Saturday, April 23, 2022

ECG Blog #300 — Why Does It Happen at Night?

The ECG in Figure-1 was obtained from a 50-year old man who developed chest pain after becoming emotionally upset. As his workplace was close to his physician's office — this ECG was obtained within ~5 minutes of the event.
  • How would YOU interpret the ECG in Figure-1?
  • How might you explain that the patient reports 3 recent similar episodes — with chest pain spontaneously resolving each time within 15 minutes?

Figure-1: ECG obtained from a 50-year old man within minutes of developing chest pain after becoming emotional upset.

MY Thoughts on the ECG in Figure-1:
The rhythm is sinus at ~90-95/minute. There is a PVC (in the middle of the tracing — between the lead switch from leads aVR,aVL,aVF — to leads V1,V2,V3).
  • Regarding Intervals — The PR interval is normal. The QRS is narrow. However — the QTc looks prolonged (especially in leads V2, V3).
  • The frontal plane Axis is normal (about 0 degrees — as the QRS is isoelectric in lead aVF).
  • Regarding Chamber Enlargement — QRS amplitude appears increased in the lateral chest leads (although as we'll see in a moment — this does not necessarily reflect LVH).

Regarding Q-R-S-T Changes:
  • There are small and narrow Q waves in each of the lateral leads (ie, leads I, aVL, V5,V6). These are of uncertain significance.
  • R Wave Progression shows normal Transition in the mid-chest lead area — but there is a strange loss of voltage for the tiny QRS complex in lead V3.
  • The most remarkable finding in ECG #1 — are the tall, peaked T waves in leads V2-thru-V6 (especially marked in leads V2, V3, V4). There is also J-point ST elevation in leads V1-thru-V4 (attaining 2-2.5 mm in amplitude in leads V2 and V3). ST segments are flat but not depressed in each of the inferior leads.

The PVC and markedly tall, peaked T waves in multiple chest leads with at least 2 mm of ST elevation in leads V2,V3 in this patient with new-onset chest pain — strongly suggest acute LAD (Left Anterior Descending) occlusion until proven otherwise.

The CASE Continues:
Immediately after ECG #1 was recorded — the patient said, "My chest pain is less. It will go away by itself. I have had clusters of such pains that usually occur between 5-to-6 am in the morning".
  • Supplemental History: The patient is a heavy smoker (2 packs per day). His medical history is otherwise negative. Negative family history.
  • The initial Troponin came back negative.
  • The patient refused medication — so neither nitroglycerin nor analgesics were given. Over the next ~10 minutes — his chest pain completely resolved, at which time ECG #2 was obtained (Middle tracing in Figure-2).
  • The patient stabilized. ECG #3 was obtained about 3 hours after the initial ECG (Bottom tracing in Figure-2). Throughout this time — the patient remained without chest pain.

  • Given the above sequence of events — HOW would you interpret the serial ECGs shown in Figure-2?
  • Based on the above history — WHAT is the likely diagnosis? 
  • What do you think cardiac catheterization showed?

Figure-2: The patient's chest pain resolved quickly. He was pain-free at the time ECG #2 was obtained. He remained pain-free over the next few hours — at which time ECG #3 was obtained (See text).

MY Thoughts on the History and Serial ECGs:
The extreme ST-T wave changes seen in the chest leads of the initial ECG improved dramatically in the ECG obtained just 17-minutes later.
  • As emphasized in the History provided above — the patient was well familiar with the sequence of events in which stress or emotional distress — or simply the early morning hours, brings on a short-lived episode of severe chest pain that he knows will spontaneously resolve minutes later.

  • KEY Clinical Point: The initial ECG ( = ECG #1 in Figure-2) was obtained during this episode of severe chest pain. Minutes later, the chest pain was less — and it was essentially gone at the time ECG #2 was obtained. While several of the mid-chest leads in ECG #2 still manifest somewhat larger-than-expected T waves — the improvement from ECG #1 is obvious.

  • ECG #3 (done ~3 hours after ECG #1) — shows further reduction in T wave amplitude. There is no longer any ST elevation. Instead — leads V3-thru-V6 show 0.5-1.0 mm of ST depression.

Further FOLLOW-UP to Today's CASE:
  • Serum Troponin never became elevated.
  • Cardiac catheterization revealed normal coronary arteries! (Figure 3).
  • Acute MI was ruled out. The patient was discharged with a diagnosis of Prinzmetal Angina.

Figure-3: Cardiac catherization of the patient in today's case was completely normal — without any significant narrowing — and with normal left ventricular function.

