2007 terni, workshop interattivo, caso clinico 3

1. • A 65-year-old man presented to the Emergency
Department (ED), and he had a 2 ½ hrs history of
chest pain radiating to left arms and mandible.
Clinical Case(1)
• Anamnestic evaluation reveal that the patient’s past
medical history was of familiarity, obesity, hypertension,
for several years and for this he was taking beta-blocker
and losartan, and dyslipidemia, for which he was taking
nothing (no statin) . No ASA.
• He had a 30 pack-year previous smoking history.
• The onset of chest pain occurred when pt was
relieved by rest.
• Associated symptoms included shortness of breath,
nausea and lipotimia.

2. Clinical Case(1)
• Personal history reveal a previous AMI in ’91, treated
(HSR) with PCA on LAD artery and Posterior Inter-
ventricular right (PIV) artery whereas a pathologic
Obtuse Marginal Artery (OMA) was not treated
because complicated (no documentation).
• Pt reveal a subsequent coronary angiography evalutation in ’98
that confirm the patologic stenosis of OMA (no documentation)
with subsequent further indication to stress-test evalutation.
• Moreover, according with his cardiologist, no further stress test
evaluation was performed until now (9 yrs ago).

3. Clinical Case(1)
EKG (Emergency Departement)

4. Clinical Case(1)
- R wave ≥0.04s in V1 or V2
- ST segment depr. V1  V3
- R/S ratio ≥1 in V1 and V2.
EKG (Emergency Departement)
R
R
R
S
S
• BP was 150/80 mmHg, and
HR was 85/min, whereas
the rest of the exam was
unremarkable.

5. Clinical Case(1)
• First Line Therapy
- Oxigen
- Nitrate (iv)
- ASA 500 mg (iv)
- Eparin (bolus + cont.
infusion iv)
• No changes in symptom
• An ECHO evaluation
reveal Total Ackinesia of
apex and posterior LV wall
R
R
R
S
S
Intensive CCU

6. • Turn ECG upside down and
look at it from the back.
• Changes in V1 and V2 which
might be over-looked at
first glance, will be seen as
abnormal Q waves, ST
elevation and increased T
wave inversion(2)
.
• R>0.04s and R≥S V1, showed
a high specificity (>99%)
and a high positive
predictive value (91%).
• R≥0.04s and R≥S V2, showed
95% of specificity, and 73%
positive predictive value.
Clinical Case(1)
Intensive CCU

7. • Turn ECG upside down and
look at it from the back.
• Changes in V1 and V2 which
might be over-looked at
first glance, will be seen as
abnormal Q waves, ST
elevation and increased T
wave inversion(2)
.
• R>0.04s and R≥S V1, showed
a high specificity (>99%)
and a high positive
predictive value (91%).
• R≥0.04s and R≥S V2, showed
95% of specificity, and 73%
positive predictive value.
Clinical Case(1)
Intensive CCU

8. • Turn ECG up-side down and look at it from the
back.
• Changes in V1 and V2 which might be over-looked
at first glance, will be seen as abnormal Q
waves, ST elevation and increased T wave
inversion(2)
.
• R>0.04s and R≥S V1, showed a high specificity
(>99%) and a high positive predictive value (91%).
• R≥0.04s and R≥S V2, showed 95% of specificity,
and 73% positive predictive value.
Clinical Case(1)
• Tall R waves in anterior leads (V1, V2 and V3)
are the electrical equivalent of Q waves in
the posterior leads (V7, V8, V9) (1,2)

9. Clinical Case(1)

10. Clinical Case(1-2)
• Tall R waves in
anterior leads (V1, V2
and V3) are the
electrical equivalent
of Q waves in the
posterior leads (V7,
V8, V9) (1,2)
• Turn ECG upside
down and look at
it from the back.

