Here is a case I will never forget. A 45-year-old man with no reported prior medical history comes into the emergency department screaming of excruciating acute-onset substernal chest pains 20 minutes prior to arrival. He says he was fine prior to the onset of the chest pain, then suddenly became short of breath and describes an “elephant on his chest” with pain down the left arm. He is afebrile with a heart rate of 65, respirations of 20, blood pressure of 142/72 and normal oxygen saturations. Sublingual nitroglycerin was given three times without relief, so IV morphine was administered and his chest pain eventually subsided. Here is his ECG:
Let's think about this. His clinical picture sounds typical for acute MI, right? A little too typical. The ECG shows a little anterior ST elevation. But look closely at the ECG ... notice something?
The cath lab is activated for an anterior ST elevation MI. A coronary angiogram shows that his right coronary and circumflex coronary arteries were normal. His left anterior descending (LAD) was ... chronically totally occluded, consistent with an old remote MI.
OK, then. No acute LAD thrombus here, like the clinical picture might suggest. Notice those Q waves in the anteroseptal leads V1-V3? That is NOT consistent with acute chest pain for 20 minutes! More like an old anterior MI.
Let's talk about Q waves
The Q wave is the first downward deflection of the QRS complex that occurs before the R wave. It is normal to have small Q waves in most leads. We consider a Q wave pathologic (abnormal) when:
more than 40 ms (1 mm) wide;
more than 2 mm deep;
more than 25% of the total QRS complex amplitude; and
present in leads V1-V3.
What does "pathological" mean? This means a certain disease process is present, specifically myocardial infarction ... usually, old. These Q waves take some time to develop and would NOT be present within 20 minutes of symptom onset. They take at least a few hours, to a couple of days after an MI, to develop and can persist for a lifetime in many cases, especially if coronary revascularization is not performed quickly. Here is a comparison of normal Q waves in the inferior leads compared with pathologic Q waves:
Let's review the ECG in an acute MI briefly
Hyperacute T wave changes are the first ECG change during acute MI and are quite transient, so usually missed. Here is an example of hyperacute T waves:
The second change is ST segment elevation at the J point. Here is a picture of an acute anterior ST elevation MI with 5 mm of ST elevation at the J point. They call this "Tombstoning" since the combination of the ST segment and the T wave look like a tombstone:
Eventually the ST elevation resolves and, if the infarct completes, a "pathologic" Q wave develops like in our patient's ECG. An old anterior MI would have pathologic Q waves in the anterior precordial leads (V1-V3) and an old inferior MI in the inferior leads (II, III and aVF).
Frequently we revascularize acute ST elevation MIs quite quickly and Q waves don't develop. The term "Q-wave MI" is an old term that used to refer to "transmural" infarctions resulting in Q waves in the ECG.
The twist in the case
He remained chest-pain-free and his cardiac enzymes remained normal throughout the hospitalization. A couple of hours after the angiogram I was called to check on him due to left groin pain. There was good hematoma there. Odd ... I was pretty sure right femoral artery access — not left — was used. So, why a left groin hematoma?
A little investigating was done and we found out he DID have a prior history. Actually, this was coronary angiogram No. 20 (yes, 20) in the past 6 months! Almost every hospital in the area had records of him presenting with chest pains not relieved with nitroglycerin, and then relieved with IV morphine.
We confronted the guy. He admitted that he knew his ECG was abnormal and mimicked an anterior STEMI and he was addicted to IV narcotics. Crazy. But he got the story wrong: He should have said chest pain for 1 to 2 days in order to truly fit his ECG pattern, not acute onset of chest pain for 20 minutes.
We found out that his initial anterior MI was 6 months ago. Wait! Then how is ST segment elevation present on his ECG? Well, that's because his LV angiogram during the cath showed that he had a left ventricular aneurysm.
Here are some of the classic findings of left ventricular aneurysm:
chronic ST segment elevation;
pathologic Q waves; and
shape of the ST elevation seen in an LV aneurysm described as "coving."
Here it is again:
Two side notes
First, there is really no clinical evidence to support this classic teaching of persistent ST elevation after MI resulting from left ventricular aneurysm. Some studies show that persistent ST elevation correlates more with "dyskinetic" wall motion (myocardium moving outward instead of in during systole) and not necesarrily just with aneurysmal changes.
Second, acording to the ACC/AHA guidelines for STEMI, to diagnose an anterior ST elevation MI there must be “new ST elevation at the J point in at least two contiguous leads of ≥ 2 mm (0.2 mV) in men or 1.5 mm (0.15 mV) in women in leads V2–V3, and/or of ≥1 mm (0.1 mV) in other contiguous chest leads or the limb leads.” Thus, 1 mm in any two contiguous leads, EXCEPT leads V2 or V3 where the elevation must be 2 mm in men or 1.5 mm in women. This guy's ECG was borderline for meeting those criteria.
The ECG dilemma
How could we have figured this out? The ECG has some good Q waves in V1-V3, which is consistent with an OLD anteroseptal MI. His symptoms were quite acute, but he knew all the key words to say. Really, the only way to know for sure that the ST elevation on his ECG represents a left ventricular aneurysm is to have clinical history of a prior anterior MI and cardiac imaging showing the aneurysm. So, when a guy like this says he has no prior history and has severe chest pains with an ECG like his, the cath lab gets activated.
How about a nice universal electronic medical record (EMR) to prevent this problem?
This patient was "malingering"... attempting to fake his illness for some secondary gain, in his case for IV narcotics. Here is a nice article on malingering and why it is important.
I'll never forget another case I saw during training of fever of unknown origin that was presented in our grand rounds: A guy with recurrent bacteremia of multiple microorganisms. He had every MRI and CT scan possible, as well as a lumbar puncture and transesophageal echocardiogram, to exclude endocarditis. Multiple infectious disease specialists were consulted and no one could figure him out. We found out that he was actually malingering by injecting feces into his IV! Oh my...
- by Steven Lome, DO, RVT
1. Chou's Electrocardiography in Clinical Practice: Adult and Pediatric, Sixth Edition, Saunders, Philadelphia, 2008.