Aortic Dissection: Recognition on Common Sequences Including Nuclear Medicine

Overview

Aortic dissection is the most common nontraumatic acute aortic emergency, with an in-hospital mortality of 20-25% overall, rising sharply in complicated cases. An intimal tear allows blood to penetrate the medial layer, creating a cleavage plane - the false lumen - between the inner two-thirds and outer one-third of the media. The true and false lumina are separated by an intimomedial flap. Dissection propagates antegrade and/or retrograde; the false lumen may remain patent, thrombose, recommunicate via fenestrations, or rupture into the pericardial, pleural, or peritoneal spaces.

Clinical presentation is sudden severe chest or back pain (75-95%), classically described as tearing/ripping, radiating to the jaw, neck, or low back. This overlaps substantially with acute MI, pulmonary embolism, and other acute aortic syndromes. A small proportion have clinically silent dissection. A high index of suspicion is essential.

Acute Aortic Syndrome: Spectrum

Acute Aortic Syndrome (AAS) encompasses aortic pathologies with similar acute presentations:

The pathological boundaries between these entities overlap: thrombosed false lumen may be indistinguishable from IMH; bleeding at the base of a PAU can give rise to IMH or act as a focus for dissection.

Predisposing Factors

• Hypertension and advancing age (most common)
• Cystic medial degeneration: Marfan syndrome, Ehlers-Danlos syndrome
• Bicuspid aortic valve, aortic coarctation
• Aortitis, prior cardiac surgery or aortic instrumentation
• Pregnancy, blunt chest trauma
• Positive family history

Classification Systems

Stanford Classification (Surgical Relevance)

DeBakey Classification

Mnemonic: Type A - Ascending and Arch; Type B - Beyond brachiocephalic vessels; Type I = II + III.

Acute vs Chronic

$$\text{Acute} = \text{symptoms} < 14\,\text{days};\quad \text{Chronic} = \text{symptoms} \geq 14\,\text{days}$$

Branch Vessel Effects

• Static obstruction: Intimal flap enters branch vessel origin without re-entry point
• Dynamic obstruction: Intimal flap prolapses over/covers the branch vessel orifice like a curtain
• Resultant malperfusion can affect: coronary ostia (MI), arch vessels (stroke), anterior spinal artery (spinal cord ischaemia), coeliac/SMA (mesenteric ischaemia), renal arteries (renal failure), iliac/femoral arteries (limb ischaemia)
• Dissection flap most commonly terminates in the left iliac artery (~80%); right iliac artery less commonly

Imaging Modalities and Appearances

Chest Radiography - Initial Screening

• Often the first imaging obtained in undifferentiated chest pain
• Classic but non-specific: widened mediastinum (> 8 cm)
• Other findings: loss of aortic knuckle contour, tracheal deviation, left pleural effusion, apical pleural cap
• Normal CXR does not exclude dissection
• Can detect complications: haemothorax, pulmonary oedema from acute aortic regurgitation/heart failure
• Useful to identify device positioning (ETT, CVC, pacing leads) and concurrent pulmonary pathology

CT Angiography (CTA) - First-Line Modality

CTA is the mainstay for diagnosis and treatment planning. Standard protocol includes a non-contrast phase (for IMH/haemopericardium detection) followed by arterial-phase contrast acquisition; delayed phases assist in assessing false lumen flow and complications. ECG-gating is essential for the ascending aorta to eliminate motion artefact.

Intimal flap: Linear structure dividing the aortic lumen; seen in approximately 70% of dissections.

Distinguishing true from false lumen:

Flow velocities (average):

$$\bar{v}{\text{true}} \approx 13.4\,\text{cm/s};\quad \bar{v}{\text{false}} \approx 3.1\,\text{cm/s}$$

Retrograde flow is more common in the false lumen.

