Angiography can have bleeding complications - be more sure of your STEMI diagnosis in high risk patients

An over 90 yo patient complained of 1 hour of chest pain.  There was a h/o CAD with CABG.  The prehospital BP was 200 systolic.  The paramedics recorded an ECG which could not be obtained but which was identical to the ED ECG recorded here:

There is sinus rhythm.  There is some STE in aVL, with reciprocal ST depression in II, III, aVF, and STD in V6.  There is also a QR-wave in aVL,  consistent with old MI.  Although one might be worried about acute MI here, it is likely that the ST elevation, without large T-wave and with Q-wave, is due to old MI (LV aneurysm morphology).

The paramedics activated the cath lab.  The CP resolved with NTG and ASA, and the ED BP was 170/90.  She was given heparin and abciximab and taken to the cath lab.  There were several severe chronic calcified lesions, no culprit, and no PCI was performed.

However, there were severe bleeding complications and she died of a retroperitoneal hemorrhage.

There are several lessons one can be reminded of by this case:

1. Not all ST elevation is acute STEMI
2. Acute STEMI usually has large T-waves and, unless anterior, does not develop Q-waves rapidly.  When you see inferior or lateral QR-waves, think of old MI with persistent ST elevation.
3. Hypertension can cause ischemia with chest pain
4. If the pain goes away and the ECG is equivocal, then slow down
5. PCI has risks, mostly bleeding risks, and these are much higher in the elderly, especially women


Summary of this case:

ECG differentiation of old vs. new MI is frequently difficult, so assess risks and uncertainties:

Risks:

Age

Uncertainty:

Q-waves

Known previous MI with CABG

Chest pain resolved.

BP 200 systolic

Bleeding Risk Factors  in PCI

GRACE registry 24000 patients; Eur Ht J 24:1815; 2003

Major bleeding definition: life threatening:

• Transfusion of ≥2 units PRBC or
• Decrease in hematocrit of ≥10% or
• Intracranial hemorrhage or
• Death

The overall incidence of Major Bleeding in PCI:

• 4.8% in patients with STEMI
• 4.7% in patients with Non-STEMI

Risk Factors for Major Bleeding in PCI:

• Advanced age
• Female sex
• History of bleeding
• Renal insufficiency
• (Diabetes and stroke in other studies)
• After adjustment, major bleeding is:
• Significantly associated with increased risk of hospital death (OR 1.64, 95% CI: 1.18, 2.28).
• Also: Transfusion is associated with worse ischemic outcomes!

How to Lower Risk in High Risk Patients 
Assess risk benefit

Be more certain of diagnosis

High risk vs. lower risk STEMI

• Anterior vs. other locations
• Poor LV function on echo
• Hemodynamics (shock, blood pressure, pulse)
• Pulmonary edema
• ST score (how many leads involved? How widespread?)
• Ongoing symptoms (vs. resolved)
• Resolution of ECG findings associated with much lower risk

Appropriate dosing of Heparin
60 U/kg Loading dose: IBW + 0.4(TBW-IBW), maintenance 12 U/kg/hr: IBW + 0.4(TBW-IBW)


Use of bivalirudin

• (always with clopidogrel) vs. heparin + abciximab

• HORIZONS-AMI, 3 yr outcome, 2011
• Lower mortality (5.9 % vs. 7.7%)
• Lower cardiac mortality (2.9% vs. 5.1%
• Lower major bleeding (6.9% vs. 10.5 %)
• ISAR-REACT 2011
• No difference in ischemic outcomes or death
• Major Bleeding 4.6 % vs. 2.6%

Radial artery access

Clopidogrel 300 mg, vs. 600 mg, vs. Prasugrel, vs. Ticagrelor (the latter have less ischemia, more bleeding)

Pericarditis, or Anterior STEMI? The QRS proves it.

A young otherwise healthy man presented with 4 hours of sharp 10/10 substernal chest pain.  It has been constant since then.  He looked ill and diaphoretic.  BP was 160.

Here is his ECG at t = 0:

There is a large amount of anterior and lateral ST Elevation. 

This ECG is diagnostic of anterior STEMI.  And the Cath lab was activated immediately.

