Summary
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.
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).
Fig. 1.
A 12-lead ECG showing ST-segment depression in the anterior leads (V1 to V4).
Fig. 2.
ST-segment elevation demonstrated in the posterior leads (V7, V8 and V9).
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.
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).ft anterior oblique (LAO) caudal view demonstrated extensive coronary artery disease. There was a long segment of severe disease in the left anterior descending artery (LAD) (blue arrow).
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
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;
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.
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).
Fig. 5.
Sub-endocardial ischaemia (NSTEMI) can manifest as ST-segment depression in the anterior leads.
Fig. 6.
Acute pulmonary embolism causing right ventricular strain, which translates to ST-segment depression in the anterior leads.
Acute posterior STEMI can be accompanied with inferior STEMI if the culprit lesion is proximal to the posterior 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
Contributor Information
Charle Viljoen, Email: charle.viljoen@uct.ac.za.
Julian Hoevelmann, Department of Internal Medicine III, Klinik Für Innere Medizin III, Kardiologie, Angiologie, Internistische Intensivmedizin, Universitätsklinikum des Saarlandes, Saarland University, Homburg, Germany.
Robert Gill, Department of Medicine, University of Cape Town, Cape Town, South Africa.
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