciated during the past few decades. A growing body of literature now documents the relationship between viral and bacterial infections such as influenza, pneumonia, urinary tract infections, septicemia, and many others. The finding that risk of acute MI is greatest at the onset of infection — and is proportional to infection severity — strengthens the premise of a cause-and-effect relationship.
• 
  
• Surprisingly — the NEJM Review authors contend that demand ischemia (ie, Type 2 Acute MI) should explain no more than a minority of infection-related MI events. Instead — they feel the cause of most infection-related MIs is acute coronary occlusion ( = Type 1 Acute MI).
• 
  
• Mechanisms proposed to explain how acute infection may result in acute coronary occlusion include (among others): i) Destabilization of existing atheromatous plaque by acute inflammatory factors (ie, cytokines, interleukins, tumor necrosis factor); ii) Increased thrombogenesis with platelet activation that is associated with acute infection; iii) Gene expression linked to platelet activation, endothelial dysfunction and hypercoagulability that may be promoted by certain viruses.
• Mechanisms proposed to explain how acute infection may result in Type 2 MI (from demand ischemia) include: i) Impaired coronary perfusion despite increased metabolic needs from acute infection (ie, compensatory tachycardia shortens ventricular filling time during diastole — thereby reducing coronary perfusion); ii) Toxin-mediated vasoconstriction from acute sepsis; iii) Hypoxemia with ventilation-perfusion mismatch (especially with severe respiratory infections); iv) A direct myocardial depressor effect from circulating toxins liberated by acute infection; v) Cytokine "storm" — with sudden release of these substances that may provoke a life-threatening systemic inflammatory syndrome leading to multi-organ failure.

The message from this NEJM Review is clear — A variety of mechanisms account for depressed ventricular function and potential for inducing either Type 1 or Type 2 acute MI as a direct result from almost any serious acute infection.

• We need to remain alert to this possibility!