11. Clinical Case(1)

12. Clinical Case(1)
• No absolute or relative
CI were present to
fibrinolitic therapy, and
then was administrated
with immediately
disappeared of symptom
Intensive CCU
R
R
R
S
S
• 10 hrs after fibrinolisis,
pt develop cerebral
symptom with evidence at
TC scan of parenchimal
hemorragic expansion

13. Clinical Case(1)
Considerations
• Posterior wall of LV is typically supplied by the left
Cx coronary artery(1)
and is a challenging area for
identifying acute ischemia and AMI.
• During transmural AMI, the characteristic ST
-segment elevations seen in other areas of the
heart are not seen in I-PMI on standard 12-lead
EKG (1,2)
• Conventional ECG, even with correct placement of the
electrodes, may miss a true I-PMI

14. • Recently a consensus report from the ACC that was
endorsed by the American College of Emergency
Physicians (16)
use the presence of tall and prominent
R waves (typically defined as an R/S ratio≥1) in V1
and V2 to define posterior MI with ST horizontal or
down-sloping depression and carachteristic
symptoms .
• Different techniques have been developed to identify I-PMI,
including the use of posterior leads V7, V8 and V9
(3–10, 11, 12)
Clinical Case(1)

15. Clinical Case(1)
• It has been suggested that
tall R waves in anterior
leads (V1, V2 and V3) are
simply the electrical
equivalent of Q waves in
the posterior leads (V7, V8
and V9)(1,2)
• If acute I-PMI was
suspected in the ED, these
pt should be considered for
thrombolytic therapy or –
if possible – to immediate
interventional Cath. Lab. (3–6)

16. • This pt presented with suggestive symptom, previous
AMI and PCA procedure, several risk factor and EKG
analisis of tall R waves in V1,V2,V3 an down-sloping ST
depression in V1  V4 and a R/S ratio≥1 in V1 and V2
Clinical Case(1)
• No EKG signs reveal a previous MI
• ECHO analysis reveal ackinesia of apex and posterior
LV wall
• No Absolute or Relative CI were present for
fibrinolitic therapy
• Symptoms immediately disappeared after rTPA

17. • The true incidence of I-PMI is unknown but has been
reported between 0-12% (6,7,9,18)
of AMI when posterior
leads V7 through V9 were obtained.
• If this were the case, these two findings would
always occur simultaneously on a 15-lead ECG (a 12-
lead ECG + posterior leads).
Clinical Case(1)

19. References(1)
1. Topol EJ, Van De Werf FJ. Acute myocardial infarction: Early
diagnosis and management. In: EJ Topol, ed. Textbook of
Cardiovascular Medicine. Philadelphia: Lippincott Williams and
Wilkins, 2002: 385-419.
2. Alexander RW, Pratt CM, Ryan TJ, Roberts R. ST-segment
elevation myocardial infarction: clinical presentation, diagnostic
evaluation, and medical management. In: Fuster V, Alexander
RW, ORourke RA, eds. Hursts The Heart. New York: McGraw
Hill, 2004: 1277-349.
3. Oraii S, Maleki M, Tavakolian AA, et al. Prevalence and outcome
of ST-segment elevation in posterior electrocardiographic leads
during acute myocardial infarction. J Electrocardiol 1999; 32:275-8.
4. Schamroth L. Posterior wall myocardial infarction. In: The 12-lead
Electrocardiogram, Book 1 (of 2). Boston: Blackwell, 1989:176-80.

20. References(1)
5. Bough EW, Boden WE, Korr KS, Gandsman EJ. Left ventricular
asynergy in electrocardiographic “posterior” myocardial infarction.
J Am Coll Cardiol 1984; 4:209-15.
6. Agarwal JB, Khaw K, Aurignac F, LoCurto A. Importance of
posterior chest leads in patients with suspected myocardial
infarction, but nondiagnostic, routine 12-lead electrocardiogram.
Am J Cardiol 1999; 83:323-6.
7. Huey BL, Beller GA, Kaiser DL, Gibson RS. A comprehensive
analysis of myocardial infarction due to left circum.ex artery
occlusion: comparison with infarction due to right coronary artery
and left anterior descending artery occlusion. J Am Coll Cardiol
1988; 12:1156-66.
8. Chaitman BR. Posterior myocardial infarction revisited. J Am
Coll Cardiol 1988; 12:167-8.

21. References(1)
9. Wang SF, Drew BJ. New electrocardiographic criteria for posterior
wall acute myocardial ischemia validated by a PTCA model of AMI.
Am J Cardiol 2001; 87:970-4.
10. Madird WL, Sanmarco ME, Gaarder TG, Selvester RH. Circum.ex
occlusion and posterior MI, diagnostic criteria and automated ECG
analysis programs. In: Bailey JJ, ed. Computerized Interpretation of the
ECG. XI. Proceedings of the Engineering Foundation Conferences. New
York: Engineering Foundation, 1986: 37-44.
11. Casas RE, Marriott HJL, Glancy DL. Value of leads V7-V9 in
diagnosing posterior wall AMI and other causes of tall R waves in V1-V2.
Am J Cardiol 1997; 80:508-9.
12. OKeefe JH, Sayed-Taha K, Gibson W, et al. Do patients with
left circum.ex coronary artery-related AMI without ST-segment
elevation bene.t from reperfusion therapy?Am J Card. 1995; 75:718-20.

