ECG Blog #209 (ECG MP-26) — Is this Wellens’ Syndrome?

The ECG shown in Figure-1 was obtained from a 53-year-old African American man. No additional information about this patient was available. The computer interpretation of this tracing read as follows — “Sinus bradycardia; LVH with repolarization abnormality; abnormal ECG.”  

• Do you agree with the computer interpretation?
• In the absence of any history — WHAT are your diagnostic considerations?
• Is this ECG diagnostic of Wellens’ Syndrome?

 

Figure-1: Is this ECG diagnostic of Wellens’ Syndrome? (See text).

 

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NOTE #1: Some readers may prefer at this point to listen to the 6:00 minute ECG Audio PEARL beforereading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-26).

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Today’s ECG Media PEARL #26a (7:40 minutes Audio) — What Wellens’ Syndrome is — and what it is not ... (P.S. — I updated this Audio Pearl on 9/28/2021).

 

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NOTE #2: I have excerpted a brief written summary regarding Wellens’ Syndrome from my ECG-2014-ePub. This appears below in the Addendum (in Figure-3 and Figure-4).

• CLICK HERE — to download a PDF of this 3-page file on Wellens’ Syndrome.

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MY Approach to this Tracing:

As always — I favor a Systematic Approach for interpretation of every ECG I encounter (This Systematic Approach reviewed in ECG Blog 205). The 1st Step in interpretation is Descriptive Analysis — which I find especially helpful for organizing your thoughts with complex tracings, such as the ECG shown in Figure-1. My Descriptive Analysis for this ECG is as follows:

• The rhythm is fairly (albeit not completely) regular at ~45-50/minute. Upright P waves with a constant PR interval are seen in lead II — so the rhythm is sinus bradycardia. 
• The PR interval is normal at 0.20 second. 
• NOTE: Given the uncertain clinical significance of 1st-degree AV block as an isolated conduction defect finding — the term “borderline” 1st-degree is essentially meaningless. As a result, my bias is not to call the PR interval “prolonged” (ie, abnormal) — unless the PR interval clearly exceeds 1 large box ( = 0.20 second) in duration, which it does not in Figure-1.
• Assessing QRS duration from the lead(s) in which the QRS appears to be longest — I measure QRS duration in leads III, V2 and V3 at 0.11 second, which is slightly prolonged (ie, the QRS is prolonged if it clearly measures more than half a large box [ = >0.10 second] in duration).
• I measure a QT interval of ~0.52 second — which is long. That said, assessment of the clinical significance of QTc prolongation is much more difficult when there is marked bradycardia — as the bradycardia itself may be associated with some QT lengthening. Serial QT readings may be insightful (ie, if on serial recordings there is clear increase or decrease from the baseline QT value) — but as an isolated finding, I find it difficult to know what to do with a QT value ~0.52 second when the heart rate is under 50/minute.
• The frontal plane axis (which is about +45 degrees) is normal.
• QRS amplitude is markedly increased — easily satisfying voltage criteria for LVH (See ECG Blog #73 for review of the LVH voltage criteria I favor). Criteria for atrial abnormality and RVH are not satisfied.

 

Regarding Q-R-S-T Changes:

• There are no Q waves in Figure-1 (NOTE: Given how common and normal it is to see a QS complex in lead aVR — I generally don’t even mention this finding).
• R wave progression is remarkable in Figure-1 for a taller-than-expected R wave in lead V1 (that measures 9mm!). That said — transition (where the R wave becomes taller than the S wave is deep) is normal (occurring between leads V2-to-V3 in this tracing).

 

Assessment of ST-T waves:

• The most remarkable finding for the ECG shown in Figure-1 is the deep, diffuse and symmetric T wave inversion seen in no less than 9 of the 12 leads of this tracing. The depth of T wave inversion reaches a maximum of 14 mm in lead V3!
• The J-point is depressed in virtually all of the leads that manifest deep T wave inversion (except in leads aVF and V2). The amount of J-point depression attains 2 mm in lead V3.
• The shape of ST segments in several leads that manifest J-point ST depression is coved (ie, with a “frowny”-configuration). This abnormal ST segment shape is best appreciated in leads I, aVL; V3 and V4.
• There is ~2 mm of J-point ST elevation in leads V1 and V2. The T wave in lead V2 is biphasic with terminal negativity.

