Post by Smith, with short article by Angie Lobo (https://twitter.com/ALoboMD), a third year intermal medicine resident at Abbott Northwestern Hospital
CaseA 30-something woman with no past history, who is very fit and athletic, presented with 1.5 hours of substernal chest pressure. It was non-radiating and without other associated symptoms except for nausea. She had zero CAD risk factors.
Here was her ECG at time zero:
|What do you think?
There is ST elevation in V2 with large fat T-wave. There is ST depression in II, III, and aVF, and V3 to V6.
I saw this before any other information and knew immediately that it represented an LAD occlusion.
There is 1 mm of STE in lead V2. This must be explained, and normally would be explained by “normal variant,” or “early repol.” However, normal variant never has associated ST depression, and here we see ST depression in II, III, aVF and V3-V6. Moreover, there are large, fat T-waves in V2 and V3. The T-waves in V3-V6 are subtle “de Winter’s” T-waves (ST depression followed by a large upright T-wave).
The physicians told me that they “knew something was wrong” with the ECG, but couldn’t express exactly what.
The pain was resolving after nitroglycerine when this ECG was recorded at time 44 minutes:
|The ST depression is less
The T-waves are smaller
The physicians did not notice this either. But this is what you are looking for if you do an ECG after pain resolution!! You MUST look for it. And then if you see it, it must make you realize that you missed the ST depression and hyperacute T-waves on the first ECG.
Next management step?
If you would not have activated the cath lab based on the first ECG, you really should strongly think about it now. This patient clearly has an unstable LAD lesion that at one point was occluded or nearly so. It is equivalent to a transient STEMI. It was late evening and the patient will be in the hospital overnight with a potentially very unstable LAD lesion.
The first troponin I returned at 0.022 ng/mL (99% URL = 0.030 ng/mL)
Not having seen the ECG findings, the providers discussed her very low risk with her and whether she would like to go home and follow up if her 2nd troponin remained negative, or be admitted to observation.
She felt more comfortable being admitted.
Later, before being taken to her room, the 2nd troponin returned at 1.01 ng/mL. This is diagnostic of myocardial infarction.
Heparin was started, but there does not seem to have been discussion of cath lab activation.
About 3 hours after admission, just after midnight, she had a 30 beat run of non-sustained VT.
They recorded a 3rd ECG at time 7 hours:
|Now you can see complete resolution of hyperacute T-waves.
There is no longer any STE in V2
There remains a bit of ST depression.
About this time, the 4th troponin, drawn at 8 hours after onset of pain, peaked at 20.956 ng/mL.
(For those of you who are accustomed to the units of high sensitivity troponin (ng/L), this is equivalent to 20,956.00 ng/L.)
Now you have ECG and troponin evidence of ischemia, AND ventricular dysrhythmia, which means this is NOT a stable ACS.
Again, cath lab was not activated.
What does this troponin level mean? Not much, but studies of STEMI and NonSTEMI show that about 70% of those diagnosed with STEMI have a peak troponin I above 10 ng/mL and that about 70% of those diagnosed with NonSTEMI have a peak troponin I below 10 ng/mL. Troponin elevation is dependent on presence or absence of occlusion (remember many OMI receive a diagnosis of NSTEMI), duration of occlusion (which is dependent on rapidity of therapy or the luck of spontaneous reperfusion), area of myocardium at risk, collateral circulation, and more.
Fortunately, the patient remained stable. Next day, the patient was taken for an angiogram and found to have a reperfused LAD lesion with good flow that appeared to the angiographer as if it was a spontaneous coronary artery dissection. It seems that there was some uncertainly about this. The lesion was stented.
ECG at time 19 hours after cath:
|Wellens’ Pattern A T-waves are present (terminal T-wave inversion)
Pattern A is in contrast to Pattern B, which is a further evolutionary stage of Wellens and is more deep and symmetric.
These are reperfusion T-waves (the same thing as Wellens’ waves)
Regional wall motion abnormality-distal septum and apex.
Regional wall motion abnormality-distal inferior wall.
ECG recorded at time 38 hours:
|A further evolutionary stage of T-wave inversion.
This is beyond Pattern A but not quite Pattern B yet.
See examples of Pattern A and Pattern B at the very bottom of this post
All ischemic ST Elevation and/or hyperacute T-waves evolve. The best evidence that ST elevation or large T-waves are ischemic comes from subsequent ECGs. It they are static, then they are not due to ischemia.
