ECG Blog #508 — Tall, Pointed T Waves ...

The ECG in Figure-1 was obtained from a middle-aged man who presented to the ED (Emergency Department) with severe, new-onset CP (Chest Pain).

• BP = 130/90 mm Hg.
• Initial hs-Troponin was normal.

QUESTIONS:

• How would you interpret this ECG?
• Should you activate the cath lab?

Figure-1: The initial ECG in today's case — obtained from a patient with new-onset, severe chest pain.

MY Thoughts on the Clinical Scenario:

The history of severe, new-onset CP in this middle-aged man that was worrisome enough to him to prompt his presentation to the ED, immediately places him in a higher-risk group for having an acute cardiac event.

• PEARL #1: To emphasize that although one may be momentarily comforted by the initial normal hs-Troponin value — this in no way rules out an acute cardiac event. Wereski et al (JAMA Cardiology, 2020) — found that 14% of patients with an acute STEMI had a normal initial hs-Troponin (and ~25% had hs-Troponin levels below the infarction “rule-in” level).
• On occasion — even the 2nd hs-Troponin level may still be normal in a patient who goes on to develop an acute STEMI. The reasons for this are simple: i) Troponin values (including hs-Troponin values) provide a “rear-view” mirror as to what has already happened — but not to what will happen in the future; — and, ii) Whether hs-Troponin increases or not depends not only on the size of the infarct — but especially on the duration of time that the “culprit” vessel is occluded — which means that if the amount of time that the “culprit” vessel is closed was brief (because of rapid spontaneous reperfusion) — then hs-Troponin may be no more than minimally (if at all) elevated.

MY Thoughts on the Initial ECG in Figure-1:

The rhythm is sinus arrhythmia — at a rate just under 60/minute. The PR interval is prolonged ( = 1st-degree AV block) — but QRS duration and the QTc interval are normal. The frontal plane axis is normal at +50 degrees. There is no chamber enlargement.

• There is appreciable artifact in lead V1. That said — the baseline artifact in the limb leads is minimal, and does not impair interpretation.
• My “eye” was immediately drawn to the chest leads — beginning with lead V2. Each of these 5 chest leads that follow manifest distinct J-point ST elevation with hyperacute-looking, tall, and pointed T waves (RED arrows in leads V2-thru-V6 — as shown in Figure-2). 
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• PEARL #2: As opposed to the peaked T waves that may be seen with repolarization variants — the T waves seen in Figure-2 are more pointed, taller and more symmetric (ie, Repolarization variants tend to be less symmetric, with a slower upslope compared to their more rapid downslope).
• Note: Distinct J-point notching is seen in lead V6. Despite this finding (that is commonly seen with repolarization variants) — the above described hyperacute appearance of the T waves in this patient with new-onset, severe CP is clearly of concern.
• P.S.: Although good to verify that serum K+ is normal (which it was) — the peaked T waves of hyperkalemia tend to have an even narrower base than that seen in Figure-2.

Figure-2: I’ve labeled today’s initial ECG.

Regarding the limb leads in Figure-2:

• ST segments are elevated and T waves are peaked in leads I,II,III and aVF (although not quite as much as they are in the chest leads).
• I was unsure if the tiny, artifact-laden QRS complex in lead aVL had some ST depression (therefore my BLUE question mark in this lead).
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• BOTTOM Line: In this middle-aged man who presents with severe, new-onset CP — ST elevation is seen in 9 (if not 10) of the 12 leads, with hyperacute T waves until proven otherwise in 5 consecutive chest leads.

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The Case Continues:

Based on the above clinical presentation and findings in the initial ECG — the cath lab was activated. Results from the cardiac cath:

• LMain: Normal.
• LAD: Mild-to-moderate atherosclerosis in the mid-LAD region with severe Coronary Spasm resulting in total occlusion (TIMI-0 flow). Normal (TIMI-3 flow) was achieved following intracoronary NTG.
• LCx: No more than minimal atherosclerosis.
• RCA: No more than minimal atherosclerosis.
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• Impression: Insignificant coronary atherosclerosis. Acute coronary spasm that initially resulted in total LAD occlusion — but with normal flow restored by intracoronary NTG. Normal LV function following IC-NTG. Medical management advised.

