The Electrocardiographically Silent Circumflex Artery

A 39 yo otherwise healthy man with no risk factors was walking at the mall when he developed chest pressure.  He presented to the ED after 30 minutes, now also feeling weak.  He was diaphoretic.  Here was his initial ECG:

There is sinus rhythm.  There is abnormal T-wave inversion in V2 which is abnormal and very suspicious There is minimal, nondiagnostic ST elevation in inferior leads with possibly a suggestion of reciprocal ST depression in aVL.  There are thin and normal inferior Q-waves. Thus, there are some suspicious abnormalities, but no definite signs of ischemia.   There is also minimal, nondiagnostic ST elevation in V5 and V6. 

Because of persistent symptoms, another ECG was recorded 30 minutes later:

There is only one new finding on this ECG which suggests ischemia.  It is very subtle but real.  What is it?  

See V3, where there is now some ST depression.  The previous ECG has a small amount of appropriate ST elevation in V3; any ST depression in a young male is abnormal, especially if changed from previous.  This is worrisome when combined with the abnormal T-wave in V2.

Let's look at both V3's, magnified:

The later ECG (bottom panel) shows minimal ST depression in V3.  The top shows minimal ST elevation (normal).  The difference is significant and highly suggests posterior ischemia.

This abnormality in V3 was apparently not seen by the treating MD, who is a nationally recognized expert in STEMI care (showing how difficult these diagnoses can be).

The initial troponin was negative. The patient was admitted to telemetry.  At 4 AM, his second troponin returned at 1.8 ng/mL.  Another ECG was recorded:

T-waves in V2 and V3 are now upright and larger, evolving. 
Are these posterior reperfusion T-waves?

He went for cath at 6 AM because of ongoing symptoms and a "positive" troponin.  He had an occluded OM-2 that was opened and stented.  

Troponin I peaked at 99 ng/mL (large MI)!

So this is a NonSTEMI, right?  Technically, yes, because there is not 1 mm of STE in 2 consecutive leads.  But the definition misses the point.  It is a coronary occlusion with a substantial myocardial territory at risk, that showed only very subtle ST changes.

Should you activate the cath lab for this?

Not from the ECG alone.  However, if you notice the ST depression, you then realize that this is ischemic chest pain, not esophageal spasm.  Once you know that the chest pain is ischemic in origin, and you cannot control it medically, then you must go urgently to the cath lab.

The patient should be treated with NTG, Aspirin (and clopidogrel, if your institution allows), metoprolol, antithrombotics, and GP IIb IIIa inhibitors.  If the pain persists, and the ST depression persists, then talk to your interventionalist immediately.

Here is the followup ECG:

The ST abnormalities have resolved.  There are new inferior Q-waves diagnostic of inferior MI.  The R-wave is increased in V2, consistent with posterior (now called lateral, to my dismay) MI (analog of a Q-wave).  There is no apparent resolution of the minimal and non-diagnostic inferior ST elevation.
Notice the T-waves are smaller in V5 and V6 now.

I don't have all the data on this case, and do not know if there is an inferior wall motion abnormality, or if this OM-2 supplied the inferior wall.  It  probably did, as evidenced by the Q-waves; but it is very interesting that during the acute phase, there were no diagnostic ST changes in inferior leads, and the minimal ST elevation that was present did not evolve.

Many MIs are electrocardiographically "silent," especially when in the circumflex territory.  I do wonder whether, in the studies that show this phenomenon, if an ECG expert evaluated the ECG for the subtle signs of ischemia.  I suspect that many or most that are thought to be "silent" are really just "subtle."  But many show nothing!

Here are more electrocardiographically subtle MI.

Why is the lateral wall, and the circumflex artery territory, electrocardiographically silent?

1. The lateral wall stretches far around to the posterior wall.  I, aVL, V5, and V6 just don't go posterior enough.  Posterior leads may help with this.

2. As you go lateral, the heart has more lung between it and the chest wall, so lead strength is buffered by air.

Anterior ST depression can help with assessing the posterior wall.   The combination of 1) accepting a lower threshold in lateral leads (0.5 mm), 2) considering ST depression in V1-V4 as posterior STEMI, and 3) using posterior leads at a threshold of 0.5 mm, will all improve the sensitivity.

Looking for a wall motion abnormality can lead you astray

A Middle-aged male presented with chest pain of 3 hours duration. He has a history of hyperlipidemia only.  There is pressure to mid-chest, radiating to the right arm, associated with diaphoresis.   He never had this before.  It was not related to eating.  There was no cough or fever, nor trauma.  There was no recent surgery, and no h/o thromboembolism.

Exam and BP were normal.

