Wellens' syndrome: to stent or not? IVUS negative, Symptoms persist, Stress Testing, Instantaneous Wave Free Ratio, and Fractional Flow Reserve.

A 55 y.o. male with no cardiac PMHX presented for 2 weeks of exertional chest pain, worsened on the day prior to presentation.  On the day of presentation, the chest discomfort was particularly intense, and associated with diaphoresis and nausea.  It was resolved (pain free) when the ECG was recorded:

This ECG was read as "nonspecific" by the providers.  

What do you think?

These is classic Wellens' pattern A (biphasic, terminal T-wave inversion), and it is Wellens' syndrome (Angina, resolved -- pain free -- with preserved R-waves and Wellens' pattern A T-waves).  The morphology of these T-waves is very distinct and most T-wave inversion does not fit the pattern.  The pattern manifests a rising ST segment with a sudden fall into the slightly negative T-wave.   If you recognize this pattern, then you are not so dependent on troponin for your diagnosis.  

Wellens' syndrome does not mandate emergent cath lab activation, since the artery is open and the patient is pain free; there is no persistent ongoing ischemia. When the patient was suffering pain prehospital, the artery was occluded, but it spontaneously reperfused (autolysis).  However, the patient is at high risk for re-occlusion at any time and cath lab activation is optimal because this should be considered a transient STEMI in which the ST elevation would have been there had the ECG been recorded during pain.

The initial Abbott high sensitivity troponin I was 60 ng/L (upper reference limit for men = 34 ng/L).

This initial troponin in this context is all but diagnostic of acute MI.  The actual definition of acute MI by the 4th Universal Definition requires a rise and/or fall of troponin.

The 2nd troponin also returned at 60 ng/L.  No rise, no fall.

Often, low or non-dynamic troponins may be explained away by "type 2 MI" or non-MI "myocardial injury" and so this physician did not want to risk such dismissal by an inpatient team.  

He therefore ordered a CT coronary angiogram:

--Calcium score (Agatston method): 0.

Followed by contrast scan:
--LAD: Noncalcified plaque in the proximal LAD, with a linear intravascular filling defect, concerning for dissection with likely severe stenosis.  Appearance is concerning for a severe stenosis. 

In fact, all 4 troponins were at plateau:

So this LAD is completely consistent with LAD thrombosis and Wellens syndrome.

He went to the cath lab within hours: Angiogram result:

Moderate hazy Eccentric plaque in the ostial/proximal LAD assessed via intravascular ultrasound (IVUS), which showed that the lesion on the Proximal LAD had 50% stenosis but without evidence of ruptured plaque.  "The lesion was discrete and eccentric."

LAD: Type III LAD is noted.  The LAD is a large caliber vessel.

Summary: No angiographic significant obstructive disease.

Medical Rx. Aggressive risk factor modification.

In the absence of proven ruptured plaque on IVUS, the interventionalist did not place a stent. This was also because the lesion was very close to the ostium (close to the takeoff from the left main) and thus higher risk.

Subsequent events

He was treated overnight with heparin and nitroglycerine infusions.

ECG the next day:

This shows evolution of Wellens waves to deeper and symmetric (Wellens Pattern B).  In spite of absence of rise and/or fall of troponin, this confirms that there is acute MI here.  In spite of the definition requiring rise and/or fall, any elevated troponin may be called acute MI under the right circumstances.

Cardiology note

EKG showed Wellens' waves, and Coronary CT in ED showed proximal LAD plaque. Flat troponin trend most consistent with unstable angina. He was treated overnight with nitro and heparin drips.  Angio today showed proximal LAD lesion with 50% stenosis, no PCI given TIMI3 flow, lack of rupture on IVUS, and proximity to left main. He does have area of soft plaque, and has continued risk of rupture. Plan is to treat patient medically with dual antiplatelet therapy and high intensity statin, and obtain a stress test.

Strangely, he did not get an echocardiogram.  

The patient was discharged on dual antiplatelet therapy,

He continued having angina for the next month.  He had no further troponins or ECGs.  He was scheduled for a Sestamibi stress test with Regadenoson.  (Regadenoson is an adenosine receptor agonist that is a vasodilator and is used in place of exercise to stress coronary flow)   

This stress test was markedly positive.  It showed: 

1) wall motion abnormalities of the anterior and anteroseptal walls, consistent with LAD ACS.  

2) Inducible and reversible perfusion of these walls, consistent with a flow limiting lesion.  This is in contrast to the angiogram, which only showed 50% stenosis. 

He was taken back to cath lab because of positive stress test.

Culprit Lesion (s): 50% eccentric ostial LAD stenosis, unchanged.

iFR (see below) with pressure transducer in distal LAD 0.94, suggestive of no hemodynamic significance (less than or equal to 0.89 is significant; greater than or equal to 0.90 is not).  

Angiographers note: "Given discrepancy between iFR and regadenoson MPI, FFR was performed; FFR was 0.82 at maximal hyperemia.  While this value is above our traditional threshold for intervention, N Johnson et al. have suggest that a higher threshold should be utilized for LAD or left main disease (0.83 or 0.86, respectively; Johnson, Nils P., et al. "Prognostic value of fractional flow reserve: linking physiologic severity to clinical outcomes." Journal of the American College of Cardiology 64.16 (2014): 1641-1654.)"

"Given these factors and limiting chest pain at cardiac rehab, episode of nocturnal angina, and abnormal MPI, decision was made to proceed with PCI following discussion with the patient."

FFR = Fractional flow reserve.  Requires administration of vasodilators so that vessel distal to lesion is not obstructing flow.  It measures the pressure distal to the lesion, divided by the pressure proximal to the lesion.  Reported in fractions of 1 (e.g., 0.92)

iFR = instantaneous wave-Free Ratio.  Similar, but done during diastole.  "iFR represents a diastolic resting index that allows the assessment of coronary lesions during the phase in the cardiac cycle where microvascular resistance is at its lowest, allowing for increased myocardial perfusion and coronary flow."  Quote is from this article in Circulation: Cardiovascular Interventions: 

Instantaneous Wave-Free Ratio or Fractional Flow Reserve for Hemodynamic Coronary Lesion Assessment?  Yes, Just Do It!

Unlike FFR, iFR does not require administration of vasodilators because hyperemia is not necessary when measuring pressure during the wave-free diastolic period of the cardiac cycle.  iFR is proven to reduce procedure time, patient discomfort and cost compared to FFR.

Learning Points: 

1. First, Recognize Wellens' waves and Wellens' syndrome.

2. Wellens' syndrome implies an unstable lesion.  

3.  It is a truism that, if ACS does not received a stent on the index visit, it is likely to need one later.  See this post: "Pay me now, or pay me later"  

4.  Wellens' waves may diagnose LAD ACS in spite of absence of rise and/or fall of troponin.

5. Troponin may plateau in acute MI and not manifest rise and/or fall.

6. Stenting a lesion is complex

7. IVUS may not always adequately characterize a coronary lesion.

8. Multiple modalities may be needed to inform the stenting decision.

9. FFR and iFR are useful in determining the need for stenting.