But there was some doubt as to whether it might be pericarditis because of the ST elevation in I and II, without ST depression in III.  Add that to "sharp" pain and a 33 year old, and it is easy to convince yourself that this is, indeed, pericarditis.

However, look closely! 

1. There is a fragmented QRS in lead V2 (potential goes up, then down, then up again).  This is a good sign for myocardial infarction and does not happen in pericarditis.
2.  The voltage in V2 is very small.  This is a sign of MI, either acute or old.
3.  There is terminal QRS distortion in V2 and V3 (you might dispute that V3 has what looks like a J-wave, but I would argue this is not what a true J-wave looks like)

After nitroglycerine, his systolic BP was 120 and his pain was improving.  Heparin and aspirin were given.  Another ECG was recorded at t = 27 minutes:

Now the T-wave in V2 is clearly hyperacute.  There is slightly less anterior ST elevation.    This is typical of a reperfusing artery, which may have hyperacute T-waves as the ST segments are resolving.

The patient went to the cath lab and had an 80% occluded mid LAD with fresh thrombus.  It was a "type III" LAD, meaning it wraps around to the inferior wall.  The distal inferior apical LAD was cut off by distal embolization from LAD culprit.  The Right Posterior Descending Artery off the RCA was small, so that the RCA did not adequately supply the inferior wall.

Thanks to spontaneous reperfusion (helped by aspirin and nitroglycerin), the artery was open and the peak Troponin I only 12.2ng/mL.

Echo showed an apical, but not inferior, wall motion abnormality.  This is likely because 1) the ischemia to the inferior wall was only partial and 2) it reperfused quickly.

Lessons:

1. Occlusion of a Type III (wraparound) LAD that supplies both the anterior and inferior wall can have "widespread ST elevation" that can be confused with pericarditis.
2. The QRS is at least as important as the ST segment in diagnosing STEMI

Spontaneous Reperfusion and Re-occlusion - My Bad Thinking Contributes to a Death

This is a case I had about a decade ago.

This is a 51 year old who was playing cards with his friends when he started to have left hand numbness.  They were worried he was having a stroke and so called 911.  The medics had just learned to do ECGs, and so recorded one.  Here it is, at 1915:

Diagnostic of Anterior STEMI.  It cannot be anything else.

I activated the cath lab at 1929 based on this ECG.

Then, I questioned the patient at length and his only symptom was subjective left hand paresthesias.  He had no pain, discomfort, or tightness of any kind, no weakness, and no SOB.  So I had a hard time believing the ECG.  I thought perhaps it was recorded with lead misplacement.

So I did the first ED ECG at 1931:

STE is resolved (but there are de Winter's T-waves in V2 and V3 (hyperacute T-wave with depressed ST takeoff)        
Previously published in:  Harrigan (Ed.). The ECG in Emergency Medicine.  
Smith SW and Whitwam W.  The ECG in Acute Coronary Syndromes.   
EM Clinics of N Am 24(1):53-89; Feb 2006]

With no more overt STEMI, and (through bad thinking and "Nah, couldn't be.....") I thought that there must have been some mistake in recording the first ECG.  At worst, if it was a STEMI, I thought that it is reperfused.  I cancelled the cath lab activation for the team that would have to come in from home.   

(Today I would have unequivocally interpreted leads V2 and V3 as LAD occlusion).

At 1942, the patient started becoming hypotensive, so I recorded another ECG at 1946:

Need I say more?  Obvious anterior STEMI.
Previously published in:  Harrigan (Ed.). 
The ECG in Emergency Medicine.  
Smith SW and Whitwam W. The ECG in Acute Coronary Syndromes.   
EM Clinics of N Am 24(1):53-89; Feb 2006

I activated the cath lab again at 1946, so that I had caused a 17 minute delay by cancelling.

He went to the cath lab, had an LAD occlusion, then died just before it could be opened.

I learned 2 major lessons from this:

1. STEMI, even if it spontaneously resolves, is very high risk and must go to the cath lab.
2. A clearly diagnostic ECG is diagnostic even if it does not match the symptoms.
  (One cannot make the same conclusion about ECGs that are only highly suspicious - these are more likely to be false positives in the context of atypical symptoms.)

