Monday, March 2, 2009

Circumflex Occlusion May be Subtle or Invisible on the ECG

Case 1

Below are 2 cases of circumflex or obtuse marginal (branch of circumflex) occlusions showing how subtle they may be:

A 52 y.o. male presents because he "thought he might be having a heart attack." He reports intermittent CP and SOB for 2-3 days. Pain worsened and became sharper after lifting a bookcase up the stairs. He continued to have worsening pain and diaphoresis, and associated left arm pain down to the fingers. Pt. reports MI in 2001 with a stent placed in the "marginal" artery. Pain is similar, but associated with less SOB. Exam is unremarkable. Here is the EKG at 1810:

There is subtle ST elevation in II, III, and aVF. It is not 1 mm. There is sublte reciprocal ST depression (but no T-wave inversion) in aVL, suggesting acute inferior MI.  There are also Q-waves in II, III, and aVF, but this may be due to a previous MI. There is no ST depression in the precordial leads, or significant ST elevation in the lateral leads, any of which would have supported the diagnosis of inferior MI. This is a non-diagnostic, but highly suggestive, ECG.

A repeat ECG 1 hour later is subtly changed, with some evolving T-wave inversion best seen in V5 and V6.

A stat echocardiogram would have helped to make this diagnosis and facilitate timely reperfusion. Angiography and PCI were undertake 8 hours after the initial ECG and showed a completely occluded OM-1. Echo revealed inferior-posterior wall motion abnormality and troponin peaked at 100!

It is not unusual for occlusions of the circumflex or its branches to show little on the ECG even though they represent a large amount of ischemic myocardium at risk for complete infarction. The circumflex territory is known as being "electrocardiographically silent".

How can you make the diagnosis? First, this patient had a known stent in the "marginal" artery and thought he was having a heart attack. In such a situation, when you know that the circumflex is the likely culprit artery, you may suspect that an MI will not be obvious on the ECG. In this case the ECG was very suspicious for MI, but not diagnostic. Therefore, additional diagnostic testing is warranted. Possibilities include: serial ECGs (which were done but still nondiagnostic), stat echocardiogram, or posterior ECG. Use of the PRIME ECG 80 lead body surface mapping shows great potential for improving diagnosis in such cases.

By definition, this is a non-STEMI because there is not 1 mm of ST elevation in 2 consecutive leads. However, ST elevation is only an imperfect surrogate for complete acute persistent occlusion of an epicardial coronary artery without collateral circulation. It is neither fully sensitive nor specific. Even though the patient's ECG did not meet criteria for STEMI, he had all the pathology of a STEMI.

Case 2

A 38 year old male with h/o smoking only c/o a few hours of severe substernal chest pain; he thinks he is having a heart attack. The pain is very nitroglycerine responsive. The first ECG with pain (unavailable) showed T wave flattening in V2 and V3. After resolution of pain with sublingual nitroglycerine, the second ECG was changed to near normal:

There are nondiagnostic T abnormalities in I and aVL, but little to suggest ischemia except that the precordial T waves are normalized. I was suspicious of LAD disease.

73 minutes later, the patient developed pain again:

The precordial T-waves are again flattened, without any other abnormality.
Nitroglycerine again eventually resolved the pain, and the following ECG was recorded at 2234:

Now the ECG is more normal appearing than ever.  In fact, the anterior T-waves are enlarged.
These T-waves represent reperfusion of the posterior wall, what I call "posterior reperfusion T-waves."   Click here for more such cases. 

The troponin returned at 0.81 ng/ml, so the patient was started on heparin and eptifibatide, in addition to IV nitroglycerine and Metoprolol (and, of course, aspirin).

His angiogram the next day revealed a 100% mid dominant circumflex occlusion that supplied the inferior and posterior walls. There was a large LAD that collaterally supplied some of the inferior wall. Echo showed an inferior-posterior wall motion abnormality. The troponin peaked at only 13, probably because of the collateral circulation from the LAD.

How could we have gotten him to angiography and PCI faster? Patients with objective evidence of acute coronary syndrome (positive troponin or ECG) AND uncontrollable pain should get emergent PCI even if they do not have ST elevation. This patient did become pain free on maximal medical therapy, so PCI was not indicated.

Fortunately, his MI was not large by biomarkers. Although he had a wall motion abnormality, this may go away over time.

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