Ischemic ST elevation will increase, decrease, or resolve. Hyperacute T-waves will get larger, smaller, normalize, or invert.
This is better evidence for ischemia than any other data point. Wall motion abnormalities may disappear with rapid reperfusion. Angiograms may be negative due to spasm or thrombus lysis or small vessel disease, or it may be a type 2 MI. Troponins may be negative with very rapid reperfusion, or measured too late, or chronically elevated due to cardiomyopathy or renal failure. But the ECG, if it has a finding which is the result of acute ischemia, (and it does not always), will be dynamic. If the ECG findings are due to a pre-existing chronic pathology, or to normal variant, they will almost always be relatively static over 48 hours.
What is Spontaneous Coronary Artery Dissection (SCAD)?
I asked Angie Lobo (https://twitter.com/ALoboMD), a third year intermal medicine resident at Abbott Northwestern Hospital (and Minneapolis Heart Institute) and an aspiring cardiologist, to write a couple paragraphs on SCAD. She has done quite a bit of research on the topic.
Spontaneous Coronary Artery Dissection
Spontaneous coronary artery dissection (SCAD) is an infrequent but increasingly recognized cause of acute coronary syndrome (1- 4%) 1, most commonly affecting women (90%) 2. In middle age women, it accounts for 22-35% of all ACS presentations 1,3, and the reported incidence of ST-elevation myocardial infarction in this subset of patients is variable, but estimated to be between 24-50%4. SCAD is a non-atherosclerotic, non-iatrogenic and non-traumatic form of ACS, defined as a dissection occurring within the wall of one or more coronary arteries (LAD being the most commonly affected 2), leading to an obstruction of the lumen caused by formation of an intramural hematoma (IMH) or intimal disruption rather than atherosclerotic plaque rupture or intraluminal thrombus 2. SCAD occurs in patients with few or non-traditional cardiovascular risk factors. There has been multiple factors associated with SCAD that may predispose to a weaken arterial wall, fibromuscular dysplasia (FMD) and pregnancy being the most common 2,5.
There are no randomized controlled trials for treatment strategies in SCAD. The current American Heart Association (AHA) consensus recommends a conservative approach (avoiding invasive therapies) in hemodynamically stable patients with good TIMI flow. Invasive therapies, such as percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG) should be reserved for patients with ongoing ischemia, left main artery dissection, or hemodynamic instability 6. It is of extreme importance to suspect SCAD in this population (specifically women) in order to deliver the adequate management (avoid management as atherosclerotic ACS, unnecessary invasive strategy) and decrease the rate of complication.
1. Nishiguchi T, Tanaka A, Ozaki Y, Taruya A, Fukuda S, Taguchi H, Iwaguro T, Ueno S, Okumoto Y, Akasaka T. Prevalence of spontaneous coronary ar- tery dissection in patients with acute coronary syndrome. Eur Heart J Acute Cardiovasc Care. 2016;5:263–270. doi: 10.1177/2048872613504310.
2. Tweet MS, Hayes SN, Pitta SR, Simari RD, Lerman A, Lennon RJ, Gersh BJ, Khambatta S, Best PJ, Rihal CS, Gulati R. Clinical features, management, and prognosis of spontaneous coronary artery dissection. Circulation. 2012;126:579–588. doi: 10.1161/CIRCULATIONAHA.112.105718.
3. Nakashima T, Noguchi T, Haruta S, Yamamoto Y, Oshima S, Nakao K, Taniguchi Y, Yamaguchi J, Tsuchihashi K, Seki A, Kawasaki T, Uchida T, Omura N, Kikuchi M, Kimura K, Ogawa H, Miyazaki S, Yasuda S. Prog- nostic impact of spontaneous coronary artery dissection in young female patients with acute myocardial infarction: a report from the Angina Pecto- ris-Myocardial Infarction Multicenter Investigators in Japan. Int J Cardiol. 2016;207:341–348. doi: 10.1016/j.ijcard.2016.01.188.
4. Saw J, Mancini GBJ, Humphries KH. Contemporary review on spontaneous coronary artery dissection. J Am Coll Cardiol. 2016;68:297–312. doi: 10.1016/j.jacc.2016.05.034.
5. Saw J, Poulter R, Fung A, Wood D, Hamburger J, Buller CE. Spontaneous coronary artery dissection in patients with fibromuscular dysplasia: a case series. Circ Cardiovasc Interv. 2012;5:134–137. doi: 10.1161/ CIRCINTERVENTIONS.111.966630.