Reciprocal (Negative) Hyperacute T-waves. What is the Diagnosis?

I was shown this ECG and asked if I think it is a STEMI.  What do you think?

Answer Below

I answered that it does not meet any criteria for STEMI, but that there are hyperacute reciprocal (negative) T-waves in I and aVL and this cannot be anything other than inferior STEMI, especially since the ST depression in V2-V5 suggests concomitant posterior STEMI.

The ECG findings resolved before cath.  At cath, there was an 80% hazy thrombotic lesion in the RCA.  Thus, this was indeed an acute RCA occlusion.  Echo the next day showed an inferior wall motion abnormality.

Lesson: Reciprocal ST-T changes are often more pronounced than the ST-T changes overlying the affected myocardium.  This is particularly common when there is lateral STEMI with inferior ST depression (see these two cases).

Here is a case in which there are both inferior and reciprocal hyperacute T-waves.

Gunshot wound to the chest with ST Elevation

A 32 year old presented with a gunshot wound that seems to have entered the anterior chest with a downward trajectory, traversing his chest wall on the interior, and exiting his left flank.  He had anterior chest pain with movement or breathing.  An ECG was done as part of the evaluation at 0300:

There is ST elevation injury pattern in V3-V6, I and aVL, consistent with either myocardial injury or pericardial inflammation.



ED Echo showed no pericardial effusion and good myocardial contractility and no major wall motion abnormality.

A CT of the chest was done:

The arrow shows air (in the pericardium?) where the bullet passed directly anterior to the heart.  There were no major organ injuries other than diaphragmatic injury and omental hernia

 

A repeat ECG was done at 0454 (114 minutes later):

ST elevation is almost entirely resolved

Troponin I quickly rose to 5.26 ng/ml and an echocardiogram showed a definite, but small, anteroapical wall motion abnormality.

This could be due to direct contusion or to coronary injury, so a CT coronary angiogram was done which showed all coronaries to be patent with no evidence of damage.

The troponin trended down from that peak.

The patient was taken to the OR for repair of a diaphragmatic and omental hernia.

He was discharged on day 4 with no adverse events, including no dysrhythmias.

Diagnosis: myocardial contusion from a bullet

Crushing Chest pain, but the ECG is not obvious; later there is both RBBB and LBBB

A 63 year old male presented with crushing chest pain.  Prehospital BP was 70, but higher in the ED.

Here is the initial ECG at 1033 PM:

There is ST segment elevation in V1 - V3.  Is it normal ST elevation?  There are several reasons why it is NOT normal STE and is due to LAD occlusion.  1) there is ST segment depression in inferior leads, and STE in aVL 2) there is ST depression in V5 and V6. These two features alone make it diagnostic.  But one can also use the formula:  3)  The QTc is 448, and thus the formula for differentiating normal anterior STE from anterior STEMI has a value of 24.41.  (See the side bar of the front page of this blog for the formula).

Although the ECG is subtle and many or most physicians will not recognize it, it is diagnostic of anterior STEMI.  Nothing else has this morphology. 

It is important to know that 40-50% of anterior STEMI have upward concavity of the ST segments on the initial ECG.(1, 2, 3) 

1. Kosuge M.  Am Ht J 1999; 137:522-7. 2. Smith SW. J Em Med 2006;31:69-77  3. Smith SW.  Annals of EM 2012;60:45-56

The emergency physician knew that the patient was ill, but did not initially diagnose STEMI.  He then noticed the STE in aVL, but not the anterior injury.  He did not activate the cath lab immediately, but did immediately consult both an interventionalist and a general cardiologist.  They did not see the STEMI, but agreed that this sounded serious and the cath lab was activated.

While waiting for the cath lab, this was recorded at 2303:

There is now right bundle branch block, still with pathologic STE in V1-V3 and aVL, and STD in V5 and V6

At cath, there was severe 3 vessel disease, with an ostial LAD occlusion that was opened.  The patient underwent a balloon pump for cardiogenic shock.

