A Tough ECG, But Learn From It!. I have to tell this story from my point of view because I don't want anyone to think that the recognition of LAD occlusion was made in retrospect. I want all to know that, with the right mind preparation, and the use of the early repol/LAD occlusion formula, extremely subtle coronary occlusion can be detected prospectively, with no other information than the ECG.
The Case:
I was reading dozens of leftover ECGs from over a weekend and saw this one:
This was my thought: if this patient presented to the ED with chest pain, then this is an LAD occlusion. So I went to look at the chart and here is the history:
This patient with no h/o CAD had a couple of episodes of chest pain during the day, then presented with one hour of substernal chest pain that had some reproducibility but also improved from 10/10 to 5/10 with nitroglycerine.
This is such a subtle ECG that I was worried that it had gone unnoticed, and, in fact, it did go unnoticed:
His pain continued and his ECG was read as normal. His first troponin was normal. He was admitted to the hospital for a "rule out." His second troponin I returned at t = 5 hours and was + at 3.8 ng/ml. His ECG was repeated at this point:
The cath lab was activated and an LAD occlusion was opened. The peak troponin I was over 100. On echocardiogram, there was a 40% ejection fraction with anterior wall motion abnormality.
I applied the LAD occlusion/early repol formula and, with a QTc of 402ms, STE60V3 of 1.5, and R-wave amplitude in V4 of 3 mm, the result was = 24.5, which is in the range of LAD occlusion (even if you read the STE as 1.0, the result is 23.9, greater than 23.4). The formula results in such a high number because of the very low R-wave amplitude, which (in comparing subtle LAD occlusion to early repol) is the single best predictor of LAD occlusion, better than ST elevation.
To not see these findings is very common, and this patient would be given the diagnosis of NonSTEMI, with subsequent development of STEMI.
It is not a missed STEMI, but it is a missed coronary occlusion. As you can see, the subtle findings are apparent and, with a prepared mind, can be detected. Studies show that 30% of NonSTEMI have an occluded infarct artery at the time of angiography done 24 hours after presentation. This is because of subtle ECG findings. These patients have worse outcomes: higher mortality, more CHF, higher biomarkers, and worse ejection fractions than the NonSTEMI patients with open arteries.
This patient had continued and ongoing pain. If there had been serial ECGs, then the evolution of ST elevation would have been detected much earlier and there would be less myocardial injury.
Fesmire et al. showed that, with continuous ST segment monitoring, the sensitivity of the ECG for STEMI rises from 48% to 62% of all MI as diagnosed by CK-MB. In other words, NonSTEMIs are frequently diagnosed as STEMIs if you give them time to evolve.
The Case:
I was reading dozens of leftover ECGs from over a weekend and saw this one:
 | ||
| There are symmetric T-waves and poor R-wave progression. There is 1 mm of ST elevation at the J-point in leads V2 and V3. This formerly met "criteria" for thrombolytics in the ACC/AHA guidelines of 2004, though of course this amount of ST elevation is very nonspecific. It is nonspecific because normal variant ST elevation can be even much greater. However, normal variant ST elevation always has better R-wave progression and asymmetric T-waves which have a slow upstroke and a rapid downstroke. See image below: |
 |
| Slow upstroke, fast downstroke. Asymmetric. |
This was my thought: if this patient presented to the ED with chest pain, then this is an LAD occlusion. So I went to look at the chart and here is the history:
This patient with no h/o CAD had a couple of episodes of chest pain during the day, then presented with one hour of substernal chest pain that had some reproducibility but also improved from 10/10 to 5/10 with nitroglycerine.
This is such a subtle ECG that I was worried that it had gone unnoticed, and, in fact, it did go unnoticed:
His pain continued and his ECG was read as normal. His first troponin was normal. He was admitted to the hospital for a "rule out." His second troponin I returned at t = 5 hours and was + at 3.8 ng/ml. His ECG was repeated at this point:
 |
| This shows a well developed anterior STEMI. |
The cath lab was activated and an LAD occlusion was opened. The peak troponin I was over 100. On echocardiogram, there was a 40% ejection fraction with anterior wall motion abnormality.
I applied the LAD occlusion/early repol formula and, with a QTc of 402ms, STE60V3 of 1.5, and R-wave amplitude in V4 of 3 mm, the result was = 24.5, which is in the range of LAD occlusion (even if you read the STE as 1.0, the result is 23.9, greater than 23.4). The formula results in such a high number because of the very low R-wave amplitude, which (in comparing subtle LAD occlusion to early repol) is the single best predictor of LAD occlusion, better than ST elevation.
To not see these findings is very common, and this patient would be given the diagnosis of NonSTEMI, with subsequent development of STEMI.
It is not a missed STEMI, but it is a missed coronary occlusion. As you can see, the subtle findings are apparent and, with a prepared mind, can be detected. Studies show that 30% of NonSTEMI have an occluded infarct artery at the time of angiography done 24 hours after presentation. This is because of subtle ECG findings. These patients have worse outcomes: higher mortality, more CHF, higher biomarkers, and worse ejection fractions than the NonSTEMI patients with open arteries.
This patient had continued and ongoing pain. If there had been serial ECGs, then the evolution of ST elevation would have been detected much earlier and there would be less myocardial injury.
Fesmire et al. showed that, with continuous ST segment monitoring, the sensitivity of the ECG for STEMI rises from 48% to 62% of all MI as diagnosed by CK-MB. In other words, NonSTEMIs are frequently diagnosed as STEMIs if you give them time to evolve.
