Smith comment: When Pendell and I taught version 1 of the Queen, we taught it OMI active or reperfused, acute or subacute. We would have taught her "acute reperfused" for this ECG. However, for version 1 she only reports OMI or not OMI (and level of confidence). So even though it is an ECG clearly diagnostic of reperfused OMI, the Queen only says "OMI -- high confidence". She does not specify whether active or reperfused.
Get access to Queen of Hearts:
My immediate reaction was reperfused LAD occlusion, but you would expect this in a patient with resolved or improving symptoms. The patient told me she had been driving when she developed acute onset, substernal, severe, sharp, stabbing pain along with warmth and pain in her ears. She said the symptoms had been coming in waves, and that her pain had been improving, but was getting a bit worse at the moment. With this history, I activated the cath lab.
While awaiting the arrival of the team, I gathered more history. Just a few weeks ago, she had learned of a sibling’s terminal diagnosis. This was of course devastating news to her, and she told me she had been experiencing terrible grief the past few weeks. I performed bedside echocardiography.
Given her lack of risk factors for coronary disease, and the fact that she was a 53 year old woman with compatible history and echo findings, stress cardiomyopathy rose to the top of my differential. Of course, stress cardiomyopathy is a diagnosis of exclusion. In this patient with stuttering symptoms and rising troponin, there is no other option but to perform emergent coronary angiography. Hers is shown below.
The final diagnosis was spontaneous coronary artery dissection (SCAD) starting in the mid LAD and continuing distally where it wraps around the apex. This is shown in a still frame below. The red arrow points to an area of abrupt narrowing in the mid LAD which signifies the beginning of the dissection. The blue arrow points to the apex of the heart, and the LAD is seen wrapping around inferiorly.
The angiography fits perfectly with the EKG. If she had undergone angiography at the onset of her symptoms, we would have seen a dissection causing complete occlusion. In the interceding ~8 hours, the dissection decompressed and produced TIMI 3 flow. This explains the reperfusion T waves in the precordial leads. The distal portion of the LAD was the last to reperfuse, which is why the V6 T wave is more biphasic compared to V2 which is more inverted. We see that the LAD wraps around the apex, which explains the T wave inversion in III and aVF, and the hint of terminally negative T wave in II.
SCAD wasn't on my differential per se, but in retrospect it should have been. Most patients presenting with SCAD report a preceding emotional or physical stressor. Unfortunately, there are no prospective trials to guide management of SCAD, so optimal management is uncertain. Revascularization is associated with high failure rates, and most patients exhibit spontaneous healing with conservative management. SCAD is strongly associated with fibromuscular dysplasia (72% of patients in one series), and can impact other vascular beds, most commonly the renal arteries, cerebrovasculature, and iliac arteries.
Saw, J., Aymong, E., Sedlak, T., Buller, C. E., Starovoytov, A., Ricci, D., Robinson, S., Vuurmans, T., Gao, M., Humphries, K., & Mancini, G. B. J. (2014). Spontaneous coronary artery dissection. Circulation: Cardiovascular Interventions, 7(5), 645–655. https://doi.org/10.1161/circinterventions.114.001760
The patient was managed conservatively and started on medical therapy including nitrates with resolution of her symptoms. HsTnI peaked at 20,762 ng/L the day of presentation and trended down. Repeat EKG the following morning is shown below.
EKG 2
On hospital day 3, the patient had recurrence of symptoms and the following EKG was obtained.
EKG 3
Here is the Queen of Hearts interpretation with explainability.
Notice that the precordial T waves are not quite as deep, and there’s a bit more convexity to the ST segments. Lead III’s ST segment has gone from relatively flat to convex. T waves in II and aVF were previously inverted and are now biphasic, on their way back to upright and hyperacute. After additional nitroglycerin, the patients symptoms resolved, and the following EKG was obtained.
EKG 4
Here is the Queen of Hearts interpretation with explainability.
The inferior leads show near resolution of the coving, and the T waves are mostly inverted again. This proves effective treatment of the recurrent ischemia. The patient had no further symptoms of ischemia. Here was her final EKG prior to discharge.
EKG 5
Here is the Queen of Hearts interpretation with explainability.
This EKG shows almost completely flattened ST segments, and deeper T wave inversion inferiorly, confirming persistent reperfusion since the prior EKG. You also appreciate the overly upright T waves in I and aVL which are reciprocal to the inferior T waves.
- Type 1 MI is the type we are most familiar with: rupture of atherosclerotic plaque with production thrombus or platelet fibrin aggregates.
- But not all OMI is atherosclerotic in nature. This is an example of a patient with a OMI due to coronary dissection. Most Type 2 OMI are due to supply-demand O2 mismatch that do NOT involve a dynamic change in the coronanry artery:
- 1) decreased O2 supply from (a) low blood pressure, especially in the presence of fixed coronary stenosis (b) hypoxia, (c) anemia (d) hemoglobinopathies such as CO poisoning or (e) oxidative phosphorylation problems (CN or HS) [(d) and (e) also causes direct injury]
- 2) increased O2 demand: (a) tachycardia (b) elevated BP (high afterload) (c) increased wall stretch
- But Coronary Artery Dissection is also classified as type 2, even though it involves an acute change in the coronary artery structure, because it does not involve ruptured plaque.
