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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 6, November/December 2020
AFRICA 331
Posterior infarction: a STEMI easily missed
Lina Hähnle, Charle Viljoen, Julian Hoevelmann, Robert Gill, Ashley Chin
Abstract
Anterior ST-segment depression encompasses important
differential diagnoses, including ST-segment elevation
myocardial infarction, non-ST-segment elevation myocardial
infarction and pulmonary embolism. Diagnostic accuracy is
crucial, as this has important therapeutic implications. This
ECG case report reviews the electrocardiographic changes
seen in patients with chest pain and anterior ST-segment
depression.
Keywords: ECG, STEMI, NSTEMI, pulmonary embolism
DOI: 10.5830/CVJA-2020-059
A 65-year-old woman with a 30 pack-year smoking history,
hypertension, dyslipidaemia and type 2 diabetes mellitus woke
up with severe central crushing chest pain and autonomic
symptoms. She was rushed to her nearest emergency centre
where a 12-lead electrocardiogram (ECG) was performed (Fig.
1). This showed a sinus tachycardia, with narrow QRS complexes
and no Q waves. The ST-segment depression in the anterior leads
(V1 to V4) prompted the attending physician to acquire another
ECG, which extended the recording to include posterior leads
(V7, V8 and V9) (Fig. 2). This showed ST-segment elevation
in V7 to V9, confirming the diagnosis of an acute posterior
ST-segment elevation myocardial infarction (STEMI).
The patient was given loading doses of dual antiplatelet
therapy and taken for primary percutaneous coronary
intervention (PCI). Coronary angiography showed an acute
occlusion of the proximal circumflex artery (LCx), which was the
culprit lesion. The patient also had severe coronary artery disease
in both the right coronary artery and the left anterior descending
artery (LAD). (Fig. 3A, B). A drug-eluting stent (DES) was
inserted in the LCx to treat the culprit lesion, resulting in good
reflow. The patient was stabilised in the coronary care unit and
discharged on guideline-directed medical therapy. Percutaneous
intervention of the non-culprit lesions was planned as an elective
procedure.
Discussion
All patients who present with chest pain should have a 12-lead
ECG.1 The ECG should be scrutinised for any features that
might suggest myocardial ischaemia, infarction or pulmonary
embolism (Table 1). Prompt recognition of these life-threatening
conditions will aid in the institution of timeous and appropriate
revascularisation therapy.1,2
Hatter Institute for Cardiovascular Research in Africa,
University of Cape Town, Cape Town, South Africa
Lina Hähnle, BSc, MB BCh
Charle Viljoen, MB ChB, MMed, FCP (SA), charle.viljoen@uct.ac.za
Julian Hoevelmann, MD
Division of Cardiology, University of Cape Town, Cape
Town, South Africa
Charle Viljoen, MB ChB, MMed, FCP (SA)
Ashley Chin, MB ChB, FCP (SA), MPhil
Department of Internal Medicine III, Klinik Für Innere
Medizin III, Kardiologie, Angiologie, Internistische
Intensivmedizin, Universitätsklinikum des Saarlandes,
Saarland University, Homburg, Germany
Julian Hoevelmann, MD
Department of Medicine, University of Cape Town, Cape
Town, South Africa
Robert Gill, MB ChB, Dip HIV Man (CMSA), FCP (SA)
ECG Series
Table 1. ECG features of acute posterior STEMI, NSTEMI and acute PE
Acute posterior STEMI NSTEMI Acute PE
Q wave in III Only present if inferior STEMI involvement Should not be present May be present as part of SIQIIITIII
Dominant R in V1 Usually present and develops over days Should not be present Only present if RVH developed from chronic
pulmonary thromboembolic disease. Severe PE
may cause incomplete or complete RBBB.
S wave in I Should not be present Should not be present May be present as part of SIQIIITIII
ST-segment depression V1–V3 Usually present May be present May be present
ST-segment elevation V7–V9 Usually present Should not be present Should not be present
ST-segment elevation elsewhere Inferior ST-segment elevation may be present Should not be present Should not be present
T-wave inversion in V1–V3 May be present in the acute setting, followed
by upright T wave in V1
May be present (Wellens’ pattern) May be present
T-wave inversion in III May be present May be present May be present as part of SIQIIITIII
STEMI, ST-segment elevation myocardial infarction; NSTEMI, non-ST-segment elevation myocardial infarction; PE, pulmonary embolism; RBBB, right bundle
branch block; RVH, right ventricular hypertrophy;.
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 6, November/December 2020
332 AFRICA
Fig. 2. ST-segment elevation demonstrated in the posterior leads (V7, V8 and V9).
Fig. 1. A 12-lead ECG showing ST-segment depression in the anterior leads (V1 to V4).