Here is the first ECG:  0526

There is ST elevation in V1-V4, with concave ST segments.  Is it ischemic, or is it early repol?
It does not meet STEMI "criteria," but we know they are insensitive
First, look for any reciprocal ST depression and you see it in lead III, plus some subtle STD in II and aVF.
There is a bit of ST elevation in I and aVL as well.
When there is reciprocal ST depression, it is likely to be LAD occlusion and the LAD occlusion formula may be falsely negative.
Indeed, if you do make the calculation, with STE60V3 = 4, QTc was 385, and R-wave amplitude in V4 = 20 results in 20.98, which is quite low

There was a previous ECG for comparison:

This is truly normal, without any significant ST elevation
You can see that the T-wave are now much larger than on the previous ECG.
These changes are diagnostic!

But the clinicians were not convinced.

So they did a bedside echo.  Here are 3 parasternal short axis views:








They read the echo as normal, without a wall motion abnormality.

Is it normal?



Comment: I think I see a clear wall motion abnormality of the anterior wall (closest to the transducer), but wall motion abnormalities are hard to see, especially for the non-expert, and especially without contrast or stress echocardiography (speckle tracking -- see these cases).



And then a repeat ECG at 0540

Not much different.

They proceeded to look for other pathology with ultrasound:

A bedside ultrasound showed a normal aortic root and distal aorta.  The gall bladder had no stones and a normal duct.  There was no abdominal free fluid and no hydronephrosis.  Chest X-ray showed no infiltrate and a normal mediastinum.  D Dimer was normal, and lipase was minimally elevated.

Cardiology was consulted by our Pathway B, and Nitroglycerine (NTG) initiated with a plan to maximize it to eliminate pain.

Another ECG was recorded at 0556:

Then the first troponin returned at 0.036 ng/mL (99% reference = 0.030 ng/mL).

Comment: A negative troponin does not help in acute coronary occlusion, because it may be too early to be "positive."  But a positive one in a patient with no baseline pathology (heart failure, renal failure) or reason for demand ischemia (sepsis, resp failure, etc.), but only with ischemic symptoms such as chest pain, tells you that an equivocal ECG is a positive ECG.

With a nitroglycerine dose titrated up to 60 mcg/min and a systolic BP of 90-100, the nitro could not be increased further.

The decision was made to activate the cath lab in the setting of elevated troponin, concerning ECGs, refractory typical pain, and no alternative explanation such as pericarditis or aortic dissection.

Another ECG was recorded at 0629:

Now there is more ST elevation and the change in the ECG itself is clearly diagnostic.

0822

At angiogram, there was a 100% mid-LAD occlusion, without good collateral circulation.  It was stented.

Here is the troponin profile:

Notice how the troponin suddenly rises after reperfusion and  release of troponin from the cardiac circulation.
The levels are quite high, consistent with a very large infarction.

Here is the ECG the next morning:

There is still significant ST elevation, now with T-wave inversion.  The persistent STE suggests that there is continued microvascular obstruction and is not a good sign.

An echo the next day showed:
Normal left ventricular size, thickness and systolic function.
The estimated left ventricular ejection fraction is 56%.
Regional wall motion abnormality-distal septum anterior and apex
hypokinetic.



Learning Points:

1. In a patient with real suspicion of MI and anterior ST elevation that does not meet STEMI "criteria," if there is inferior reciprocal ST depression, it is LAD occlusion until proven otherwise.  This is true even if the "early repol -- LAD occlusion" formula value is less than 23.4 (specific) or even if less than 22 (otherwise, a very sensitive cutpoint).

2. Compare with a previous ECG.  If there is a marked change, then it is likely to be due to ACS/coronary occlusion.    

Unfortunately, early repol is not completely stable: Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation. Elevations in inferior leads were less than 0.5mm in 18 of 20 cases. Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.

3. Bedside echo has many great uses.  In suspected ACS, visualization of a wall motion abnormality may help to make the diagnosis of coronary occlusion, especially with speckle tracking; the positive predictive value is probably good.  But it is hazardous to try to rule out MI with limited bedside echo.  In this case, its use delayed care.

4.  Finally, the clinicians did a superb job by remaining vigilant, continuing to search for alternative causes and to monitor for ACS through serial ECGs, troponin, Nitroglycerine use and more.  This patient could easily have been just admitted for "rule out MI" and been left with a crippling cardiac injury.

5. Many NonSTEMI are due to coronary occlusion.  Early angiography with PCI saves myocardium.

Inferior STEMI with AV Block, Cardiogenic Shock and ST elevation in V1

This is a case I had with one of our superb internal medicine/emergency medicine residents, Marco Salmen, MD.  He wrote it up for this blog, with some help from me.