- The absence of risk factors for coronary artery disease does not mean a patient is not at risk for OMI.
- Stress cardiomyopathy can be a very convincing mimic for OMI, particularly LAD OMI. But it is a diagnosis of exclusion. If a patient’s presentation is suggestive of stress cardiomyopathy, the onus is on the treating clinician to rule out other causes including OMI.
- Serial EKG is very high yield diagnostic test in patients with stuttering angina. EKG 3 is diagnostic for developing re-occlusion, and EKG 4 proves that the nitrates relieved the ischemia.
- Reason #1: Attention is not directed at ensuring that we are "comparing apples with apples and not with oranges" as we look at serial tracings. By this I mean that IF there is significant variation in either the frontal plane axis or in precordial lead placement (ie, R wave progression) — then instead of ischemic change — the reason for a difference in ST-T wave morphology might be the result of a difference in recording technique.
- Reason #2: The tendency to skip meticulous correlation between the presence and severity of symptoms at the time each serial ECG is recorded.
- Reason #3: Diligent lead-by-lead comparison is simply not made. Instead — there is a tendency to look at each ECG in its entirety without comparing lead I in each tracing — then lead II in each tracing — and so on, for each of the 12-leads.
- For clarity in Figure-1 — I have placed side-by-side limb leads (on TOP) and chest leads (on the BOTTOM) from each of today's 5 ECGs to faciliate this comparison.
- CONFESSION: I fully acknowledge that I did not optimally appreciate all of the subtle-but-real observations described by Dr. Frick when I first went through the 5 ECGs in today's case. It was only after I put each tracing next to each of the other tracings that I could clearly see all of the subtle-but-important findings.
-USE.png) |
| Figure-1: Lead-to-lead comparison of evolving ST-T wave changes over the course of the 5 ECGs in today's case. |
- First — Lead-by-lead comparison between each of the 5 ECGs in today's case is valid because: i) There is no appreciable change in the frontal plane axis over the course of these 5 tracings; and, ii) There is no more than minimal variation in QRS morphology and R wave progression — such that our lead-by-lead comparison will not be affected.
- Dr. Frick's immediate reaction on seeing ECG #1 — was "reperfused LAD occlusion". He notes (after having a chance to learn the history) — that his impression of ECG #1 is "as you would expect in a patient with resolved or improving symptoms".
- But because the patient's symptoms were now returning — Dr. Frick activated the cath lab. After reviewing results of the cath, he noted that angiography fit perfectly with the findings in ECG #1 — in that we see reperfusion T waves in the chest leads. He added the insightful clinical points that: i) Since "the distal portion of the LAD is the last to reperfuse — the V6 T wave is more biphasic compared to V2 which is more inverted" — and, ii) The cath film shows "the LAD wraps around the apex — which explains the T wave inversion in III and aVF, and the hint of terminally negative T wave in II".
- Medical therapy resulted in resolution of symptoms — with ECG #2 obtained the following morning. Dr. Frick astutely noted, "The precordial T waves are now much more deeply inverted — and the T waves in II and aVF which were previously biphasic are now inverted. This is reassuring, as it indicates persistent reperfusion compared to ECG #1.
- CP recurred the next day — prompting ECG #3 — in which Dr. Frick notes, "the precordial T waves are not quite as deep, and there’s a bit more convexity to the ST segments compared to ECG #2. Lead III’s ST segment has gone from relatively flat to convex. T waves in II and aVF were previously inverted and are now biphasic, on their way back to upright and hyperacute."
- ECG #4 was obtained shortly after ECG #3 — because the patient's symptoms were relieved with nitroglycerin. Compared to ECG #3 — Dr. Frick notes that "the inferior leads in ECG #4 show near resolution of the coving that was present in ECG #3". Instead, "the inferior T waves in ECG #4 are now mostly inverted again. This proves effective treatment of the recurrent ischemia."
- CP did not recur during the remainder of the hospital stay. ECG #5 was obtained prior to discharge. Dr. Frick notes, "this pre-discharge ECG shows almost completely flattened ST segments, and deeper T wave inversion inferiorly — which confirms persistent reperfusion since ECG #4." Dr. Frick notes that an additional sign of inferior wall reperfusion is "the overly upright T waves in I and aVL — which are reciprocal to the inferior T wave inversion."
- QUESTION: Isn't it so much EASIER with the lead-to-lead comparison facilitated by Figure-1 — to see the subtle-but-important evolution of ST-T wave changes that so closely correspond to clinical events?
No comments:
Post a Comment
DEAR READER: I have loved receiving your comments, but I am no longer able to moderate them. Since the vast majority are SPAM, I need to moderate them all. Therefore, comments will rarely be published any more. So Sorry.