Acute Aortic Syndrome: The Evidence Behind the Pathway

It is two in the morning in a district hospital casualty. A 54-year-old lorry driver was lifting a spare tyre when a sudden, severe pain tore through his chest and went straight through to his back. He has had high blood pressure for years and stopped his tablets three months ago. His pressure is 188/104 mmHg and his pulse 108. The electrocardiogram shows left ventricular hypertrophy and no ST elevation. The intern beside you has already written “ACS?” on the sheet and is asking whether to start the heparin. This is an illustrative case, not a real patient.

The Acute Aortic Syndrome tool will help you with him: the aortic dissection detection risk score, what a D-dimer can and cannot do, the targets, the doses for his weight, and the operations and the referral. What it no longer carries is some of the why. The table of the three lesions, the study figures behind the score and the description of Indian practice that sat in its Evidence tab have moved here, so that the tool stays quick at the bedside. By the end of this article you will know why the tool asks what it asks, and where its numbers come from.

1. Three lesions, one pain

Acute aortic syndrome is a presentation, not a diagnosis. Three different lesions of the aortic wall produce the same pain, share the same risk factors and most of the management, and are told apart only on the scan. Here they are, as the tool carried them on 4 November 2026.

The intima is the thin inner lining of the aorta; the media is the thick muscular and elastic layer outside it. The vasa vasorum are the tiny vessels that feed the wall of the aorta itself. So a dissection begins with a tear from the inside, an intramural haematoma begins with a bleed inside the wall with no tear at all, and a penetrating ulcer begins as an atherosclerotic plaque that eats its way outwards.

“If they look different on the scan, why put them on one sheet?” Because they share their cause and their first treatment. Two factors drive all three: wall stress raised by hypertension or by dilatation, and a media that is inherently weak or degenerated. That is why the treatment is anti-impulse therapy rather than blood pressure control alone, and why the commonest risk factor by a distance is ordinary hypertension rather than any of the named aortopathies. Our lorry driver has no Marfan features and no family history. He has untreated hypertension, which is the usual story.

2. The score and the D-dimer

The national workflow lists risk features but offers no way to combine them. The aortic dissection detection risk score, from the guideline the workflow itself cites, does that: one point for each of three groups in which anything is present. The groups are high-risk conditions, high-risk features of the pain, and high-risk findings on examination. Our patient scores 1: his pain was abrupt, severe and tearing, and nothing else is present.

“Can a low score and a normal D-dimer send him home?” This is where the study figures come in. Paired with a D-dimer below 500 ng/mL in the ADvISED study of 1850 patients, a score of 0 missed 1 case in 294, and a score of 1 or less missed 3 in 924 (Nazerian 2018). Both strategies failed in 0.3 per cent. The difference is how many patients they spare a scan: 15.9 per cent against 49.9 per cent. In plain words, the looser rule, a score of 1 or less, spares about half the patients a scan, at the same small miss rate. The tool prints these figures in the result for the score you have entered.

The common mistake is to read that as permission to stop thinking. The tool keeps three cautions beside the score, and each one is there because of a patient who was missed. D-dimer alone is not a rule-out. A score of 0 is not a discharge: in the registry that derived the score, 108 of 2538 confirmed dissections scored 0, and of the 72 of those who had a chest radiograph, 35 showed a widened mediastinum (Rogers 2011). And a normal D-dimer virtually rules out dissection, but an intramural haematoma or a penetrating ulcer may still be present.

Our lorry driver’s D-dimer comes back far above 500 ng/mL. The computed tomography angiogram shows a dissection that spares the ascending aorta: a type B dissection, with no malperfusion.

3. Why the heart rate comes down before the pressure

Look at what the tool asks you to aim for: a systolic pressure of 100 to 120 mmHg and a heart rate of 60 to 70 per minute. Why the rate as well as the pressure? Because the aim is not a number on the monitor. It is the force with which each ejection strikes the dissection flap, which depends on the velocity of ventricular contraction, the rate of contraction and the pressure together. A beta blocker lowers all three. A vasodilator lowers one and, through reflex tachycardia, raises another.

