Tearing Back Pain with Inferior ST Elevation: Antiplatelets Before Imaging?
A 58-year-old man with a 15-year smoking history and treated hypertension presents 25 minutes after the sudden onset of severe tearing pain between the scapulae while lifting a gas cylinder. The pain migrated to the mid-back and he calls it 'the worst of my life'. He is pale and diaphoretic. Blood pressure is 178/96 mmHg in the right arm and 148/84 mmHg in the left; heart rate 104/min and regular; SpO2 96% on room air. Both radial pulses are palpable but the left is noticeably weaker. The ECG shows 2 mm ST elevation in leads III and aVF with reciprocal depression in aVL. Chest radiograph shows a widened upper mediastinum. Point-of-care troponin is 0.08 ng/mL (cut-off 0.04). The CT angiography suite is in the adjacent building and is free now; the catheterisation laboratory is 40 minutes away. Potassium 4.1 mmol/L, creatinine 96 µmol/L.
1. Do you give aspirin and heparin and activate the cath lab for primary PCI, or do you obtain CT angiography first? Justify your decision against the alternative.
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Decision: withhold aspirin, heparin and P2Y12 inhibitors, and go to CT angiography now.
Reasoning:
- This man has several high-risk features for acute aortic dissection: abrupt tearing pain, migration to the back, a pulse deficit and an interarm systolic difference of 30 mmHg. With high-risk features present, a D-dimer cannot exclude dissection and imaging is mandatory; risk scores exist to select patients for CT, not to replace it.
- The inferior ST elevation is entirely compatible with right coronary ostial involvement by a type A dissection. Treating this as a primary STEMI would mean heparin, dual antiplatelet therapy and catheter manipulation of the ascending aorta, all of which risk extension, tamponade, and uncontrollable bleeding at surgery. Thrombolysis in this setting is a recognised cause of death.
- Practicality: the CT suite is adjacent and free, the cath lab is 40 minutes away, and CT still leaves the cath lab available if dissection is excluded and true STEMI confirmed.
What to do while waiting: IV opioid for pain, continuous bilateral BP monitoring, large-bore access, group and save, and have esmolol ready. Do not start rate control on suspicion alone in a patient who may have a STEMI needing PCI, but be ready to bring heart rate to around 60/min and systolic BP to 100-120 mmHg the moment dissection is confirmed.
Exceptions: if he becomes unstable with tamponade or arrest, do a bedside echo first and take him to theatre rather than CT.
2. CT confirms a Stanford type A dissection from the aortic root to the iliac arteries, with no pericardial effusion. Outline your immediate management, including haemodynamic targets, and explain what should happen about the ST elevation.
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Immediate priority: emergency cardiothoracic surgery. Type A dissection is a surgical emergency; every hour of delay increases mortality, so the call to the surgeon and the operating theatre happens in parallel with stabilisation, not after it.
Haemodynamics:
- Anti-impulse therapy: IV esmolol titrated to heart rate around 60/min, then add a vasodilator (nitroprusside or nicardipine) to bring systolic BP to 100-120 mmHg. Reduce heart rate first: vasodilators alone cause reflex tachycardia and increase dP/dt, which propagates the false lumen.
- If a new early diastolic murmur of aortic regurgitation is heard, be cautious with beta-blockade, because the compensatory tachycardia maintains forward flow; use a vasodilator and involve the surgeon urgently.
- Analgesia with IV opioid, two large-bore cannulae, cross-match 4-6 units, correct coagulopathy, keep the patient calm and strictly bed-rested.
- Do not give heparin before cardiopulmonary bypass unless the surgeon asks; do not give antiplatelets or thrombolysis.
The ST elevation is not treated with reperfusion. It reflects ostial RCA compromise and usually resolves after aortic root repair; the surgeon must know about it, and the patient should be consented for concomitant coronary revascularisation. If there is limb, mesenteric or renal malperfusion, that is an additional reason for immediate surgery, not for endovascular fenestration in a type A.
Afterload reduction alone, or a delay to repeat troponin or echocardiography, is the classic error in this scenario.