Clinical IMPRESSION:

Unfortunately — Our interpretation of the ECG shown in Figure-1 needs to proceed without the benefit of any history. The only information available is that the patient is a 53-year-old African American man. With this in mind — my Clinical Impression was as follows:

• The rhythm is sinus bradycardia at 45-50/minute.
• There is marked LVH with diffusely abnormal ST-T waves consistent with LV “strain” and/or ischemia, that could be recent or acute. Clinical Correlation is essential!

COMMENT: There is a lot to discuss about the ECG findings on this tracing. 

• Given the age and race of the patient in today’s case (ie, a 53-year-old African American man) — there should be little doubt about the presence of severe LVH. The increase in QRS amplitude is extreme (ie, a 22 mm R wave in lead II; S waves exceeding 20 mm in leads V1 and V2; 20-25 mm R waves in leads V3 and V4). Likely diagnoses include: i) Severe, longstanding hypertension; ii) Hypertrophic or apical cardiomyopathy; iii) Congestive (dilated) cardiomyopathy; and/or, iv) Other forms of severe underlying heart disease.
• The overly slow heart rate is of potential concern. Whether this is the result of rate-slowing medication (ie, such as a beta-blocker) — an early sign of SSS (Sick Sinus Syndrome) — or part of this patient’s underlying (acute or chronic) cardiac disorder needs clinical explanation.
• Although severe LVH with longstanding hypertensive heart disease may produce fairly deep and symmetric T wave inversion in multiple leads — there are a number of additional findings on this tracing that prompt concern for potential recent or acute ischemia. These findings include: i) Marked J-point depression in multiple leads (which is usually not seen to this extent in so many leads with simple LVH); ii) ST segment coving in leads I, aVL, V3, V4 (ST coving is generally not seen with simple LVH); iii) Excessively deep T wave inversion (over 10 mm deep in lead V3); iv) Potential reciprocal (mirror-image opposite) changes for the ST-T waves in leads III and aVL; and, v) The marked sinus bradycardia.

 

Returning to 2 ECG findings I noted earlier:

• The QRS complex is slightly prolonged (ie, at ~0.11 second). That said — QRS morphology does notresemble that of any conduction defect (ie, neither RBBB, LBBB nor a hemiblock). Although some clinicians might call this a nonspecific IVCD — I believe the “theme” of this tracing is marked LVH. A thicker left ventricle takes more time to depolarize — so I thought the slight QRS widening that we see here is most likely the result of the LVH.
• The QT interval appears to be prolonged (ie, ~0.52 second). That said — it is difficult clinically to “correct the QT for rate” with a bradycardia in the 40s. Clinically, once we learn the history — common potential causes of QT prolongation should be inquired about (ie, medication effect; serum electrolyte disorders; CNS catastrophes — which I review in ECG Blog #89 and Blog #152) — but if no other obvious cause of QT prolongation is elicited, the increased QT interval seen here may be the result of the marked ST-T wave abnormalities.

BOTTOM Line regarding the ECG in Figure-1: 

The computer interpretation picked up sinus bradycardia and LVH with “strain”. It said nothing about the possibility of ischemia that could be acute (For more on the Pros & Cons of the Computer ECG Report — See ECG Blog #207).

• Finding a prior ECG on this patient would be invaluable for determining whether the above-noted ST-T wave changes are new or old. 
• Clinical Correlation is the essential next step!

Is the ECG in Figure-1 Diagnostic of Wellens’ Syndrome?

I review the essentials of Wellens' Syndrome in today's ECG Media PEARL #26 (above) — and in the 2 Figures shown below in the Addendum. In a word — this ECG is not diagnostic of Wellens' Syndrome.

• As emphasized in my review of Wellens’ Syndrome — a history of recent chest pain that has now resolved is an essential part of the diagnosis of Wellens’ Syndrome. The history is unknown in today’s case.
• The picture of modest ST elevation in lead V2 with very sharp (steep) descent of the T wave in this lead, that goes on to terminal negativity is identical to the shape of a Wellens’-like T wave. That said — there are 2 reasons why we can not make the diagnosis of Wellens’ Syndrome from this tracing: i) There is marked LVH — which is notorious for producing false positive T wave findings that simulate the T wave appearance in Wellens’ Syndrome; and, ii) I suspect the reason for the Wellens’-like T wave in lead V2 — is that V2 is a transitional lead between the all-positive T wave (with slight ST elevation) that we see in lead V1 — and— the ST segment coving with very deep and symmetric T wave inversion in lead V3 (See Figure-2).
• BOTTOM Line: As discussed in my Clinical Impression and Comment above — there are a number of ECG findings in Figure-1 that should prompt concern for possible ischemia that may be acute. But the diagnosis of Wellens’ Syndrome can not be made from this tracing alone.