Common entry tear locations (helical flow pattern):

Complication assessment on CTA:

• Pericardial effusion / haemopericardium (extension into aortic root)
• Aortic valve involvement → aortic regurgitation
• Coronary artery involvement → acute MI (RCA most commonly, producing inferior MI)
• Pleural effusion / haemothorax (left > right)
• Arch vessel compromise → stroke
• Branch vessel occlusion: mesenteric ischaemia, renal infarction, limb ischaemia
• Extension into iliac arteries

CTA pitfalls:

• Linear streak artefacts from metallic lines/leads or adjacent contrast-filled veins (especially the SVC) can simulate an intimal flap - compare with non-contrast series
• Thrombosed false lumen may be mistaken for IMH
• Motion artefact in the ascending aorta is the most common cause of false-positive dissection on CT - ECG-gating is essential

MRI/MRA - High Accuracy, Second-Line in Acute Setting

MRI sensitivity and specificity for aortic dissection both approximate 100%, based on excellent inherent contrast between flowing blood and aortic wall.

MRI limitations in the acute setting: prolonged acquisition time, limited haemodynamic monitoring capability, contraindication with certain implanted devices - restricts use in unstable patients. Valuable for chronic dissection surveillance and when CT contrast is contraindicated.

The cobweb sign and beak sign are primarily CT signs and are less reliably demonstrated on MRI.

Echocardiography

Transthoracic echocardiography (TTE): - Rapid bedside assessment - Demonstrates proximal ascending aorta dissection flap, aortic regurgitation, and pericardial effusion - Limited visualisation of descending aorta and arch - Standard views: parasternal long/short axis, apical four-chamber and two-/three-chamber, subcostal (including IVC for volume status assessment)

Transoesophageal echocardiography (TEE): - Superior visualisation of the thoracic aorta; directly images posterior cardiac and aortic structures (oesophagus is directly anterior to the posterior heart) - Identifies intimal flap, true/false lumen, coronary ostial involvement, and left atrial appendage thrombus - Blind spot at mid-ascending aorta (tracheal/bronchial interposition) - Limitation: invasive, requires sedation

Nuclear Medicine: Role in Acute Aortic and Myocardial Assessment

Nuclear medicine has a limited direct role in the acute diagnosis of aortic dissection but is important for evaluating ischaemic complications, particularly acute MI complicating dissection.

Myocardial Perfusion Imaging (MPI)

One of the most widely used nuclear cardiology techniques. Provides information on myocardial perfusion, function, and viability.

Mechanism: A radiolabelled tracer ($^{99m}$Tc-sestamibi, $^{99m}$Tc-tetrofosmin, or $^{201}$Tl) distributes in the myocardium proportional to regional blood flow. A perfusion defect is identified as relatively reduced tracer uptake in the abnormal territory compared with adjacent normal myocardium.

Stress modalities:

Stress increases coronary blood flow, revealing the flow differential between normal and diseased territories.

Interpretation:

Indications for MPI: - Evaluation of non-acute chest pain or ischaemia equivalent - Risk stratification in known chronic stable CAD - Preoperative risk assessment for non-cardiac surgery - Post-acute coronary syndrome risk assessment - Post-revascularisation assessment - Myocardial viability assessment

Patient preparation: - Fast ≥ 4 hours (reduces splanchnic tracer activity → better image quality) - Caffeine avoidance ≥ 24 hours before (caffeine antagonises adenosine/dipyridamole vasodilation) - Withhold beta-blockers 24-48 hours, calcium channel blockers 24 hours, long-acting nitrates 24 hours before (if clinically permissible)

Relevance to dissection-complicated MI: When retrograde dissection occludes the RCA origin (most common), the result is an acute inferior MI. On MPI:

Viability Assessment with PET

$^{18}$F-FDG PET combined with $^{13}$N-ammonia (NH$_3$) or $^{82}$Rb perfusion PET is the most accurate viability modality:

This distinction is particularly relevant post-dissection when coronary revascularisation or surgical repair is being planned.

