A 70-something presented with stuttering chest pain for a couple days that became constant shortly before presentation to the ED.
I was shown this ECG and asked for my opinion:
I did not know there was a previous to compare with (see below).
I said: "There is a ventricular paced rhythm (VPR). There is 1 mm of concordant ST Elevation in lead V5 All other leads have appropriate discordance, whether discordant ST elevation or depression. When there is just a single lead that meets the Smith modified Sgarbossa criteria, then the full criteria are met. Our PERFECT study had 96% specificity of this finding for Occlusive MI (OMI)."
One question posed: "Isn't this discordant STE? There is an S-wave prior to the ST segment" Answer: "We use the majority of the QRS."
"However, among all patients who come to the ED with chest pain (whether with LBBB, paced rhythm, or normal conduction), only about 2% have an acute coronary occlusion. So the low pretest probability results in a much lower positive predictive value (PPV) than one might think."
The PPV for sens = 81%, spec = 96% and prior probability of OMI = 2% is 29.2%.
The NPV for sens = 81%, spec = 96% and prior probability of OMI = 2% is 99.6%.
I recommended cath lab activation even though the PPV is only ~30%.
Then I was told that his first troponin I was 6.0 ng/mL. This result elevates the PPV to near 100%.
How did we already know the troponin? It turns out that the patient had presented almost 2 hours prior. After return of the troponin at 6 ng/mL, a 2nd ECG was recorded and was identical.
I am not certain if the findings on the first ECG (before troponin result) were not seen or not believed, but this would be typical: OMI in paced rhythm is frequently missed.
It is believed by many that OMI cannot be diagnosed in the presence of VPR. And therefore patients with VPR are denied reperfusion therapy routinely. Rathore et al. showed that these patients are extremely undertreated.
The cath lab was activated.
The cardiologist came down to the ED. He performed a bedside echo which confirmed an apical wall motion abnormality.
He also found a previous ECG. Here it is:
The angiogram did indeed show mid-LAD occlusion of a wraparound LAD. It was stented.
Post PCI, the troponin rose to 78 ng/mL.
The formal echo showed:
Learning Points
1. New or increased ST Elevation compared to previous VPR ECG is very specific for OMI.
2. Even without the previous ECG, the Smith Modified Sgarbossa Criteria have very high sensitivity, specificity, and accuracy for OMI in VPR.
Criteria are:
1. Any single lead with 1 mm concordant ST Elevation
2. Any of leads V1-V3 with 1 mm of concordant ST depression.
3. Any single lead with excessively discordant ST elevation as defined by 25% of preceding S-wave.
I was shown this ECG and asked for my opinion:
 |
| What do you think? |
I did not know there was a previous to compare with (see below).
I said: "There is a ventricular paced rhythm (VPR). There is 1 mm of concordant ST Elevation in lead V5 All other leads have appropriate discordance, whether discordant ST elevation or depression. When there is just a single lead that meets the Smith modified Sgarbossa criteria, then the full criteria are met. Our PERFECT study had 96% specificity of this finding for Occlusive MI (OMI)."
One question posed: "Isn't this discordant STE? There is an S-wave prior to the ST segment" Answer: "We use the majority of the QRS."
"However, among all patients who come to the ED with chest pain (whether with LBBB, paced rhythm, or normal conduction), only about 2% have an acute coronary occlusion. So the low pretest probability results in a much lower positive predictive value (PPV) than one might think."
The PPV for sens = 81%, spec = 96% and prior probability of OMI = 2% is 29.2%.
The NPV for sens = 81%, spec = 96% and prior probability of OMI = 2% is 99.6%.
I recommended cath lab activation even though the PPV is only ~30%.
Then I was told that his first troponin I was 6.0 ng/mL. This result elevates the PPV to near 100%.
How did we already know the troponin? It turns out that the patient had presented almost 2 hours prior. After return of the troponin at 6 ng/mL, a 2nd ECG was recorded and was identical.
I am not certain if the findings on the first ECG (before troponin result) were not seen or not believed, but this would be typical: OMI in paced rhythm is frequently missed.
It is believed by many that OMI cannot be diagnosed in the presence of VPR. And therefore patients with VPR are denied reperfusion therapy routinely. Rathore et al. showed that these patients are extremely undertreated.
The cath lab was activated.
The cardiologist came down to the ED. He performed a bedside echo which confirmed an apical wall motion abnormality.
He also found a previous ECG. Here it is:
 |
| Notice that there is only minimal discordant ST elevation in inferior leads, and none elsewhere. Therefore, the discordant ST Elevation seen on the new chest pain ECGs is new or increased. There is increased ST elevation in II, III, aVF, with increased reciprocal STD in aVL. There is new STE in V3-V6. So this must be a wraparound LAD to the inferior wall. |
The angiogram did indeed show mid-LAD occlusion of a wraparound LAD. It was stented.
Post PCI, the troponin rose to 78 ng/mL.
The formal echo showed:
Regional wall motion abnormality-anterior and apex akinetic.
Regional wall motion abnormality-distal inferior wall .
The estimated left ventricular ejection fraction is 51 %.
The anterapical/distal inferior WMA is consistent w/ new wrap-around LAD-territory infarct.
Learning Points
1. New or increased ST Elevation compared to previous VPR ECG is very specific for OMI.
2. Even without the previous ECG, the Smith Modified Sgarbossa Criteria have very high sensitivity, specificity, and accuracy for OMI in VPR.
Criteria are:
1. Any single lead with 1 mm concordant ST Elevation
2. Any of leads V1-V3 with 1 mm of concordant ST depression.
3. Any single lead with excessively discordant ST elevation as defined by 25% of preceding S-wave.
While not directly related to this case, is there any significance to a concordant t wave without any st elevation in a LBBB or ventricular paced rhythm?
ReplyDeleteNot much. We have studied it and found little correlation with ACS.
DeleteYes, QRSs originating from the ventricle (e.g. PVCs, QRSs during VT, accelerated idioventricular rhythm, or ventricularly paced rhythm) can reveal STEMI very effectively. Here, one is looking for ST segment deviation (elevation or depression) concordant with the major component of the QRS, either
ReplyDelete"up up", or down down.
Yes, but this is a different meaning of the word "concordant". We use concordance in ST segments to indicate ischemia, but we also use a different definition of "concordant" (all precordial leads without RS or rS or Rs AND in the same direction) to differentiate VT from SVT with aberrancy.
DeleteThere is also straightening of the slope of the T wave in V4. This would be abnormal and concerning in an otherwise normal EKG, but does it have the same significance in the setting of LBBB and pacing? If so, it would be a useful thing to look for in evaluating for ischemia in these cases, no?
ReplyDeleteIndeed. We studied this and found it to be specific but not sensitive. https://www.sciencedirect.com/science/article/pii/S0736467916002134
DeleteACO, non-STEMI, and no MI groups consisted of 33, 24, and 105 patients. The sum of the maximum deflection of the QRS amplitude across all leads (ΣQRS) was smaller in patients with ACO than those without ACO (101.5 mm vs. 132.5 mm; p < 0.0001) and a cutoff of ΣQRS < 90 mm was 92% specific. For ACO, non-concave ST-segment morphology was 91% specific, any ST concordance ≥ 1 mm was 95% specific, and any ST concordance ≥ 0.5 mm was 94% sensitive. For non-STEMI, terminal T-wave concordance, analogous to biphasic T-waves, was moderately sensitive at 79%.