Here is an EKG shortly after leaving the cath lab:

This appears to me to be sinus rhythm with alternating LBBB and RBBB (not multiform PVCs).  There is persistent ST elevation, consistent with poor microvascular reperfusion.  The ST/S ratio in the LBBB complexes in V1-V3 is proportionally excessive (>0.25). There is concordant ST elevation in lead V4.  There is nearly excessive proportionally discordant ST depression (0.28) in V5 and V6.  As for  the RBBB complexes

He went for CABG x 4.

Hyperacute T-waves that one might attribute to hyperkalemia and acidosis

A 32 yo type I diabetic woman presented with chest pain, nausea, vomiting and diffuse abdominal pain.  She was in DKA with an anion gap of 35, a glucose of 1128, and a K of 5.5. 

pH = 7.17, pCO2 = 24, HCO3 =  8. 

Here is here ED EKG:

There is sinus tach.  The T-waves are somewhat peaked, suggesting hyperkalemia.  But what is atypical is that the T-wave in V3 towers over the R-wave, and there is terminal QRS distortion in lead V3 (meaning there is neither a J-wave nor an S-wave).  QTc is 462 ms.  These are suspicious findings for a hyperacute T-wave and anterior injury.  Her equation/formula score is 24.8, also consistent with anterior injury.

In any case, one would not expect profound T-wave changes from a K of only 5.5.  Some might argue that acidosis would exacerbate this, but I would not attribute peaked T-waves to a pH of 7.17.

The possibility of anterior STEMI was not noticed.  I noticed it much later on looking through a random stack of EKGs.

Troponin I were followed and rose to a peak of 12.4 ng/ml. 

Here is her ECG the next day (with a normal K):

T-waves are much more normal, less peaked, but also with better R-wave amplitude.  The ST segment is back to 0.  Equation value is 23.0.

Also the next AM, echocardiography (done for the positive troponins) showed a wall motion abnormality in the anterior, anterolateral, and apical walls, consistent with LAD myocardial infarction.  Therefore, she underwent angiography and had a 95% LAD culprit that fortunately had opened on its own (that's why the troponin was only 12).  It was stented.  Had it not opened on its own, it could have resulted in a very large anterior wall MI.

The possibility of anterior STEMI was not noticed during patient care.  I noticed it much later on looking through a random stack of EKGs.  I mention this only to point out that these findings can be noticed, and differentiated from more benign etiologies, prospectively.

Lesson: Hyperacute T-waves and hyperkalemia may be confused, and they may be simultaneous.  Here the potassium was barely high enough to result in a change in T-waves, so one should be especially suspicious in this case.

Subtle ECG, seen well in PVC's, and 2 arteries are involved.

An elderly female with h/o HTN presented with chest pressure.  She awoke with bilateral upper sternal chest pressure and tightness, with some SOB, starting at 6 am.  Here was her first prehospital ECG at 0623:

There is sinus rhythm with one PVC.  There is subtle ST elevation in aVL and I, with reciprocal ST depression in III and aVF, indicative of a circuflex (or obtuse marginal - OM - branch), or possibly and first diagonal, occlusion.  There are also hyperacute T-waves in V4-V6, with some ST elevation, suggesting more widespread STEMI, such as LAD or very large OM or diagonal.  The ST elevation is even easier to see in the PVC in lead aVL: it is discordant, as it should be, but out of proportion.

Here was another at 0627:

This is similar, except that the PVC is now seen in V4-V6, and this time the T-wave appears more hyperacute in the PVC than in the normal beat.

She received nitroglycerin and had near resolution of chest pain.  She arrived in the ED at 0639.  I looked at the ECG and immediately activated the cath lab.  We then recorded another at 0651 while waiting for the cath team:

There is less high lateral STE (aVL), but still some "inferior" ST depression.  Interestingly, there is now new ST Depression in V2 and V3, with a new Q-wave in V2.  This is suggestive of LAD disease.  The T-waves in V4-V6 are much less hyperacute.

She went to the cath lab immediately and had co-culprit lesions:
1) 99% thrombotic lesion in the proximal segment of a large obtuse marginal, with TIMI-2 flow
2) 99% mid LAD occlusion with TIMI-2 flow.

Both were stented.