Radionuclide Ventriculography

• Accurate, reproducible assessment of ventricular volumes and ejection fraction
• Can quantify regional wall motion abnormalities from coronary occlusion complicating dissection
• Less commonly used given CMR availability; useful when CMR is contraindicated

Differential Diagnosis of Acute Chest Pain

Complications and Their Imaging Correlates

Systematic Approach to Reporting CTA for Aortic Dissection

1. Classification: Stanford A vs B; DeBakey type
2. Primary entry tear location and re-entry tear(s)
3. True vs false lumen: size, enhancement, position, patency (patent/thrombosed/partial)
4. Extent: ascending aorta → arch vessels → descending thoracic → abdominal aorta → iliac vessels
5. Aortic measurements: maximal diameters of true and false lumina and total aortic diameter at key levels
6. Branch vessel involvement: coronary ostia (RCA, LCA), innominate, left carotid, left subclavian, coeliac, SMA, renals, iliacs
7. Complications: pericardial effusion, pleural effusion/haemothorax, end-organ ischaemia, signs of rupture
8. Aortic valve and root: regurgitation, root involvement
9. Incidental/relevant findings: pre-existing aneurysm, BAV, other pathology

Key Pitfalls and Errors

CT Diagnosis

• Streak artefacts: Metallic leads, central lines, and SVC opacification create linear artefacts mimicking an intimal flap - compare with non-contrast series and assess continuity
• Thrombosed false lumen: May resemble IMH; look for a residual flap or hyperdense crescent on non-contrast images
• Motion artefact (ascending aorta): Most common cause of false-positive diagnosis - ECG-gating is mandatory for this segment
• Missed coronary involvement: Actively trace RCA and LCA origins when root/ascending aorta is involved

Clinical Overlap with Acute MI

• Dissection can directly cause MI via coronary ostial occlusion - thrombolysis administered for presumed MI in unrecognised dissection is potentially catastrophic
• Consider dissection when MI is accompanied by unequal blood pressures, widened mediastinum, or pulse deficit
• The triple rule-out CTA protocol (pulmonary arteries + coronary arteries + thoracic aorta) can be applied in selected patients with indeterminate acute chest pain; requires tailored contrast administration to ensure adequate opacification of all three vascular beds - clinical utility remains under evaluation

Nuclear Medicine Pitfalls

• MPI is not a first-line investigation for acute aortic dissection; its role is characterising ischaemic complications once dissection is identified
• Avoid pharmacological stress (adenosine/dipyridamole) in haemodynamically unstable patients or those with uncontrolled hypertension
• Pre-test preparation requirements (caffeine avoidance, fasting, medication withholding) are impractical in the acute setting
• A fixed perfusion defect in a patient with known dissection should prompt consideration of coronary malperfusion rather than chronic CAD

MRI

• Do not delay surgery for MRI in an unstable Type A dissection patient - CTA is faster and sufficient
• Cobweb and beak signs are CT findings, less reliably seen on MRI
• Adequate cardiac gating is essential; ungated acquisitions degrade flap visualisation

Management Summary

Type A Dissection

• Emergency open surgical repair - standard of care for all patients
• Mortality > 50% within 48 hours if untreated; fatal complications include aortic rupture, cardiac tamponade, acute aortic regurgitation, and acute MI
• CTA used for preoperative planning: coronary ostia patency, arch vessel involvement, extent of dissection
• Initial medical therapy in all patients: IV beta-blockers + peripheral vasodilators to reduce systolic BP and the rate of pressure rise ($\text{d}P/\text{d}t$)

Type B Dissection

• Uncomplicated: Medical therapy (IV beta-blockers, vasodilators); similar mortality to emergency surgery
• Complicated (refractory pain, impending rupture, malperfusion): TEVAR - stent-graft across primary entry tear to depressurise false lumen and restore true lumen flow
• High-risk features warranting intervention:
• Total aortic diameter $> 44\,\text{mm}$
• False lumen diameter $> 22\,\text{mm}$
• False lumen to total aortic lumen area ratio $> 0.7$
• Early surgery recommended for patients with Marfan syndrome
• Post-TEVAR surveillance CTA: monitors for endoleak, false lumen thrombosis, and aneurysmal progression