 

Figure-2: Magnified view of leads V1, V2 and V3. I suspect that the ST-T wave changes seen in lead V2 are most likely the result of this being a “transition” lead. IF you were to “average out” R wave amplitude, S wave amplitude, and the ST-T wave appearance in lead V1 with that of lead V3 — Wouldn’t you expect to see a QRST complex similar to what we see here in lead V2?

 

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ADDENDUM (3/30/2021): In the following 2 Figures — I post written summary from my ECG-2014-ePub regarding Wellens’ Syndrome. 

• CLICK HERE — for a PDF of this 3-page file on Wellens’ Syndrome that appears in Figure-3 and Figure-4.

 

Figure-3: Regarding Wellens’ Syndrome (from my ECG-2014-ePub).

Figure-4: Wellens’ Syndrome (Continued).

 

 

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Relevant ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23-LINK in Blog #205).
• ECG Blog #73 — Reviews “My Take” on the ECG Diagnosis of LVH.
• ECG Blog #207 — The ECG Computer Report: Friend or Foe?
• ECG Blog #152 — Tachycardia with a long QTc.
• ECG Blog #89 — ECG Basics: Assessment of Intervals (PR, QRS, QTc).

ECG Blog #208 — ST Elevation but No History

The computer interpretation of the ECG shown in Figure-1 said the following — “Sinus rhythm; Normal ECG.”  

• Do you agree with the computer interpretation?
• In the absence of any history ... — WHAT are your diagnostic considerations?
• WHICH of these considerations is most likely?

 

Figure-1: How would you interpret this ECG? (See text).

 

 

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NOTE #1: Some readers may prefer at this point to listen to the 9:50 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-25).

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 Today’s ECG Media PEARL #25 (9:50 minutes Audio) — Pearls & Pitfalls regarding the ECG diagnosis of Acute Pericarditis.

 

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NOTE #2: I have excerpted a written summary on “My Take” for ECG diagnosis of Acute Pericarditis from my ECG-2014-ePub. This appears below in the Addendum (in Figure-3 through Figure-7).

• CLICK HERE — to download a PDF of this 9-page file on Pericarditis.

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MY Approach to this Tracing:

As always — I favor a Systematic Approach for every ECG I encounter (This Systematic Approach reviewed in ECG Blog 205). My descriptive analysis of the ECG shown in Figure-1 is as follows:

• The rhythm is regular at ~80/minute. Upright P waves with a constant PR interval are seen in lead II — so the rhythm is sinus. Intervals (PR, QRS, QTc) and the axis (which is about +70 degrees) are normal. There is no chamber enlargement.

 

Regarding Q-R-S-T Changes:

• There are small and narrow Q waves in the inferior and lateral chest leads.
• R wave progression is remarkable for the presence of a taller-than-expected R wave in lead V1 — with early transition occurring between lead V1-to-V2. Normally, there is no more than a very small r wave in right-sided lead V1 — and transition (where the R wave becomes taller than the S wave is deep) does not occur until at least lead V2-to-V3.

 

Assessment of ST-T waves:

• There is subtle-but-real ST elevation in multiple leads (horizontal dotted RED lines in Figure-2). There is an upward concavity (ie, “smiley”-configuration) to the elevated ST segments — with suggestion of J-point notching in several of them (best seen in leads V2 and V6).
• Assessment of ST elevation in Figure-2 is made more difficult by the presence of subtle-but-real PR depression in a number of leads (best seen in the inferior leads, and in leads V4 and V5). There is also slight PR elevation in lead aVR.
• There is T wave inversion in lead aVL (within the dotted BLUE oval in Figure-2).

Figure-2: Horizontal dotted RED lines show subtle-but-real ST elevation in multiple leads. The T wave in lead aVL is inverted (See text).

PEARL #1: The term PR depression will often come up when a diagnosis of acute Pericarditis is contemplated. 