22. • A 72-year-old woman complained of intermittent
chest pain for 3dys, which became severe and
continuous 4hs before presentation.
Clinical Case(2)
• Her cardiovascular risk factors were NIDDM for 30
yrs, hypertension for ten yrs and dyslipidaemia.
• BP was 148/74 mmHg, and HR was 82/min, whereas
the rest of the examination was unremarkable.

23. Clinical Case(2)

24. • Normal SR, tall R waves in V1  V3
• R wave >0.04s in V1, V2 and V3
• ST segment depression in V1-V4.
• Lateral and inferior leads did not
demonstrate T elevation.
• The EKG done in the ER; what
is the diagnosis?
Clinical Case(2)

25. • Coronary angiography showed an
occlusion of the proximal LCxCA
• Distal L-ADA 80% stenosis, a
dominant RCA with a 60-70%
stenosis in the postero-lateral
branch.
• PCA to the proximal LCxCA was
performed and balloon angioplasty
was also done to the obtuse
marginal branch of the LCxCA.
• A good final result with TIMI3
flow was obtained with resolution
of chest pain.
Clinical Case(2)

26. Clinical Case(2)
BEFORE AFTER

27. • I-PMI occurs in the posterior or postero-basal LV wall,
is rare and usually associated with an inf. or lat. MI(1,2)
.
DISCUSSION
Clinical Case(2)
• Incidence has been estimated at 3-4% of all AMI(3)
.
• ECG of posterior MI as described by Schamroth(4)
are:
- R wave ≥0.04s in V1 or V2
- Upright T waves in contiguous right
precordial leads
- ST segment depression in V1  V3
• R/S ratio ≥1 in leads V1 and V2.
• As MI evolves ST segment depression
decreases and the upright T amplitude
increases.

28. - R wave ≥0.04s in V1 or V2
- Upright T waves in contiguous right
precordial leads
- ST segment depression in V1  V3
• R/S ratio ≥1 in leads V1 and V2.
• As MI evolves ST segment
depression decreases and the
upright T amplitude increases.
EKG criteria
Clinical Case(2)

29. • Turn ECG upside down and
look at it from the back.
• Changes in V1 and V2 which
might be over-looked at first
glance, will be seen as abnormal
Q waves, ST elevation and
increased T wave inversion(2)
.
• R>0.04s and R≥S V1, showed a
high specificity (>99%) and a
high positive predictive value
(91%).
• R≥0.04s and R≥S V2, showed
95% of specificity, and 73%
positive predictive value.
Clinical Case(2)

30. • I-PMI has been found to be always due to LCX
occlusion(6)
.
• In another study, an abnormal R wave in V1 had a 96%
specificity for LCxCA vs RCA-related infarction, but
a sensitivity of only 21%(7)
.
• In addition, all patients with LCxCA-related MI and
abnormal R wave in lead V1, had multivessel disease(7)
• In spite of these, true posterior MIs are usually well-
tolerated(1)
.
• Conventional ECG, even with correct placement of the
electrodes, may miss a true I-PMI
Clinical Case(2)

31. • The use of additional chest leads on the posterior
thorax between the angle of the scapula and the
vertebral column, at the level of the 5th
intercostal
space (leads V7-9), will increase the sensitivity
through detection of Q waves(8)
.
• Some have questioned whether the conventional 1mm
ST elevations in the posterior leads were appropriate
and it has been found that the currently-used
criterion of 1mm to detect ischaemia is inadequate to
demonstrate ST segment elevation in the posterior
leads during LCxCA occlusion.
Clinical Case(2)

32. Possible mimics of ECG changes in a posterior
MI include other causes of tall R waves in V1:
– Right ventricular hypertrophy
- Right bundle branch block
- Wolf-Parkinson-White syndrome
- Normal variants
- Ischaemia of the anterior wall of the LV also
produces ST segment depression in leads V1-3 and
this must be differentiated from posterior MI.
Isolated PMI
Clinical Case(2)

