A middle-aged patient with lung cancer had presented to clinic complaining of generalized malaise, cough, and chest pain. He had an ECG in clinic which worried the providers because of possible inferior MI, and they sent him to the ED.
Here is that ECG:
There is sinus tachycardia.
There is ST Elevation at the J-point, relative to the PQ junction (end of PR segment) in II, III, aVF.
There is some T-wave inversion in aVL (which is a soft sign of inferior MI, but no reciprocal ST depression).
Notice, however, that there is profound PR depression. The apparent ST elevation is mostly just relative to the depressed PR segment.
He was sent to the ED and had this ECG at t = 1 hour:
There are several issues which mitigate against acute inferior MI, and these are the Learning Points:
1. Symptoms other than chest pain (malaise, cough in a cancer patient)
2. Sinus tachycardia, which exaggerates ST segments and implies that there is another pathology. I have always said that tachycardia should argue against acute MI unless there is cardiogenic shock or 2 simultaneous pathologies. We showed this in a recent analysis of UTROPIA data (see abstract below).
3. PR depression, which suggests pericarditis
4. Absence of large inferior T-waves, which are very common in OMI (acute occlusion MI).
5. Absence of any ST depression in aVL. (We showed that absence of STD i aVL rules out inferior MI, even subtle inferior MI, with 99% accuracy. We also showed that, of 47 cases of pericarditis with ST elevation, none had ST depression in aVL.) T-wave inversion in aVL was also very sensitive, but not as good as ST depression.
The patient underwent an emergent formal echocardiogram to look for wall motion abnormality:
The patient turned out to be septic from pneumonia, received 3 liters of fluids and antibiotics, and had the following ECG recorded:
ECG (t = 7 hours)
Here is that ECG:
 |
| What do you think? |
There is sinus tachycardia.
There is ST Elevation at the J-point, relative to the PQ junction (end of PR segment) in II, III, aVF.
There is some T-wave inversion in aVL (which is a soft sign of inferior MI, but no reciprocal ST depression).
Notice, however, that there is profound PR depression. The apparent ST elevation is mostly just relative to the depressed PR segment.
He was sent to the ED and had this ECG at t = 1 hour:
 |
| Similar |
There are several issues which mitigate against acute inferior MI, and these are the Learning Points:
1. Symptoms other than chest pain (malaise, cough in a cancer patient)
2. Sinus tachycardia, which exaggerates ST segments and implies that there is another pathology. I have always said that tachycardia should argue against acute MI unless there is cardiogenic shock or 2 simultaneous pathologies. We showed this in a recent analysis of UTROPIA data (see abstract below).
3. PR depression, which suggests pericarditis
4. Absence of large inferior T-waves, which are very common in OMI (acute occlusion MI).
5. Absence of any ST depression in aVL. (We showed that absence of STD i aVL rules out inferior MI, even subtle inferior MI, with 99% accuracy. We also showed that, of 47 cases of pericarditis with ST elevation, none had ST depression in aVL.) T-wave inversion in aVL was also very sensitive, but not as good as ST depression.
The patient underwent an emergent formal echocardiogram to look for wall motion abnormality:
The estimated left ventricular ejection fraction is 63 %.
No wall motion abnormality .
Pericardial effusion very small
No evidence for pericardial tamponade.
Multiple fibrin strands in (lateral) pericardial space, c/w fibrinous pericarditis
FINDINGS C/W WITH FIBRINOUS PERICARDITIS AND SUSPICIOUS FOR
EFFUSIVE-CONSTRICTIVE PERICARDITIS
Here is a still image from a bedside cardiac ultrasound:
 |
| See small effusion in upper right of image |
The patient turned out to be septic from pneumonia, received 3 liters of fluids and antibiotics, and had the following ECG recorded:
ECG (t = 7 hours)
 |
| Fluids have resolved the sinus tachycardia. ST elevation persists, but there is less PR depression (interesting!) Still no reciprocal ST depression in aVL |
TITLE:
The Negative Predictive Value of Tachycardia for Type I MI in
Hemodynamically Stable Patients with Chest Pain
AUTHORS:
Daniel H. Lee, MD – Department of Emergency Medicine, Hennepin County
Medical Center, Minneapolis, MN
Yader Sandoval, MD - Department of Cardiovascular Medicine, Mayo Clinic,
Rochester, MN.