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 6, November/December 2020
AFRICA 333
In normal physiology, the vectors at the end of depolarisation
and the beginning of repolarisation neutralise each other. On
the ECG, this manifests as a J point (start of ST-segment),
which is not deviated from the isoelectric line.3 This balance of
charge is maintained by Na+/K+ ATPase channels, which are
dependent on glucose. In coronary artery occlusion, the lack
of glucose supply causes malfunctioning of these ion-gated
channels, resulting in an imbalance of electrical charge across
the myocardial cell membrane. This imbalance in electrical
charge manifests as ST-segment deviation. Transmural ischaemia
leads to ST-segment elevation in leads overlying the ischaemia,
whereas sub-endocardial ischaemia can manifest as ST-segment
depression or T-wave inversion.4 However, in some cases,
ischaemia can be electrocardiographically silent.5
ST-segment depression can represent reciprocal changes of
ST-segment elevation recorded by leads opposite those overlying
the acute infarction (Table 1). Because the standard 12-lead
ECG does not include leads that overlie the posterior aspect of
the heart, ST-segment depression in the anterior leads should
prompt the acquisition of posterior leads (V7, V8 and V9) to
rule out posterior ST-segment elevation (Fig. 4).6,7 ST-segment
elevation in the posterior leads confirms the diagnosis of
posterior STEMI. If no ST-segment elevation is recorded in the
posterior leads, non-ST-segment elevation myocardial infarction
(NSTEMI) (Fig. 5) or pulmonary embolism (PE) (Fig. 6) should
be considered as alternative diagnoses.
Acute posterior STEMI can be accompanied with inferior
STEMI if the culprit lesion is proximal to the posterior
A
LAO CAU RAO CAU
B
Fig. 3. A. Left anterior oblique (LAO) caudal view demonstrated extensive coronary artery disease. The proximal left circumflex
artery (LCx) was totally occluded (culprit lesion) (red arrow), and the left anterior descending artery (LAD) was severely
diseased (blue arrow). The posterior descending artery (PDA) filled competitively from left to right collaterals (green arrow).
B. The culprit lesion was the proximal occlusion of the left circumflex artery (LCx), as shown in this right anterior oblique
(RAO) caudal view (red arrow). There was a long segment of severe disease in the left anterior descending artery (LAD)
(blue arrow).
V1 V2
V3
V4
V5
V6
Fig. 5. Sub-endocardial ischaemia (NSTEMI) can manifest as
ST-segment depression in the anterior leads.
V1 V2
V3
V4
V5
V6
V7
V8
V9
Fig. 4. Posterior transmural myocardial infarction (STEMI)
would cause ST-segment elevation in the posterior
leads, which in the anterior leads will manifest as
ST-segment depression (reciprocal changes).
A B
CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 6, November/December 2020
334 AFRICA
descending artery of the right coronary artery. However, isolated
posterior STEMI can occur if the culprit occlusion is in a
posterior lateral wall branch of the right coronary artery or in
the circumflex artery (as in this case). In a posterior STEMI, the
evolution of changes over days includes the development of a
dominant R wave in V1 (a reciprocal Q wave) or Q waves in V7
to V9 with a T wave that is usually upright in V1 (Table 1).
PE is an important differential diagnosis to be excluded in
the patient presenting with chest pain. This life-threatening
condition can be clinically indistinguishable from MI, as both
conditions may present with chest pain and/or dyspnoea. In
addition, a further confounder is that a massive PE can mimic a
MI on the ECG. Both posterior MI and PE could be associated
with a dominant R wave in V1 and ST and/or T-wave changes in
the anterior leads (Table 1).
Chronic pulmonary thromboembolic disease can cause right
ventricular hypertrophy (RVH) with a dominant R wave in
V1, but in acute PE the right ventricle has not had time to
hypertrophy. Severe cases of PE may cause incomplete or
complete right bundle branch block (RBBB).8 However, RBBB
could also be caused by MI.
Occasionally, patients present with the pathognomonic
SIQIIITIII (S wave in lead I, Q wave in lead III, T-wave inversion
in lead III), ST-segment changes and/or widespread T-wave
inversion. The mechanism for the ST-segment deviation and
T-wave inversion in the anterior leads seen in PE could be
explained by the strain on the right ventricle caused by the
sudden rise in pulmonary artery pressure.9 Whenever suspected,
compacted tomography pulmonary angiography (CTPA) would
be the diagnostic modality of choice for PE.2 As sinus tachycardia
is the most common ECG feature of acute PE, its absence makes
the diagnosis less likely.8
Because biomarkers such as troponins and CK-MB could be
elevated in STEMI, NSTEMI and PE, they should not be relied
on as the sole diagnostic modality. In this setting, imaging such
as coronary angiography and/or CTPA should be performed. 10
Accurate diagnosis of STEMI, NSTEMI or acute PE allows
for the timely institution of appropriate therapy. STEMI requires
emergency revascularisation in the form of PCI, or thrombolysis
if a PCI centre cannot be accessed within two hours of
diagnosis,1 whereas angiography is indicated within 24 hours
after presenting with a NSTEMI.4
Pain management and appropriate antiplatelet therapy form
part of the mainstay of therapy in both STEMI and NSTEMI.1,4
PE, however, requires anticoagulation. Systemic thrombolytic
therapy is recommended for PE with haemodynamic instability.
In centres with the necessary skill, percutaneous catheter-directed
therapy or surgical embolectomy could be considered in high-risk
PE when thrombolysis has failed or is contra-indicated.2
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V1 V2
V3
V4
V5
V6
Fig. 6. Acute pulmonary embolism causing right ventricular
strain, which translates to ST-segment depression in
the anterior leads.
