Aortic Dissection and Acute Aortic Syndromes
MRCS Part A & B — Comprehensive Study Notes
Pathophysiology of Aortic Dissection
Mechanism of Dissection
Aortic dissection occurs when the intima (innermost layer) of the aorta is torn, allowing blood to enter and dissect within the media (muscular middle layer). The basic mechanism is an intimal tear that allows pressurised blood from the true lumen to enter the potential space between the intima and external elastica. The dissecting blood plane propagates along the aortic wall—longitudinally along the aorta (propagation) and circumferentially around the aorta. The dissected space (false lumen) becomes pressurised, pushing the intimal flap and compressing the true lumen. The compression of the true lumen reduces its diameter and flow capacity, causing downstream ischaemia. Additionally, the intimal flap may act as a valve: in systole, the flap bows into the false lumen (expanding it); in diastole, the flap may move back to the centre, restricting true lumen flow. This dynamic obstruction worsens if the false lumen is pressurised more than the true lumen (as occurs when the intimal tear is distal and re-entry points allow false lumen pressurisation).
The false lumen may thrombose over time (especially if the intimal tear is proximal and re-entry points are few), or it may remain patent and progressively enlarge, ultimately eroding through the aortic wall (rupture) or chronically aneursymal dilatation. The pericardium is only distensible to a limited degree; if the ascending aorta ruptures into the pericardium, the pericardium fills with blood rapidly, causing tamponade (haemodynamic collapse from raised pericardial pressure preventing venous return to the heart).
DeBakey vs. Stanford Classification
| Feature | DeBakey Classification | Stanford Classification (Clinical Use) |
|---|---|---|
| Type I | Ascending aorta + arch + descending (entire aorta involved). 60% of dissections. | Type A = ascending aorta involved (DeBakey I + II). SURGICAL EMERGENCY. |
| Type II | Ascending aorta only (no arch or descending involvement). 10% of dissections. | Classified as Type A (ascending involved) → SURGICAL. |
| Type III | Descending aorta only (distal to left subclavian artery). 30% of dissections. IIIa = above diaphragm; IIIb = below diaphragm. | Type B = descending aorta only (DeBakey III). MEDICAL MANAGEMENT (unless complicated). |
The Stanford classification is used clinically because it directly guides management: Type A dissections involve the ascending aorta and carry risk of acute catastrophic complications (tamponade, acute AR, MI) requiring emergency surgery; Type B dissections spare the ascending aorta and are managed medically unless complications develop (branch vessel malperfusion, rupture, rapidly expanding dissection).
Predisposing Factors
Hypertension is the most important predisposing factor (~70% of dissection patients are hypertensive). Chronic elevated blood pressure causes medial hypertrophy and degenerative changes in the aortic wall, predisposing to intimal tears. Marfan syndrome (fibrillin-1 mutation causing FBN1 mutations) leads to cystic medial necrosis—characteristic histopathological finding of aortic wall degeneration with mucoid material filling the media, loss of elastic fibres, and VSMC apoptosis. Marfan patients have dilated aortic roots and are at high risk of dissection, particularly when aortic diameter exceeds 50 mm (beta-blockers and/or ARBs recommended to slow aortic dilatation; prophylactic root replacement if diameter >50 mm). Loeys-Dietz syndrome (mutations in TGFBR1 or TGFBR2, genes encoding TGF-beta receptors) causes diffuse arterial aneurysms and dissections, often at smaller aortic diameters than Marfan; prophylactic surgery recommended at 50 mm diameter or smaller if family history of dissection. Bicuspid aortic valve carries increased dissection risk, particularly if aortic root is dilated. Aortic coarctation causes proximal hypertension, increased dissection risk. Turner syndrome features aortic dilatation and dissection risk.
Trauma: Deceleration injury (high-speed motor vehicle accident, fall from height, sudden chest compression) causes shear forces that can tear the aortic intima, typically at the aortic isthmus (the fixed point between the mobile ascending/arch and fixed descending aorta). Iatrogenic: Cardiac catheterisation (guidewie perforation), intra-aortic balloon pump (IABP) insertion, aortic cross-clamping during cardiac surgery. Pregnancy: Pregnancy increases dissection risk 2–10 fold, particularly in third trimester and early postpartum (hormonal effects on collagen metabolism, haemodynamic changes). Cocaine use: Cocaine causes acute hypertension and increases myocardial contractility (increased dP/dt—rate of pressure change), accelerating dissection propagation.