Fred S. Apple, Ph.D. - Department of Laboratory Medicine, Hennepin
County Medical Center; Professor, University of Minnesota School of Medicine
Stephen W. Smith, MD – Department of Emergency Medicine, Hennepin County
Medical Center, Professor, University of Minnesota School of Medicine,
Minneapolis, MN
ABSTRACT:
Background:
Patients with type 1 myocardial infarction with normal left ventricular
function that are hemodynamically stable do not usually manifest with sinus
tachycardia. The goal of the present analysis was to examine whether the
presence of tachycardia identified patients unlikely to have type 1 myocardial
infarction.
Methods:
This was a secondary post-hoc analysis of a prospective, observational
data study of 1927 consecutive ED patients over 4 months who had at least 1
contemporary troponin I (cTnI) resulted.
Inclusion criteria were chest pain, ≥ 2 serial cTnI, sinus rhythm, and ≥
1 ECG.
Exclusion criteria included age <18 b="" years="">SBP <100 b="" echocardiogram="" ejection="" fraction="" mi="" mmhg="" st-elevation="" with="">, pregnancy, and
trauma.
All cases with at least one elevated cTnI were adjudicated into
specific MI type (or no MI) by two clinicians who reviewed all medical records.
Patients were stratified according to presence or absence of type I MI, and of
heart rate (HR) > 99 bpm, and > 120 bpm on presenting ECG. All ECGs were
coded by an expert clinician as having ST-elevation, ST-depression, T-wave
inversion [ST/T abnormalities, (ST/T-A)], or none of the above.
Results:
877 patients were included, of whom 135 had HR > 99 bpm (742 ≤ 99
bpm) and 23 had HR > 120 bpm (854 ≤ 120 bpm). Of the 877, 58 (6.6%) had type I MI and 819
did not; 4 of 58 (6.9%) with type I MI, and 131 of 819 (16.0%) without, had HR
> 99 (P=0.02). The negative
predictive value (NPV) of HR > 99 for type I MI was 97.04% (95%CI 92.6-98.8)
and the negative likelihood ratio [(-)LR] was 0.43 (95%CI 0.17-1.12). 23 had HR > 120 bpm (854 ≤ 120 bpm);
0/23 with HR > 120 bpm had type 1 MI.
The NPV of HR > 100 bpm for type I MI among those with ST/T-A was the
same as in those without, at 92.0% (95%CI 74.7.6-97.8). Of 23 patients with HR > 120 bpm, 4 had
ST/T-A. See Table for diagnostic
utility.
Conclusion:
In hemodynamically stable patients with chest pain, sinus tachycardia
aids in the identification of patients unlikely to have type I MI, especially
in those with HR > 120 bpm.
-----------------------------------------------------------
Comment by KEN GRAUER, MD (6/17/2018):
-----------------------------------------------------------
Excellent case with insightful learning points explaining why these serial tracings are not indicative of acute inferior infarction. I’ll add the following 2 comments:
- i) This patient presumably has effusive-constrictive pericarditis. ECG findings of constrictive pericarditis are generally not overly helpful clinically. Low voltage and nonspecific ST-T wave abnormalities are commonly seen but non-diagnostic. Electrical alternans is generally only seen with a large pericardial effusion. Other nonspecific findings may include P wave abnormalities, PR segment deviations, and atrial arrhythmias — though none of these findings are seen in a majority of patients. So while the ECG will often not be normal with constrictive pericarditis — nonspecificity of ECG findings offers little diagnostic assistance.
- ii) All 3 of the ECGs in this case manifest Schamroth’s Sign! This is the presence of an almost “null vector” in standard lead I (ie, P wave, QRS complex and T wave all under 2mm in size). While sensitivity of this sign is very low — its presence is highly suggestive of longstanding and severe pulmonary disease. A small percentage of patients with effusive-constrictive pericarditis are found to have RVH — with potential explanation for this finding as a sequela of fibrous band narrowing of the RV outflow tract (Mehta A et al: Constrictive Pericarditis. Clin Cardiol 22:334-344, 1999).
The ECG diagnosis of RVH is often challenging. On occasion, I have found awareness of Schamroth’s sign to be helpful in recognizing probable severe pulmonary disease with RVH when other ECG findings were inconclusive.
