A 58-year-old man with long-standing hypertension arrives forty minutes after sudden chest pain that went straight through to his back. The ECG shows ST elevation in II, III and aVF with reciprocal change in aVL. The nearest cath lab is three hours away, and a nurse is already drawing up the thrombolytic. Everything points to inferior STEMI, until someone notices that his left radial pulse is weaker than the right. In that moment, one question separates a life-saving treatment from a fatal one.
Key points
- Type A aortic dissection can extend into the coronary ostia, most often the right, and present as inferior STEMI.
- Before any thrombolytic, anticoagulant or antiplatelet loading dose, ask: could this be aortic dissection?
- Bedside clues include tearing or migrating pain, a pulse deficit or inter-arm systolic difference above 20 mmHg, a new aortic regurgitation murmur and a neurological deficit with pain.
- The Aortic Dissection Detection Risk Score (ADD-RS) structures that suspicion; it does not replace imaging.
- Bedside echo can raise suspicion quickly, but CT aortography is the test that confirms or excludes the diagnosis.
Why the right coronary artery?
In Type A dissection the intimal tear usually begins in the ascending aorta, and the false lumen can propagate proximally into the aortic root. When it reaches a coronary ostium, flow is compromised either by the dissection flap obstructing the ostium or by the dissection extending into the coronary artery itself. The right coronary ostium is the one most commonly involved, which is why the ECG so often looks like an inferior, and sometimes right ventricular, infarction. Left main involvement is less frequent and is often catastrophic.
The ECG is genuinely abnormal, the troponin will rise and the pain is real. Nothing about the coronary picture is false. The error lies only in assuming the cause is plaque rupture.
The question to ask before any thrombolytic or anticoagulant
Thrombolysis, heparin, potent P2Y12 loading and glycoprotein IIb/IIIa inhibitors are all routine in STEMI and all potentially lethal in dissection, where they can convert a contained false lumen into rupture, haemopericardium or uncontrollable bleeding. The pause needed is short. Before giving any of these, the team should be able to answer: is there anything in the history, examination or imaging to suggest aortic dissection?
This is one of the classic traps covered in our pillar guide to the ten cardiac emergencies every physician must know, and it deserves its own checklist.
Bedside clues worth sixty seconds
| Clue | What to look for | Caution |
|---|---|---|
| Pain character | Abrupt onset, maximal at the start, tearing or ripping, radiating to the back or migrating downward | Painless dissection occurs, particularly in older patients and those presenting with syncope or stroke |
| Pulse deficit | Absent or weak radial, carotid or femoral pulse; systolic difference of more than 20 mmHg between arms | Measure both arms routinely; absence does not exclude dissection |
| New AR murmur | Early diastolic murmur at the left sternal edge, wide pulse pressure | Easily missed in a noisy department; listen sitting forward if possible |
| Neurological deficit | Hemiparesis, altered consciousness, paraplegia or limb ischaemia with chest pain | A “stroke with chest pain” is dissection until proven otherwise |
| Chest radiograph | Widened mediastinum, abnormal aortic contour, left pleural effusion | A normal film does not exclude dissection |
| Haemodynamics | Hypotension or shock out of proportion to the infarct territory | Consider tamponade, rupture or severe AR |
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Using the ADD-RS
The Aortic Dissection Detection Risk Score, used in ESC and AHA/ACC guidance, groups features into three categories. One point is scored for each category with at least one feature present, giving a total of 0 to 3.
- High-risk conditions: Marfan syndrome or other connective tissue disease, family history of aortic disease, known aortic valve disease, known thoracic aortic aneurysm, recent aortic manipulation.
- High-risk pain features: chest, back or abdominal pain that is abrupt in onset, severe in intensity, or ripping or tearing.
- High-risk examination features: pulse deficit or systolic blood pressure differential, focal neurological deficit with pain, new aortic regurgitation murmur with pain, hypotension or shock.
A score of 2 or 3 indicates high probability and should lead directly to aortic imaging. A score of 0 or 1 does not exclude dissection; in that group, guideline algorithms use D-dimer and bedside imaging to help decide whether CT is needed. Two cautions apply in the STEMI context. First, the score was not designed for patients whose ECG already shows ST elevation. Second, a single convincing clue, such as a clear pulse deficit, is enough to justify imaging regardless of the total.
Bedside echo and CT aortography
Focused transthoracic echo is quick and available in most emergency departments. In the parasternal long-axis view look for a dilated aortic root, an intimal flap, aortic regurgitation on colour Doppler and a pericardial effusion; the suprasternal view may show the arch. A pericardial effusion in a patient with apparent inferior STEMI should immediately raise the question of dissection. Transthoracic echo can strengthen suspicion, but a normal study does not exclude the diagnosis.
CT aortography, ideally ECG-gated, is the definitive test: it confirms the diagnosis, classifies it, shows coronary and branch involvement and guides surgery. Transoesophageal echo is the alternative when the patient is too unstable for CT, typically in theatre or the intensive care unit. When dissection is plausible and the patient can be moved safely, a short delay for CT is far less harmful than an incorrect thrombolytic.
What not to give, and what to give instead
- Do not give a thrombolytic, unfractionated or low-molecular-weight heparin, bivalirudin, a P2Y12 loading dose or a glycoprotein IIb/IIIa inhibitor until dissection has been excluded.
- Do not give a vasodilator alone; reflex tachycardia increases aortic wall stress. Beta-blockade comes first.
- Do not perform blind pericardiocentesis for haemopericardium from Type A dissection unless the patient is in extremis and surgery is not immediately available; even then, aspirate only enough to restore perfusion.
- Be cautious with beta-blockers in hypotension or severe acute aortic regurgitation, where the compensatory tachycardia may be sustaining output.
- Do give adequate IV opioid analgesia, an IV beta-blocker titrated towards a heart rate of about 60/min, and a vasodilator if needed to bring systolic pressure towards 100–120 mmHg as tolerated.
- Do call the cardiothoracic surgical team as soon as Type A dissection is confirmed; this is a surgical emergency.
A practical sequence for the emergency team
- Record the ECG and confirm inferior ST elevation.
- Before reperfusion drugs, take a focused history of pain onset and character.
- Check pulses and blood pressure in both arms; auscultate for aortic regurgitation; perform a brief neurological check.
- Perform a focused echo for root dilatation, flap, aortic regurgitation and effusion.
- If any red flag is present, withhold antithrombotic therapy and obtain CT aortography.
- If dissection is excluded, proceed with the reperfusion strategy without further delay.
Free live webinar: 10 Cardiac Emergencies Every Physician Must Not Miss
Saturday 14 November 2026 · 7:30 pm IST · 60 minutes online, with live Q&A. Every registrant gets the recording and a one-page summary.
If you want to practise this kind of reasoning through structured cases, the 12-week Practical Cardiology Certificate for Physicians begins with its founding cohort on 23 November 2026.
This article is educational content intended for registered medical practitioners. It does not replace clinical judgement. Always follow your local protocols and current national and international guidelines when managing patients.
