🩸 Aortic Pathology
Stanford Type A vs B dissection, DeBakey classification, aortic aneurysm, TEVAR, and the key management principle: IV beta-blockers before vasodilators.
Aortic Dissection — Overview
Aortic dissection occurs when a tear in the aortic intima allows blood to enter the media, creating a false lumen that propagates along the length of the aorta. It is a cardiovascular emergency with mortality of ~1–2% per hour untreated in Type A. Understanding the classification, presentation, and management principles is essential for MRCS.
Classical Presentation — “Tearing / Ripping” Chest Pain
The characteristic symptom is sudden onset, severe, tearing or ripping chest pain radiating to the back (interscapular). Unlike ACS pain which builds gradually, dissection pain is maximal at onset (“worst pain of my life, instant”). Pain may migrate as the dissection propagates distally. Critical distinguishing features from MI: pain maximal from onset (not building), tearing quality, pulse differential (unequal BP or pulses between arms — >20 mmHg), aortic regurgitation murmur (Type A), neurological deficits.
Pathophysiology
- Intimal tear: Usually starts just above the aortic valve (ascending aorta — Type A) or just distal to the left subclavian artery (descending aorta — Type B). High mechanical stress at these locations. Bicuspid aortic valve, Marfan syndrome → weakened aortic wall → earlier and more severe dissection.
- False lumen propagation: High-pressure blood dissects along the media. Can propagate proximally (towards the heart) or distally (towards the legs). False lumen may remain patent (bad — higher pressure, continued growth) or thrombose (better).
- Complications from branch vessel involvement: Coronary ostia (MI), carotid arteries (stroke), subclavian (arm ischaemia), visceral vessels (bowel/renal ischaemia — malperfusion syndrome), iliac arteries (leg ischaemia), intercostal arteries (spinal cord ischaemia — paraplegia).
Risk Factors
| Category | Risk Factors |
|---|---|
| Hypertension | Most common risk factor (~75% of dissections). Chronic hypertension weakens the aortic media through accelerated atherosclerosis and cystic medial necrosis. |
| Connective tissue disorders | Marfan syndrome (FBN1 mutation — fibrillin-1; aortic root dilatation, lens dislocation, tall stature). Ehlers-Danlos type IV (COL3A1 — collagen III). Loeys-Dietz syndrome. |
| Bicuspid aortic valve | Associated with aortic root/ascending aortic dilatation and dissection, independent of stenosis. Common (1–2% population). |
| Aortic dilatation/aneurysm | Pre-existing aneurysm is the strongest single risk factor for dissection at that level. |
| Iatrogenic | Cardiac catheterisation, intra-aortic balloon pump insertion, cardiac surgery (aortic cannulation). Accounts for ~5% of dissections. |
| Other | Cocaine use (acute hypertension), pregnancy (3rd trimester — hormonal changes weaken aortic wall, especially Marfan’s), trauma (deceleration). |
Classification Systems
| Classification | Type | Description | Treatment |
|---|---|---|---|
| Stanford (most used clinically) | Type A | Involves the ascending aorta (regardless of origin of tear) | Emergency surgical repair |
| Type B | Does not involve the ascending aorta (confined to descending aorta, distal to left subclavian) | Medical management; TEVAR if complicated | |
| DeBakey | I | Originates in ascending, extends to descending (whole aorta) | Surgical |
| II | Confined to ascending aorta only | Surgical | |
| IIIa / IIIb | Originates in descending aorta; IIIa = thoracic only, IIIb = extends to abdominal | Medical ± TEVAR |
Investigations
- CXR: Widened mediastinum (>8 cm at aortic knuckle — 80% sensitivity), calcium sign (intimal calcification displaced >6 mm inward), pleural effusion (haemothorax from dissection into pleural space). Normal in 20% of cases — never exclude dissection based on normal CXR alone.
- ECG: Usually normal or non-specific ST changes. Important to do to exclude STEMI (different management entirely). LVH from chronic hypertension common.
- CT aortography (CTA): Gold standard — rapid, sensitive (~98%), available. Shows: extent of dissection, true vs false lumen, branch vessel involvement, pericardial effusion. Required for surgical planning.
- Transoesophageal echocardiography (TOE): Excellent for aortic root and ascending aorta. Ideal in haemodynamically unstable patients (can be done in theatre/ICU). Identifies AR, pericardial effusion, tamponade. Blind spot = distal ascending aorta / arch (air in trachea).
- MRI: Most detailed but slow — not suitable for acute emergency. Used in stable patients or follow-up.
- Bloods: D-dimer (elevated in dissection — >500 ng/mL has 97% sensitivity; if negative, very useful to rule out). FBC, U&E, coagulation. Group & save / cross-match.
Dissection Mimicking STEMI — A Lethal Trap
Aortic dissection can occlude the right coronary artery ostium → inferior STEMI pattern on ECG. If thrombolysis or primary PCI is given to a patient with Type A dissection masquerading as STEMI, the consequences are catastrophic: thrombolysis → uncontrolled aortic haemorrhage → death. Always consider dissection before thrombolysis if: sudden-onset maximal pain, pulse differentials, widened mediastinum, or clinical features atypical for ACS. D-dimer is a useful rapid screen. CTA is definitive.