“So why not start the nitroprusside first? It brings the pressure down fastest.” That is exactly the reason not to. Nitroprusside given alone drops the pressure, the heart answers with a reflex tachycardia, and the force of each beat on the flap goes up. That is why the escalation chart never reaches the vasodilator until the rate is controlled. For our patient: a beta blocker first, labetalol or esmolol, to the rate target; then, if the systolic pressure is still high with the rate controlled, the vasodilator is added. And his pain is treated with morphine or fentanyl, because pain raises both the pressure and the rate.

4. What happens in India

There is no Indian specialty-society guideline on acute aortic syndrome. What India has instead is description, and it is worth having.

The surgical reality first. Information from the subcontinent largely remains unpublished, there are few specialised centres, and patients are often operated on without a specialised radiologist, interventionalist or anaesthetist, and without sealants, specialised grafts or stent grafts. That is the background against which both national documents agree on one line: after medical therapy has been started, move the patient to a centre that does this work, as soon as possible.

Then what surgeons say they do. In a 2025 national survey of 200 respondents (Sajja 2025): surgery within 24 hours prioritised by 68.4 per cent, antegrade cerebral perfusion by 77.7 per cent, axillary cannulation by 55.8 per cent, and surgery avoided in the over-80s by 73.5 per cent. The guideline’s position is that elderly patients still benefit. Both are printed and neither is resolved. The tool prints both in the result, because the decision belongs to the surgeon and the family, not to the tool.

And afterwards. The national workflow gives no follow-up, no surveillance interval and no discharge criterion. The 2022 American guideline asks for computed tomography or magnetic resonance imaging at 1 month, 6 months and 12 months, then annually if stable, and a long-term beta blocker for everybody. In the same survey, 88.4 per cent used computed tomography angiography for that surveillance and only 19.5 per cent used magnetic resonance angiography. For a patient who will need many scans over many years, that choice is worth discussing.

Back to the casualty

Our lorry driver did not get heparin. He scored 1, his D-dimer was high and the scan answered the question. He has an uncomplicated type B dissection, so the first treatment is medical: a beta blocker to bring his rate to 60 to 70 and his systolic pressure to 100 to 120, a vasodilator only once the rate is controlled, and proper pain relief. He is moved to a centre that does aortic work as soon as he is stable to travel, and he leaves that centre with a beta blocker for life and a date for his first surveillance scan. Each of those steps is a line in the tool.

Try this

A 62-year-old woman arrives with sudden severe chest pain. Her electrocardiogram shows ST elevation in the inferior leads. The registrar is preparing thrombolysis. You hear a new early diastolic murmur, and her left radial pulse is weaker than the right. What do you do? Illustrative case.

Answer. Stop the thrombolysis. A dissection that reaches a coronary ostium presents with ischaemic pain, ischaemic electrocardiogram changes and raised enzymes. The murmur and the unequal pulses point to the aorta. The national workflow says it in its own capital letters: if dissection is diagnosed alongside myocardial ischaemia, manage it as a dissection, and thrombolytic therapy should NOT be initiated. A gated computed tomography angiogram answers both questions at once.

Take-home points

• Dissection, intramural haematoma and penetrating ulcer share a pain and a first treatment; only the scan tells them apart.
• The risk score with a D-dimer below 500 ng/mL can spare a scan, but D-dimer alone is not a rule-out and a score of 0 is not a discharge.
• Bring the heart rate down with a beta blocker before any vasodilator; the target is the force on the flap, not the pressure alone.
• Never thrombolyse chest pain until dissection has been considered; a murmur or unequal pulses changes everything.
• Start treatment, then transfer to a centre that does aortic work, and plan surveillance imaging at 1, 6 and 12 months.

Read with this: Acute Coronary Syndrome: The Evidence Behind the Pathway, the tool this one sits beside, and Beta-Blockers: Clinical Pharmacology and Practice Pearls.

Declaration: the author built and maintains the tool. It is free to use. The figures in this article are those the tool carried in its Evidence tab on 4 November 2026, each from the source named beside it. The tool is in administrator preview, pending clinical review.

References

1. Indian Council of Medical Research, Department of Health Research. Standard treatment workflow: acute aortic syndrome (ICD-10-M31.4). New Delhi: Ministry of Health and Family Welfare; 2024.
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7. Hagan PG, Nienaber CA, Isselbacher EM, Bruckman D, Karavite DJ, Russman PL, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000;283(7):897-903. [1996 to 1998 data]
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