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NOTE: Although the initial hs-Troponin-I value was normal — the 2nd and 3rd Troponin values were greatly increased! ==> Today's patient had an MI precipitated by coronary spasm.

• At 6 hours after symptom onset — hs-Troponin I was 6.24 ng/mL (abnormal ≥0.0875; reference ≤0.0175).
• At 12 hours after symptom onset — hs-Troponin I = 66.16 ng/mL.

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MY Thoughts on this CASE:

Unfortunately, no ECG was obtained following relief by intracoronary NTG of the complete LAD occlusion. Thus, we do not have a baseline ECG when this patient was pain-free.

• Review of this patient's chart did not reveal any prior ECG.
• A repeat ECG was done after cardiac catheterization, at which time the patient was still pain-free — but this was nearly 2 hours later (shown in Figure-3).

QUESTION:

• Has there been any change in ECG #2 compared to ECG #1?
• HINT: If your answer is that there is no difference between the 2 tracings shown in Figure-3 — GO BACK and LOOK again ...

Figure-3: Comparison between today's initial ECG — and the repeat ECG done after cardiac catheterization.

ANSWER:

ST elevation with T wave peaking persists in multiple leads in ECG #2. That said — there is subtle-but-real improvement in chest lead T wave appearance.

• Chest lead T waves look less hyperacute in the repeat ECG — in that these T waves are now less symmetric than they were in ECG #1 (ie, the T wave upslope in leads V2-thru-V6 is now slower than the T wave downslope).
• Subtle J-point notching is seen in leads V5,V6 — as well as in several limb leads.
• My Thoughts: We still do not know what this patient's baseline ECG looks like. Although ECG #2 now manifests characteristics of a repolarization variant — I would have expected more normalization of this patient's ECG by this point 2 hours after intracoronary NTG completely relieved this patient's chest pain. I'd want to repeat the ECG after the patient remains pain-free for at least a day.

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CASE Conclusion:

Today's case provides an insightful example of a patient with limited, non-obstructive coronary disease — who presented with acute coronary spasm severe enough to completely occlude the mid-LAD until the administration of intracoronary NTG.

• The result was spasm-induced infarction, with marked Troponin increase.

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About VSA (VasoSpastic Angina) = Coronary Spasm:

The entity of "VSA" — has been known for more than 50 years. As opposed to Prinzmetal (or Variant) Angina that occurs at rest — it has become increasingly apparent that variations on the theme of coronary "spasm" also occur with surprising frequency in association with exercise-induced angina, unstable angina, acute infarction, and with malignant ventricular arrhythmias that may cause sudden death.

I found manuscripts by Teragawa et al ( World J Cardiol 10(11):201-209, 2018) — by Tandon et al (Cureus 11(2):e4134, 2019) — by Slavich and Patel (IJC Heart & Vasc 10:47-53, 2016) — and by Ziccardi and Hatcher (StatPearls, 2023) helpful in my review of this subject.

