Aortic Dissection: Symptoms, Causes & Treatment

Aortic dissection is among the most catastrophic cardiovascular emergencies, with an untreated mortality of 1–2% per hour and a 48-hour mortality exceeding 50% for Type A dissections. The pathological event is a tear in the aortic intima, through which blood under systolic pressure surges into and propagates within the medial layer, creating a false lumen that expands and compresses branch arteries supplying vital organs — coronary arteries (myocardial infarction), carotid arteries (stroke), renal arteries (acute kidney injury), mesenteric arteries (bowel ischemia), and spinal arteries (paraplegia).

The Stanford classification guides management: Type A involves the ascending aorta and aortic arch regardless of origin site — emergency surgery is mandated because death from aortic rupture, tamponade, or coronary ostium involvement is imminent. Type B involves only the descending aorta distal to the left subclavian artery — initial medical therapy (IV antihypertensives and heart rate control) with surveillance; thoracic endovascular aortic repair (TEVAR) is indicated for complicated Type B (malperfusion, persistent pain, rupture, or expansion).

Chest pain is present in 90% of cases — characteristically abrupt onset, maximal intensity from the start (unlike MI's crescendo), described as tearing or ripping, radiating to the interscapular region. Blood pressure differential >20 mmHg between arms or absent femoral pulses support the diagnosis. CT angiography (CTA) of the chest, abdomen, and pelvis with contrast is the standard diagnostic modality, achievable in under 5 minutes in most centers.

• Sudden, severe chest or back pain of maximal intensity from onset — tearing, ripping, or knife-like quality; unlike MI (crescendo), aortic dissection pain is abrupt and maximal
• Pain radiating to the interscapular region (Type B) or anterior chest (Type A)
• Blood pressure differential >20 mmHg between arms or pulse deficit
• Malperfusion syndromes: stroke (carotid), syncope (arch), paraplegia (spinal), abdominal pain (mesenteric), oliguria (renal), leg ischemia
• Hypotension and shock in aortic rupture or severe tamponade

• Hypertension — present in 70–80% of cases; the dominant modifiable risk factor
• Connective tissue disorders: Marfan syndrome (fibrillin-1 mutation), Ehlers-Danlos syndrome Type IV, Loeys-Dietz syndrome
• Bicuspid aortic valve with associated aortic root dilatation
• Aortitis: giant cell arteritis, Takayasu's arteritis, syphilitic aortitis
• Trauma: blunt chest deceleration injury or iatrogenic dissection from cardiac catheterization
• Pregnancy: third trimester, especially in women with connective tissue disorders or coarctation
• Cocaine use: acute hypertensive surges

CT angiography (CTA) of the entire aorta is the diagnostic gold standard (sensitivity and specificity >98%): visualizes intimal flap, true and false lumen, branch vessel involvement, and pericardial effusion. Transesophageal echocardiography (TEE) is performed in the operating room when CT is unavailable or contraindicated. Chest X-ray: widened mediastinum >8 cm (sensitivity only 60%). D-dimer elevation is sensitive but non-specific. Troponin to rule out concomitant coronary malperfusion. ECG is often normal — critically important to distinguish from STEMI before giving thrombolytics (which would be catastrophic in dissection).

Type A: immediate surgical emergency — ascending aortic replacement under cardiopulmonary bypass is the only life-saving option (30-day surgical mortality 15–25%, versus near-100% medical mortality). Type B uncomplicated: IV antihypertensive therapy targeting SBP 100–120 mmHg and HR <60/min (labetalol, esmolol, nicardipine + sodium nitroprusside); pain control; ICU monitoring. Type B complicated (malperfusion, persistent pain, hemodynamic instability): TEVAR with endovascular stent-graft deployment is standard. Lifelong antihypertensive therapy and aortic surveillance imaging every 6–12 months for all survivors.

• Aortic rupture with massive hemorrhage and cardiac arrest
• Stroke from carotid or innominate artery malperfusion
• Acute renal failure, intestinal ischemia, spinal cord ischemia (paraplegia), limb ischemia
• Acute aortic regurgitation and coronary ostium compromise in Type A
• Late complications: aortic aneurysm formation or re-dissection of the false lumen

• Strict blood pressure control (<130/80 mmHg) — the most impactful modifiable preventive measure
• Smoking cessation and avoidance of cocaine and stimulants
• Lifelong aortic surveillance imaging in Marfan syndrome, bicuspid aortic valve, familial thoracic aortic disease, and prior aortic surgery
• Beta-blockers for Marfan syndrome patients to reduce aortic wall stress
• Prophylactic aortic replacement when aortic root diameter exceeds 5.0 cm (Marfan) or 5.5 cm (general population)