Also, see this case: http://hqmeded-ecg.blogspot.com/2011/01/rv-mi-diagnosed-by-st-elevation-in-v1.html

Case

If you prefer to watch this case presented on video, here it is presented by Marco Salmen:
https://hqmeded.com/stabilization-series-right-ventricular-mi/
Marco makes some mistakes in reporting epinephrine dosing.  5 mcg should be 50 mcg, and 10 should be 100.

An elderly woman called 911 for acute onset of nausea and chest pain of 30 minutes duration.  A prehospital ECG was identical to this first ED ECG: 

Rhythm: There is a regular, narrow complex bradycardia, with ventricular rate of ~43 bpm. There appear to be P-waves at irregular intervals, but without relationship to the QRS.  Thus, there is third degree (complete) AV block.  The escape is narrow, thus junctional or from the bundle of HIS.  

QRST: The QRS is narrow, so any ST-T abnormalities are primary: there is significant ST elevation in leads II, III, and AVF, with reciprocal ST depression in leads I and AVL, all suggestive of an inferior STEMI. Note that the ST elevation in lead III is greater than that in lead II, but that this is not specific for culprit artery (RCA vs. Left Circumflex).  However, there is ST elevation in lead V1, the furthest right pre-cordial lead, which lies directly over the RV free wall and highly suggests a Right Ventricular MI

The medics activated the cath lab from prehospital.

The patient arrived awake, alert, with only mild chest pain.  The BP was 136/91 with SpO2 of 100% and StO2 (tissue oxygenation) of 69% (slightly below lower limits of normal at 70%).  She had no past medical history.  

Inferior STEMI with RV infarction was diagnosed, IV fluids were hung wide open, Aspirin, Ticagrelor and Heparin were given, and a cardiac ultrasound was performed. 

What do you see?

There is a large, dilated right ventricle with significantly reduced systolic function, with bulging into the left ventricle known as the “D sign”.  There is diffuse hypokinesis that appears to spare the RV apex.  This is known as “McConnell’s sign”, and is seen in both acute PE and RV MI equally. ¹  Although not seen well in this view, the left ventricle appears to have mildly reduced systolic function as well.

Additionally, there were no B-lines (with RV MI, one may get cardiogenic shock but without pulmonary edema), as the shock is due to right ventricular failure, which does not lead to the elevated pulmonary capillary pressure that causes pulmonary edema. 

A confirmatory Right Sided EKG was obtained. 

Increasing ST elevation is seen in Leads VR3 through VR6 confirm Right Ventricular MI. 

While preparing for catheterization, the patient's BP dropped to 54/25, with StO2 still at 69%.  Fluids were continued.  1 mg of atropine was given without effect.  Then there was an acute change in mental status with BP 66/53 and congruent with an acute drop in StO2 to 60% (low, indicative of inadequate perfusion).  With this cardiogenic shock, she required intubation for airway protection, as well as transient vasopressors (push dose epinephrine), sedation with ketamine, paralysis with atracurium, and transcutaneous cardiac pacing, which improved her heart rate and perfusion. 

A chest x-ray was done, again with only mild pulmonary edema:

Coronary angiography revealed an acute thrombus with 100% occlusion of the proximal Right Coronary Artery (proximal to the right ventricular marginal branch), successfully stented and reduced. The left coronary arteries were clean.  She required approximately 12 hours on a vasopressor infusion and with an intra-aortic balloon pump, but was successfully weaned, extubated, and left the hospital on Day 4. Her formal echocardiogram revealed full right ventricular function, LVEF of ~50%, and small persistent wall motion abnormality.

Right Coronary Artery Occlusion and Right Ventricular Infarction by ECG

           

            This patient’s first ECG clearly demonstrated STEMI and the need for cath lab activation.  The right coronary artery is the most common culprit artery in acute inferior MI, but a lesion in the left circumflex artery (LCx) can produce a similar pattern of ST elevation in inferior leads.  Distinguishing an RCA lesion from LCx lesion by early electrocardiogram is often important given the unique consequences of right coronary ischemia, particularly SA node ischemia causing bradycardia and AV nodal ischemia causing AV block, as well as right ventricular MI with dysfunction. Because RV dysfunction can lead to reduced LV filling (pre-load), with resultant hypotension and potentially shock (with greatly increased mortality over isolated LV inferior STEMI)2, it is important for first-line providers to quickly recognize the presence of RV dysfunction in the setting of MI.  Clinically significant RV dysfunction occurs likely in only a minority of inferior myocardial infarctions, due in part to its smaller mass, thinner walls, and extensive collateral circulation ^{3, 4}. When RV dysfunction is observed or suspected, nitrate administration must be avoided, and instead, augmentation of pre-load must be given, commonly through IV fluids.