33. • A 53-year-old man presented to the ED, and he had a
4 ½ hrs history of chest pain radiating to both arms.
• The onset of chest pain occurred while walking and
was not relieved by rest.
• Associated symptoms included shortness of breath,
nausea and diaphoresis. The patient’s only past
medical history was of hypertension, for which he was
taking losartan, and no other medications.
• He had a 30 pack-year smoking history.
Clinical Case(3)

34. • BP 177/102mmHg, HR 72b/m
RR 20 breaths/min, T. 36,5°C.
• Prompted by the ST depres-
sion and typical presentation
for MI, a reading for post.
leads V7 through V9 was
immediately obtained and
demonstrated ST elevation
• Standard management
including M.O.N.A. and heparin
• ED ECG showed downsloping
ST depression mostly
prominent in leads V1 V4
and tall R wave in V3 (not in
V1/V2)
Clinical Case(3)

35. • A cardiology consultation was obtained, and the pt
was taken promptly to the Cath. Lab, whereas
Troponin I and other laboratory values were pending
at that time.
• Cath. revealed total occlusion of the LCA, a normal
LDA, a normal left main artery, a 60% proximal lesion
of a small branch of the LCA and luminal irregularities
in LDA.
• Pt underwent uncomplicated stenting of the LCA, and
a subsequent Echo evaluation identified moderate to
severe posterior wall hypokinesis and was otherwise
unremarkable.
Clinical Case(3)

36. • Pt’s initial troponin I level was 1.4 ng/mL (range 0.0–
1.2 ng/mL) with a peak of 172 ng/mL 7 hours after
presentation. Five hours after presentation a single
CK measurement was obtained and was 3730 U/L with
a CK-MB of 191 ng/mL (relative index 5.1%).
• The only complication identified during hospitalization
was a single uncomplicated episode of hematemesis.
• The pt otherwise did well and was discharged home on
hospital day 4.
Clinical Case(3)

37. • No EKG ST elevat nor tall R
V1 or V2
• EKG reveal ST depression
in V1 and V2 and an up-right
T wave in V2
• ST elev. in leads V8 and V9.
• True incidence is unknown but has reported
between 0% to 12% (6,7,9,13,18)
when posterior
leads V7 through V9 is obtained
• Identif. pts with I-PMI with
standard EKG could be
challenging(1,2,10,12–14)
due to the
location of the AMI(1,2,14)
Clinical Case(3)

38. Clinical Case(3)
Introduction
• Posterior wall of LV is typically supplied by the left Cx
coronary artery (1) and is a challenging area of the heart
in which to identify acute ischemia and MI.
• During transmural AMI, the characteristic ST-segment
elevations seen in other areas of the heart are not seen
in isolated posterior myocardial infarctions (IPMI) on
standard 12-lead EKG (1,2)
• If A-IPMI were identified promptly in the emergency
department (ED), these patients could be considered
for thrombolytic therapy or immediate interventional
Cath. Lab. (3–6)

39. • Recently a consensus report from the ACC that was
endorsed by the American College of Emergency
Physicians (16)
use the presence of tall R waves
(typically defined as an R/S ratio ≥ 1 in V1 and V2 to
define posterior MI with ST depression and
carachteristic symptoms .
• Few techniques have been developed to identify IPMI,
including the use of posterior leads V7, V8 and V9 (3–10)
body surface mapping (11,12)
and the development of
specific EKG criteria other than ST elevation (13-15)
• We present a case of an acute I-PMI in which the ECG
lacked tall R waves in leads V1 and V2 and the use of
posterior leads identified ST-segment elevation that
changed pt management resulting in the pt going
promptly to the Cath. Lab.
Clinical Case(3)

40. • Current diagnostic criteria for acute I-PMI include:
horizontal STsegment depression, tall R waves, and
prominent upright T waves in V1, V2 and/or V3 (1,2)
Discussion
• In this case we had down-sloping ST segments and
lacked tall R waves in V1 and V2, an up-right T wave in
V2 and a tall R wave in V3 were present. It has been
suggested that tall R waves in anterior leads (V1, V2
and V3) are simply the electrical equivalent of Q
waves in the posterior leads (V7, V8 and V9)(1,2)
• If this were the case, these two findings would
always occur simultaneously on a 15-lead ECG (a 12-
lead ECG + posterior leads).
• Correlation between anterior R waves, posterior Q waves, and
the time course of their development in I-PMI needs further
study.

41. Clinical Case(1)

42. Clinical Case(1-2)