• PR depression is said to be present when the horizontal PR segment is depressed below the ST segment baseline (as determined here with respect to the T-P baseline).
• Support that the finding of PR depression is real may be derived by the finding of PR elevation in lead aVR. 
• Unfortunately — there are problems with use of PR depression as a diagnostic criterion for acute Pericarditis. These include: i) False positives (because other conditions, including acute MI and normal repolarization variants may also at times manifest PR depression); ii) False negatives (because PR depression is not always seen with acute pericarditis); and, iii) Inter- and intra-observer variability in detecting PR depression (therefore limited reliability in my experience for the validity of this finding). 
• BOTTOM Line: It is probably best not to base your diagnosis of acute Pericarditis on whether or not you see PR depression.

 

PEARL #2: While important to note the presence of symmetric T wave inversion in lead aVL of Figure-2 — this is not necessarily an abnormal finding!

• Considering the small amplitude of the QRS complex in lead aVL — the size of the inverted T wave in this lead is relatively large. That said — T wave inversion may sometimes normally be seen in lead aVL — especially when there is a relatively vertical frontal plane axis and the QRS is predominantly negative in lead aVL (as we see in Figure-2). This is because the normal T wave axis often follows fairly close behind the QRS axis in frontal plane leads (ie, isolated T wave inversion may be normal if seen in lead III, lead aVF or lead aVL when the QRS complex is predominantly negative in the lead with T wave inversion — See ECG Blog #79).
• BOTTOM Line: The T wave inversion that we see in lead aVL of Figure-2 may or may not reflect an abnormal finding.

 

PEARL #3: The larger-than-expected R wave in lead V1, with early transition (mentioned above under R-wave progression) is of unknown significance. The purpose of including an “R” in my memory aid for assessing Q-R-S-T Changes — is specifically so that the finding of early transition is not overlooked.

• BOTTOM Line: The list of clinical entities to consider whenever you encounter a taller-than-expected R wave in lead V1 were reviewed in ECG Blog #81. Among these entities is posterior infarction that occurred at some point in time. This could be relevant to today’s case — given questions regarding inferior lead ST elevation and possible reciprocal ST-T wave change in lead aVL. 

 

Putting It All Together:

Some history is needed in order to know what (if anything) to do with the ECG shown in Figure-1! This ECG was one of many in a “pile” of tracings that I was given to read in our ambulatory care clinic (during the time I was charged with “official interpretation” of ECGs for our 35 medical providers). There was no indication on the ECG of any history.

• The 1st thing I did was to cross out the computer interpretation of this ECG, which said: “Sinus rhythm; Normal ECG.”  Although subtle — there is no denying the above Descriptive Analysis findings of: i) Some ST elevation in multiple leads; ii) T wave inversion in lead aVL that could potentially reflect reciprocal changes; and, iii) Early transition with a taller-than-expected R wave in lead V1.
• I could not rule out the possibility of infero-postero MI at some point in time.
• I also could not rule out the possibility of potentially recent pericarditis — given at least slight ST elevation in more leads than is generally seen with repolarization variants.
• That said, my “sense” (intuitive feeling) — was that the above-described ECG findings in today’s case were probably not acute.
• FOLLOW-UP: It was clear that I needed to find out the history on this patient. It turned out that the patient was an elderly, non-English speaking woman. Through translators, we learned she had no cardiac symptoms in recent months. Physical examination at the time this ECG was obtained was unremarkable. The reason for obtaining the ECG appeared to be as part of a general assessment in a new patient. Whether this woman had a previous cardiac event was uncertain — as there were no medical records. Taking this history into account — I concluded there was nothing acute on her ECG, and no need for further investigation at this time given her elderly age and lack of cardiac symptoms.

 

PEARL #4: Each ECG tells a story. Without the clinical history — that story is incomplete. I find it humbling (and clinically essential) to appreciate — that identical findings on an ECG may lead to vastly different clinical interpretation depending on what is going on with the patient at the time the ECG was taken.

• Had the history in today’s case been that of a young adult with recent viral illness and pleuritic chest pain — this ECG could have been consistent with recent (or acute) pericarditis.
• Had the history been that of a middle-aged or older adult with chest pain that began over the previous day — one would not be able to rule out the possibility of recent (or acute) infero-postero MI on the basis of this single tracing.
• Therefore — clinical correlation is an essential part of our interpretation.
• That said, by definition — a computer interpretation is made without benefit of clinical history.

 

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ADDENDUM (3/27/2021): In the following 5 Figures — I post written summary from my ECG-2014-ePub on the ECG diagnosis of Acute Pericarditis.