Prinzmetal Angina:
The entity known as Prinzmetal Angina (also known as "vasospastic" or "variant" angina) — is a syndrome of recurrent chest pain episodes that occur at rest in association with transient ST-T wave changes (either ST elevation and/or depression). I summarize below KEY points from the following sources — (Ziccardi and Hatcher: StatPearls-NCBI Bookshelf- 7/31/2021) — (Bayés de Luna et al: Ann Noninvasive Electrocardiol 19:442-453, 2014 Consensus Paper) — and — (Ghadri et al: Q J Med 107:375-377, 2014).
  • Charcteristic Features of Prinzmetal Angina — are that: i) Chest pain episodes spontaneously resolve (usually within 5-15 minutes without treatment!); and, ii) Chest pain episodes often occur in clusters over consecutive (or nearly consecutive) days. Fortunately — chest pain episodes resolve faster if short-acting nitrates are promptly given. 
  • There is often a circadian pattern to symptoms — in that episodes most often occur between midnight and the early morning hours. In any given patient — episodes often occur at about the same time during the day or night.

  • Approximately 50% of patients with Prinzmetal Angina have normal coronary arteries on cath. Most of the remainder have nonobstructive coronary lesions (ie, less than 50% vessel narrowing).
  • ECG changes may include ST elevation with/without reciprocal ST depression — which may (or may not) be followed by reperfusion ST changes (ie, T wave inversionSee Below!).
  • Prompt recognition of this entity is important because potentially life-threatening malignant arrhythmias (including VT/VFib, high-grade AV block) may occur. Myocardial infarction is not common (because episodes most often spontaneously resolve within 15 minutes) — but acute MI can occur.

  • The mechanism of Prinzmetal Angina is uncertain — though the end result appears to be diffuse or localized coronary spasm, perhaps precipitated by sympathetic hyperactivity (with or without vagal tone withdrawal) — by reduced nitric oxide synthase with endothelial dysfunction — and/or by genetic predisposition. Coronary vessel hyperreactivity may be precipitated by development of underlying coronary narrowing — OR — "pure" vasospastic angina may be seen in patients with totally normal coronary arteries.

  • Among potential "trigger" factors of anginal episodes include drugs (cocaine, amphetamine, mariuana) — especially if associated with cigarette smoking! Other potential precipitating factors include cold exposure and exercise in a small percentage of patients. That said — there need not necessarily be any triggering factor.
  • Other "vasospastic" disorders (ie, Raynaud phenomenon, typical migraine) may be associated in patients with Prinzmetal Angina.

  • The average age of presentation for patients with Prinzmetal Angina is in an adult between 40-50 years of age. But it does present in other age groups.

  • Standard Treatment of Prinzmetal "Vasospastic" Angina incudes Nitrates (short and/or longterm — with the caution that longterm nitrates may lead to tolerance) — longterm Calcium Channel Blockers (ie, debate persists as to which ones are best) —  plus emphasis on complete smoking cessation! 
  • Additional treatment measures more recently considered include Nicorandil (a nitrate and K-channel activator with coronary vasodilatory properties) — and Fluvastatin (seems to benefit some patients with vasospastic angina by improving endothelial function).
  • Among the Drugs to Avoid include ß-Blockers (which may cause unopposed alpha-receptor agonism) — alpha-agonists (ie, Oxymetazoline, Pseudoephedrine) — Sumatriptan (a serotonin receptor agonist used for acute treatment of migraine — which works by promoting vasoconstriction).

  • NOTE: The diagnosis of Prinzmetal Angina may be difficult — especially because of its usual nocturnal occurrence — with spontaneous resolution of symptoms and ECG changes within minutes! (ie, often before an ECG can be done). For this reason — awareness of the above clinical features and of the expected array of ECG changes that I describe below is essential for recognition of this entity!

  • The "GOOD" News — the occurrence of Prinzmetal Angina is much less frequent than in years past (probably because of increased efficacy of antianginal measures and less smoking in the general population). In addition — the longterm efficacy of Calcium Channel Blockers has resulted in much improved symptom control with reduced morbidity in most patients (especially in those who quit smoking).
  • Editorial Comment: I remember special attention being devoted in my medical training to making us aware of this entity. That said, while some component of coronary spasm clearly occurs in a percentage of patients with coronary disease — Prinzmetal Angina in its "pure" form as described above (as was seen in today's patient) is not a common disorder.

Characteristic ECG Features of Prinzmetal Angina:
Most patients with Prinzmetal Angina have a relatively normal baseline ECG, with at most nonspecific ST-T wave abnormalities. I synthesize below the KEY ECG Features to look for in Prinzmetal patients, as detailed in the 2014 international Consensus Paper by Bayés de Luna et al:
  • The most common initial ECG change — is development of tall, symmetrical and usually peaked T waves — accompanied by a modest increase in the QTc.
  • On occasion — negative U waves may be seen.
  • T wave peaking is typically followed by progressive ST elevation. This ST elevation usually lasts less than 5 minutes — after which there is gradual return to a more normal (or minimally peaked) T wave. The patient's chest pain typically corresponds to the period of maximum ST elevation.

  • Some patients manifest reciprocal ST depression during the period of ST elevation. When this happens — it suggests regional (rather than diffuse) coronary vasospasm.

  • Of interest — R wave amplitude tends to increase — while S wave amplitude tends to decrease (if not disappear) during the phase of ST elevation.

