Cardiovascular · Moderate
This case is fictional and exists for study. It describes no real patient.
58 years · male
A 58-year-old male presents to the Emergency Department with severe, crushing substernal chest pain radiating to his left arm and jaw that started 2 hours ago. He reports associated nausea and profuse sweating. His past medical history includes hypertension and type 2 diabetes mellitus, for which he takes amlodipine and metformin. He is a current smoker with a 30 pack-year history. On clinical examination, he appears anxious and diaphoretic. Auscultation of the heart reveals normal S1 and S2 with no gallop or murmurs. Chest auscultation demonstrates clear lung fields bilaterally.
Vital signs
- HR
- 98 bpm
- BP
- 145/90 mmHg
- RR
- 20/min
- Temp
- 36.8 °C
- SpO₂
- 96%
Examination findings
- Diaphoretic and anxious appearance
- S1 and S2 present, no murmurs or friction rub
- Lungs clear to auscultation bilaterally
- 12-lead ECG shows 2.5 mm ST-elevation in leads II, III, and aVF with reciprocal ST-depression in I and aVL
Investigations
| High-sensitivity Cardiac Troponin T | 520 ng/L | reference: <14 |
| Serum Creatinine | 88 µmol/L | reference: 60-110 |
| Haemoglobin | 14.2 g/dL | reference: 13.0-17.0 |
Question 1 of 3
Based on the clinical presentation and investigation findings, what is the most likely diagnosis?
The patient presents with classic ischaemic chest pain radiating to the jaw and arm, diaphoresis, elevated cardiac troponin, and ECG evidence of ST-segment elevation (>1 mm in adjacent limb leads) in leads II, III, and aVF with reciprocal ST depression in I and aVL. This meets the criteria for acute inferior STEMI. NSTEMI would not show persistent ST elevations. Acute pericarditis typically presents with widespread concave ST elevation, PR depression, and pleuritic pain relieved by sitting forward. Gastroesophageal reflux disease does not cause troponin elevation or ST elevation.
Teaching point: ST-segment elevation in leads II, III, and aVF with reciprocal depression in I and aVL is diagnostic of an acute inferior STEMI.
Question 2 of 3
What is the most appropriate next step in management regarding reperfusion for this patient, assuming a primary PCI-capable facility can be reached within 60 minutes?
Primary PCI is the preferred reperfusion strategy for patients with STEMI presenting within 12 hours of symptom onset, provided it can be performed within 120 minutes of diagnosis. Thrombolysis is indicated only if primary PCI cannot be delivered within 120 minutes. CT pulmonary angiogram is indicated for pulmonary embolism, not STEMI. Transferring to an outpatient clinic is unsafe and inappropriate for an acute coronary syndrome.
Teaching point: Primary PCI is the treatment of choice for acute STEMI when accessible within 120 minutes of diagnosis.
Question 3 of 3
Which medical therapy regimen should be administered immediately as part of acute medical management prior to emergency intervention?
Dual antiplatelet therapy (DAPT) consisting of a loading dose of aspirin (300 mg) and a second antiplatelet agent (typically ticagrelor 180 mg or prasugrel) should be administered as soon as possible in acute STEMI unless contraindicated. Low-dose monotherapy (75 mg aspirin or clopidogrel) does not provide rapid, sufficient platelet inhibition for acute management. Heparin alone without dual antiplatelet therapy is inadequate treatment for STEMI.
Teaching point: Immediate dual antiplatelet therapy (aspirin loading dose plus a P2Y12 inhibitor) is essential early medical management in acute STEMI.
Key learning points
- Inferior STEMI is characterised by ST-segment elevation in leads II, III, and aVF with reciprocal ST-depression in leads I and aVL.
- Primary PCI is the gold-standard reperfusion treatment for STEMI if delivered within 120 minutes of diagnosis.
- Dual antiplatelet therapy (aspirin 300 mg load plus ticagrelor/prasugrel/clopidogrel load) must be initiated immediately upon diagnosis of STEMI.
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