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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

S

I

Q

III

T

III

(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.