  • There is often upsloping of the T-Q segment (or the T-P baseline) during the phase of ST elevation.
  • Occasional patients may manifest alternans (from one beat-to-the-next) of the elevated ST segment or upsloping T-Q segment.
  • During the resolution stage of ST elevation — T wave inversion may be seen, which can be deep and similar to Wellens' Syndrome ECG changes (ie, presumably reflecting evolution of reperfusion T waves).

  • PVCs including short episodes of NSVT (Non-Sustained Ventricular Tachycardia) — are common during the period of chest pain and ST elevation. Fortunatelysustained VT/VFib are uncommon. Occasional patients may manifest ventricular arrhythmias (ie, AIVR) during the reperfusion stage.

  • NOTE: While ST elevation (and other ECG abnormalities) most often occur in association with chest pain episodes — coronary spasm can be "silent" (without chest pain) in up to 20% of cases. This may account for unexplained sudden death due to ischemia in these patients without any "warning" system.

Looking CLOSER at Serial ECGs in Today's CASE:
Let's now apply the above Consensus Paper description of the KEY ECG features to look for in serial ECGs of a patient with Prinzmetal Angina. 
  • In Figure-4 — I again show the initial ECG ( = ECG #1) — and ECG #3, obtained ~3 hours after resolution of this patient's chest pain. 
  • To this, I have added ECG #4 — done 3 days later. The patient had remained pain-free during this time. MI was ruled out — and the cardiac catheterization showed normal coronary arteries.

Figure-4: Comparison of the initial ECG (obtained during the episode of chest pain) — with the follow-up ECG done 3 hours later — and a final ECG done 3 days later (See text).

Review of Serial ECG Changes in Figure-4:
As we emphasized in discussion of Figure-1 — the initial ECG in today's case (TOP tracing in Figure-4) is remarkable for the tall, peaked T waves in leads V2-thru-V6 (especially marked in leads V2, V3, V4). There is also J-point ST elevation in leads V1-thru-V4 (attaining 2-2.5 mm in amplitude in leads V2 and V3). ST segments are flat but not depressed in each of the inferior leads.
  • These ECG changes were obtained during an episode of chest pain in this patient with Prinzmetal Angina.
  • Additional findings in ECG #1 (consistent with Prinzmetal Angina) include the following: i) A PVC; ii) Loss of S wave amplitude (with near disappearance of the S wave in lead V3); iii) Increased R wave amplitude (seen in the lateral chest leads, in which there is overlap of R wave amplitude into neighboring leads); iv) Upsloping of the T-P baseline (best seen in leads V2, V3, beginning just after the T wave returns to baseline); and, v) Localization of these ST-T wave changes to the chest leads (suggesting regional rather than diffuse coronary spasm).

ECG #3 — was obtained 3 hours after ECG #1. The patient's episode of chest pain was short-lived — and he remained pain-free at the time ECG #3 was obtained.
  • Apart from shallow T wave inversion in lead III — limb lead appearance is unchanged from the initial ECG.
  • In contrast — chest lead T waves are all now normal in size. There is no longer any ST elevation. Instead, leads V3-thru-V6 now show 0.5-1.0 mm of ST depression.
  • The S wave in lead V3 has been reestablished. There is no longer upsloping of the T-P baseline. Lateral chest lead R wave amplitude remains increased.

ECG #4 — was obtained 3 days later. The patient remained pain-free throughout this time. He was discharged from the hospital.
  • There has been essentially no change in limb lead appearance.
  • R wave amplitude has decreased dramatically since ECG #3. Significant S waves are now present through to lead V6.
  • There is no longer any ST depression.
  • The upright T waves that were seen in the chest leads of ECG #3 — have now evolved into a biphasic (positive-negative) small-amplitude T wave. Presumably, this is a reperfusion change.

Acknowledgment: My appreciation to Klanseng Ng (from Kluang, Malaysia) for the case and this tracing.

Additional Relevant Material to Today's Case:
  • See ECG Blog #205 — Reviews my Systematic Approach to 12-Lead ECG Interpretation.

  • ECG Blog #183 — Reviews the concept of deWinter T-Waves (with reproduction of the illustrative Figure from the original deWinter NEJM manuscript). 
  • ECG Blog #222 — Reviews the concept of Dynamic ST-T wave changes, in the context of a detailed clinical case. 
  • ECG Blog #260 — Reviews another case that illustrates the concept of "dynamic" ST-T wave changes.

  • ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 
  • ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?"). 

  • ECG Blog #193 — Reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and — reviews the basics on how to predict the "culpritartery.

  • ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data.

  • ECG Blog #115 — Shows an example of how drastically the ECG may change in as little as 8 minutes.

  • The July 31, 2018 post in Dr. Smith's ECG Blog (Please scroll down to the bottom of the page to see My Comment). This case provides an excellent example of dynamic ST-T wave changes on serial tracings (that I illustrate in My Comment) in a patient with an ongoing acutely evolving infarction.

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