• CLICK HERE — for a PDF of this 9-page file on Pericarditis that appears in Figures-3-thru-7.
• An additional criterion that has sometimes been cited as helpful for making the diagnosis of acute Pericarditis — is the ST/T Wave Ratio in Lead V6 (Please see My Comment at the BOTTOM of the page in the December 13, 2019 post of Dr. Smith's ECG Blog).

Figure-3: How to make the diagnosis of acute Pericarditis (ie, use of the History and Physical Exam).

Figure-4: ECG findings (4 Stages of acute pericarditis — with attention on diagnostic Stage I). How helpful is PR depression?

 

Figure-5: PR depression (Continued). Spodick’s sign. Acute MI vs Pericarditis vs Repolarization variants?

 

Figure-6: Acute MI vs Pericarditis. ECG findings with acute Myocarditis. Pericarditis vs Early Repolarization?

 

Figure-7: Pericarditis vs Early Repolarization? (Continued).

 

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Relevant ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23-LINK in Blog #205).
• ECG Blog #79 — Reviews which leads may normally manifest Q waves and/or T wave inversion.
• ECG Blog #81 — Reviews the Common Causes of a Tall R Wave in Lead V1.
• ECG Blog #207 — The ECG Computer Report: Friend or Foe?
• 
  
• Please see My Comment (at the BOTTOM of the page in the December, 13, 2019 post in Dr. Smith's ECG Blog) — regarding potential use of the ST/T Wave Ratio in Lead V6.

ECG Blog #207 (ECG MP-24) — The ECG Computer Report: Friend or Foe?

You are asked to interpret the ECG shown in Figure-1, obtained from a 52-year-old woman. Unfortunately, no additional information is available to you.

• The Computer Report interpreted this tracing as, “Sinus rhythm; Nonspecific T wave abnormality; Abnormal ECG”.

QUESTIONS:

• Do you agree with the computer report?
• How would YOU interpret this ECG?
• Is there anything to be concerned about on this ECG?

 

Figure-1: ECG obtained on a 52-year-old woman. No history available. Is there anything to be concerned about? (See text).

 

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NOTE #1: Some readers may prefer at this point to listen to the 9:00 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-24).

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Today’s ECG Media PEARL #24 (9:00 minutes Audio) — Review on the Pros and Cons of the Computerized ECG Report.

 

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NOTE #2: Written summary of “My Take” on Optimal Use of the ECG Computer Interpretations appears below in the Addendum (in Figure-2 and Figure-3).

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COMMENT: This case brings up the issue of how best to use (or not use) the Computerized ECG Report. Like it or not — virtually all ECG systems in modern offices, clinics, urgent care centers and hospitals make use of a computerized ECG report. How best should the ECG interpretation be used?

• NOTE: Regardless of whether you love or hate the computerized ECG interpretation — it is part of the medical record. Therefore — IF you disagree with what it says, you should cross out those computer statements that you feel are wrong.

 

MY Approach to the ECG in Figure-1:

As I’ve emphasized previously — it is always challenging when you are given a tracing to interpret without the benefit of any history. This is the situation in today’s case. I would recommend proceeding as follows:

• PEARL #1 — Do not look at the computer report until after you have completely interpreted the ECG in Figure-1. (My rational for emphasizing this point is explained in full in the above Audio Pearl #24).
• The rhythm in Figure-1 is regular at just under 100/minute. The QRS complex is narrow in all leads. P waves are present and upright in lead II, with a constant and normal PR interval — so the rhythm is sinus at a relatively fast rate.
• All intervals (PR, QRS, QTc) and the axis are normal.
• There is no chamber enlargement. (NOTE: I did not call LAA = Left Atrial Abnormality — because the negative component to the P wave in lead V1 is not deep — and I think the reason the P wave looks “notched” in inferior leads is the baseline artifact).
• Several leads show some fine baseline artifact. This makes it difficult to appreciate if there is (or is not) a QS for the very small-amplitude complex in lead III. Other than this — there are no Q waves.
• R wave progression is fairly normal, albeit transition (where the R wave becomes taller than the S wave is deep) is slightly delayed until lead V4-to-V5. 
• NONE of the above descriptive findings are of concern. However, assessment of ST-T wave appearance for the ECG in Figure-1 is of concern (See below).