            In addition to ST elevation in inferior leads, there are several features of the ECG that suggest an RCA lesion and RV ischemia.   Commonly referenced standard of ST elevation in Lead III greater than in Lead II suggests an RCA lesion, but is not specific or sensitive for RV infarction.  Similarly, ST depression in lead aVL is very sensitive and specific for inferior MI, but non-specific for culprit artery (RCA vs. LCx) or the presence of RV infarct 5. Some series suggest the magnitude of ST depression in aVL can be more specific for RCA occlusion, while the absence of any ST depression in lead I is highly suggestive of a Left Circumflex lesion over a RCA lesion ^{6, 7}.  However, claims that ST depression in I is indicative of RV MI are incorrect except to the extent that, by indicating RCA etiology, it makes RVMI possible (circumflex occlusion does NOT cause RV MI).

           Among precordial leads, ST elevation in lead V1, the furthest right precordial lead which lies directly over the RV free wall, is nearly diagnostic of RV STEMI. Investigators have looked at the ratio of ST depression in Lead V3 compared to ST elevation in Lead II (V3:III ratio), finding that a V3:III ratio of less than 0.5 suggests a proximal RCA occlusion⁸.

Right-sided ECG:           

Confirmation of suspected RV infarction can be seen on right-sided ECG, by placing precordial leads over the right chest, as seen here:

ST elevation in Lead V4R is highly sensitive for an RV infarct, as confirmed by multiple studies.   Specificity for RV infarction approaches 100% if ST elevation in V4R is greater than any ST elevation in V1-V3⁹. One must remember, however, that a right-sided ECG should be obtained early in suspected inferior MI, as the right-sided ST elevation is transient and most prominent early in the course of infarction.

            Not all proximal RCA occlusions result in significant RV MI, especially not in hemodynamically significant RV MI. This is due to extensive collaterals from the LAD to the right ventricle.  In patients with collaterals from the LAD, a high degree of obstructive coronary disease in the LAD can limit the left to right collateral circulation and result in larger RV MI.(10) 

Learning Points:

1. In acute inferior STEMI, on the standard left-sided ECG, STE in Lead V1 predicts RV MI. 

2. Early in the course of an MI, findings on right-sided EKG, particularly ST elevation in Lead V4R, can confirm RV infarction.

3. McConnell's sign and D-sign are not specific to pulmonary embolism, but are equally suggestive of RV MI

4. RV MI can lead to profound shock and death

5. Moderate IV fluid administration can ameliorate the shock and hypotension.

6.  Intubation and paralysis lowers the metabolic needs in cardiogenic shock.

7.  External pacing improves perfusion in shock with bradycardia

References:

            ⁵ Birnbaum Y, Drew BJ. The electrocardiogram in ST elevation acute myocardial infarction: correlation with coronary anatomy and prognosis. Postgrad Med J 2003, Vol 79: 490-504

            ⁶ Birnbaum Y et al. ST segment depression in AVL: a sensitive marker for acute inferior myocardial infarction. Eur Heart Journal, 1993. Vol. 14 (1) 4-7.

                        1 Casazza F et al. Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular infarctions. European Journal of Echocardiography, 2005, Vol. 6: 11-14 

              ⁴ Haupt H, Hutchins G, & Moore G. Right Ventricular Infarction; Role of the Moderator Band Artery in Determining Infarct Size.  Circulation, 1983, 67: 1268-1271

              ⁸Kosuge M et al. New electrocardiographic criteria for predicting the site of coronary artery occlusion in inferior wall acute myocardial infarction. Am J Cardiol 1998, Vol 82: 1318–22.

            ⁹Lopez-Sendon J, Coma-Canella I, Alcasena S, et al. Electrocardiographic findings in acute right ventricular infarction: sensitivity and specificity of electrocardiographic alterations in right precordial leads V4R, V3R, V1, V2, and V3. J Am Coll Cardiol 1985, Vol 6:1273–9

            ³Ondros et al. Right ventricular myocardial infarction: from pathophysiology to diagnosis. Exp Clin Cardiology, 2013. 18 (1): 27-30.

              ⁷Turban et al. Diagnostic value of aVL derivation for right ventricular involvement in patients with acute inferior myocardial infarction.  Ann Noninvasive Electrocardiology, 2003, Vol.8 (3):185-8.

              ²Zehender et al. Right Ventricular Infarction as an independent predictor of prognosis after acute inferior myocardial infarction. NEJM, 1993, Vol 328 

                     10.  Haupt HM et al.  Right Ventricular Infarction: Role of the Moderator Band Artery in Determining Infarct Size.  Circulation 1983;67:12168-1272.