• Coronary Spasm is defined — as transient narrowing of one or more epicardial coronary arteries, with this resulting in myocardial ischemia.
• Multiple potential mechanisms have been attributed to causing coronary spasm, including — endothelial dysfunction; hyper-reactive vascular smooth muscle — magnesium deficiency; autonomic nervous system malfunction — and/or from some combination of the above factors.
• The diagnosis of VSA in today's patient was made by cardiac catheterization. In this patient who was found to have a limited amount of non-obstructive atherosclerosis — total occlusion of the mid-LAD region was initially seen on cath. Administration of IC (IntraCoronary) NTG restored normal flow — thus confirming the diagnosis of coronary spasm.
• In other cases, SPT (Spasm Provocation Testing) is needed to make the diagnosis of VSA (ie, Ergonovine or Acetylcholine are administered during cardiac cath in an attempt to provoke coronary spasm — after which the diagnosis of spasm is confirmed by restoration of coronary flow with IC-NTG).
• Additional modalities that may be helpful for diagnosing VSA include ETT (Exercise Treadmill Testing) in patients with exercise-induced spasm — and/or Holter monitoring (for patients with night-time or early morning VSA).
• Although many (most) patients with VSA have at least some degree of underlying atherosclerosis — a certain percentage of patients with VSA do not (sometimes showing "normal" coronary arteries on cath). Thus, the mechanism by which coronary spasm may produce symptoms and/or events may vary from microvascular dysfunction in seemingly normal vessels — to coronary spasm that acts on vessels with established plaque in a way that may ultimately precipitate plaque rupture (ie, See ECG Blog #415 on MINOCA — for the group of patients who develop acute MI despite "Non-Obstructive" Coronary Arteries).
• PEARL #3: Be aware of potential triggers of coronary spasm. These may include smoking, cocaine, marijuana, alcohol, amphetamines, certain migraine medications, alpha agonists (ie, clonidine; pseudoephedrine), cold exposure, psychologic stress and left heart catheterization (guidewire, balloon dilatation).

Treatment of VSA:

Full discussion of VSA extends beyond the scope of this ECG Blog. That said — several points regarding treatment are worthy of mention.

• Smoking cessation is an absolute MUST! This is one example of a clinical condition in which smoking a single cigarette — is smoking 1 cigarette too many. 
• Avoid other potential triggers of spasm (ie, = PEARL #3 above! ).
• SL (Sublingual) NTG — is 1st-line treatment for an acute VSA episode.
• CCB (Calcium Channel Blockers) — are recommended for longterm treatment. If/as needed — CCBs may be combined with long-acting nitrates.
• ß-Blockers — are best avoided (as ß-blockade may result in unopposed alpha-adrenergic activity, potentially exacerbating spasm). If ß-blockers are needed for other cardiac indications — then gradual dose titration is essential to avoid exacerbating coronary spasm.
• Consider magnesium supplementation.
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• Unresolved Issues: While great progress has been made in the recognition of VSA under a variety of conditions — some problems remain: i) How to treat refractory VSA? — and, ii) Determining which patients with VSA are in need of an ICD (Implantable Cardioverter-Defibrillator).

Another LOOK at Today's ECG:

While fully acknowledging that I was not expecting the principal pathology in today's patient to be the result of coronary spasm — in retrospect, the initial ECG is perfectly consistent with this diagnosis!

• As discussed earlier — today's initial ECG (that I've reproduced below in Figure-2) shows ST elevation with tall, pointed T waves in 5/6 chest leads (RED arrows in these leads). Although distorted by artifact — there appears to be ST elevation in lead V1.
• ST elevation with T wave peaking is also seen in 4 of the limb leads. This makes for 10/12 leads showing ST elevation with peaked T waves.
• Clear sign of reciprocal ST depression is missing.
• As opposed to an acute OMI, in which ST-T wave findings tend to be localized to that area of the heart that is ischemic — diffuse ST elevation with hyperacute T waves in the absence of reciprocal ST-T wave changes is perfectly consistent with coronary spasm!
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• PEARL #4: Although today's ECG showing diffuse ST elevation without reciprocal STdepression is typical for pure coronary spasm — VSA is not always associated with ST elevation SPT (Spasm Provocation Testing) may be needed for diagnosis on cath in certain cases.

Figure-2 — that I’ve reproduced from above. 

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Acknowledgment: My appreciation to Chun-Hung Chen = 陳俊宏 (from Taichung City, Taiwan) for the case and this tracing.

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