 

Assessment of ST-T waves:

• Looking at all 3 inferior leads in Figure-1 together — raises concern that the T waves (especially in leads III and aVF) may be hyperacute. 
• PEARL #2: The "definition" as to what constitutes a "hyperacute" T wave is sometimes admittedly elusive, and dependent on interpreter experience + the clinical context (See ECG Blog #193 for full discussion of this subject). That said — Consider the possibility of “hyperacute” T waves when you see T waves that are disproportionately tall and/or fatter-at-their-peak or wider-at-their-base than should be expected given R wave and S wave amplitude in that lead. The more leads in a given lead area that show hyperacute changes — the greater the concern for acute OMI (Occlusion-based MI).
• In Figure-1 — QRS amplitude in leads III and aVF is admittedly tiny, and this makes it that much more difficult to assess what constitutes “larger-than-expected”. That said — T wave amplitude in lead III actually exceeds QRS amplitude in this lead — and the T wave is clearly more “voluminous” than one would normally expect. While not as obvious in lead aVF — the T wave in this 2nd inferior lead also looks more “voluminous” than might be expected. That said — the 3rd inferior lead ( = lead II) does not look overly abnormal.
• PEARL #3: Despite a lack of ST elevation in lead III, and a lack of J-point ST depression in lead aVL — there does appear to be that “magical” mirror-image opposite picture for the shape of reciprocal changes for the T waves in leads III and aVF (See ECG Blog #184 for full discussion of this subject). This finding should significantly increase your concern about possible ongoing or recent OMI.
• There is subtle-but-real T wave inversion in lead I. Given the absence of voltage criteria for LVH — I felt this subtle, shallow T inversion in lead I supports concern about reciprocal high-lateral ST depression.
• There is some nonspecific ST-T wave flattening in most of the chest leads — but this does not look acute.

 

BOTTOM LINE: The KEY point is that we need some History in order to know what to do with this tracing. 

• Finding a prior ECG on this patient could prove invaluable — because it is possible that the ECG changes we see in Figure-1 are old.
• In the absence of a prior ECG on this patient — IF the clinical history suggested new or recent symptoms for possible coronary disease — then the ECG in Figure-1 could represent an acute or recent event!
• An acute or recent event would be far less likely if this patient had no new or recent symptoms — which places the onus on us to find out the clinical history!
• Although the computer did recognize that the ECG in Figure-1 is abnormal and shows “T wave abnormality” — the computer failed to recognize the possibility of a recent or acute ongoing cardiac event. Hopefully the clinicians caring for this patient did not depend solely on the computer interpretation at the time they decided on management of this patient. 

 

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Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #193 — Discusses the concept of using the term, “OMI” ( = Occlusion-based MI) instead of STEMI — and — reviews the ECG findings to look for when your patient with chest discomfort does not manifest frank STEMI-criteria ST elevation on ECG.
• ECG Blog #184 — Reviews the “magical” mirror-image OMI relationship to look for between leads III and aVL.

 

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My Publications on Computerized ECG Interpretation include the following:

• Grauer K: Chapter 21 — Does the Computer Know Better? — from Grauer K: Practical Guide to ECG Interpretation (2nd Edition) — Mosby, St. Louis, 1998, pp 374-379.
• Grauer K, Kravitz L, Ariet M, Curry RW, Nelson WP, Marriott HJL: Potential Benefits of a Computer ECG Interpretation System for Primary Care Physicians in a Community Hospital. J Am Bd Fam Prac 1:17-24, 1989.
• Grauer K, Kravitz L, Curry RW, Ariet M: Computerized Electrocardiogram Interpretations: Are They Useful for the Family Physician? J Fam Prac 24:39-43, 1987.
• Grauer K, Curry RW: Chapter 11: Use of Computerized ECG Interpretation Programs — from Clinical Electrocardiography (Grauer & Curry) — Blackwell Scientific Publications, Boston, 1992, pp 418-425.

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ADDENDUM (3/23/2021): In the following 2 Figures — I review “My Take” on the Pros and Cons of the Computerized ECG Report (Section 13, contained in Figure-2 and -3 — is excerpted from Grauer K: ECG-2014-ePub, KG/EKG Press).

 

 

Figure-2: “My Take” on the Pros & Cons of Computerized ECG Interpretations (Please listen to my 9-minute ECG Audio Pearl above, in this post = ECG MP-24).

 

Figure-3: Example of hyperacute T waves missed by the Computer Report.