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Diseases of the circulatory system

Aortic dissection

Aortic dissection is a life-threatening condition caused by a tear in the intimal layer of the aorta, allowing blood to dissect between the layers of the aortic wall. It most commonly affects hypertensive men aged 60-70 years. The classic presentation is sudden-onset tearing chest pain radiating to the back with a blood pressure differential between arms.

Practice questionsHigh-yield facts
ICD-10I71.0
Typical patientHypertensive man, 60-70 years, sudden tearing chest pain
Key findingBlood pressure differential >20 mmHg between arms
First-line treatmentIV beta-blocker, blood pressure control, urgent surgical consultation
10 min readFor medical studentsUpdated 2026-10-14

Definition and epidemiology

Aortic dissection occurs when blood passes through an intimal tear into the aortic media, creating a false lumen that propagates along the length of the vessel. This separation of aortic wall layers can compromise branch vessels and lead to catastrophic complications including rupture, tamponade, or acute organ ischemia.

The incidence is approximately 3-4 per 100,000 persons per year. Men are affected 2-3 times more frequently than women, with peak incidence in the sixth and seventh decades. Without treatment, mortality is approximately 1-2% per hour in the acute phase, with 50% dying within 48 hours and 90% within one month.

Classification

Two main classification systems are used:

Stanford classification:

  • Type A: involves the ascending aorta (regardless of origin site) – accounts for 60-70% of cases
  • Type B: involves only the descending aorta distal to the left subclavian artery – accounts for 30-40%

DeBakey classification:

  • Type I: originates in ascending aorta, extends at least to the aortic arch
  • Type II: confined to ascending aorta only
  • Type III: originates in descending aorta, extends distally (IIIa: above diaphragm; IIIb: below diaphragm)

The Stanford system is more commonly used clinically because it directly guides management: Type A requires emergency surgery, Type B is usually managed medically unless complicated.

High-yield for exams
  • Type A dissection (ascending aorta) requires emergency surgery; Type B (descending) is usually managed medically unless complicated.
  • Classic presentation: sudden tearing chest/back pain, blood pressure differential >20 mmHg between arms, pulse deficits.
  • Hypertension is present in 70-80% of patients and is the most important modifiable risk factor.
  • Marfan syndrome causes dissection at younger age (30-40 years) due to cystic medial degeneration.
  • CT angiography is first-line imaging; shows intimal flap and true/false lumens.
  • Initial management: IV beta-blocker first to reduce heart rate and blood pressure, then add vasodilator if needed.
  • Never give vasodilators alone (causes reflex tachycardia); always beta-block first.
  • Chest X-ray is normal in 10-20% of cases; normal CXR does not exclude dissection.

Etiology and risk factors

The primary cause of aortic dissection is degeneration of the aortic media, which weakens the vessel wall and predisposes to intimal tear.

Major risk factors

  • Hypertension: present in 70-80% of patients; the single most important modifiable risk factor
  • Age: progressive medial degeneration increases risk with advancing age
  • Male sex: 2-3 fold increased risk
  • Atherosclerosis: contributes to wall stress and weakening

Connective tissue disorders

  • Marfan syndrome: cystic medial necrosis causes aortic root dilation; dissection occurs at younger age (mean 30-40 years)
  • Ehlers-Danlos syndrome type IV: defective type III collagen
  • Loeys-Dietz syndrome: aggressive aortic disease
  • Turner syndrome: associated with bicuspid aortic valve and coarctation

Other associations

  • Bicuspid aortic valve: 5-10 fold increased risk due to associated aortopathy
  • Aortic coarctation: causes proximal hypertension and post-stenotic dilation
  • Giant cell arteritis: inflammation weakens aortic wall
  • Cocaine and amphetamine use: acute hypertension and increased sympathetic tone
  • Pregnancy: especially third trimester and early postpartum in women with underlying aortopathy
  • Iatrogenic: cardiac catheterization, aortic cannulation, intra-aortic balloon pump
  • Trauma: rapid deceleration injury

Familial thoracic aortic aneurysm and dissection (FTAAD) accounts for approximately 20% of cases and may occur without syndromic features.

Pathophysiology

Aortic dissection begins with an intimal tear, most commonly in areas of high mechanical stress: the ascending aorta (within several centimeters of the aortic valve) and the descending aorta just distal to the left subclavian artery at the ligamentum arteriosum.

Blood enters the media through the tear, creating a false lumen that propagates along the length of the aorta. The dissection typically extends anterograde (distal direction) but can extend retrograde. The false lumen is bounded by the torn intima internally and the outer media and adventitia externally.

Pulsatile aortic blood flow drives progressive extension of the dissection. The false lumen may remain patent, thrombose completely, or show partial thrombosis. A re-entry tear may create a double-barrel aorta with both true and false lumens perfused.

Complications arise from:

  • Aortic rupture: into the pericardium (tamponade), pleural space (hemothorax), mediastinum, or retroperitoneum
  • Aortic regurgitation: from disruption of the aortic root or valve commissures in Type A dissection
  • Branch vessel compromise: dissection flap obstructs coronary, carotid, spinal, visceral, or renal arteries causing end-organ ischemia
  • Propagation into pericardium: hemopericardium and cardiac tamponade

Cystic medial degeneration is the underlying histologic finding in many cases, characterized by smooth muscle cell loss, elastic fiber fragmentation, and accumulation of basophilic ground substance. This process is accelerated by hypertension, genetic connective tissue disorders, and aging.

Clinical features

The presentation of aortic dissection is variable, and a high index of suspicion is essential. Misdiagnosis is common because symptoms overlap with more common conditions.

Cardinal symptom: Pain

Sudden-onset severe pain occurs in 85-95% of patients. The pain is:

  • Quality: tearing, ripping, sharp, or stabbing (though any severe pain should raise suspicion)
  • Location: anterior chest (Type A), interscapular back (Type B), or both
  • Radiation: may migrate as dissection propagates
  • Maximal at onset: unlike myocardial infarction where pain crescendos

Approximately 10-15% present without pain, particularly elderly patients and those with prior aortic surgery.

Physical examination findings

  • Blood pressure differential: >20 mmHg systolic difference between arms (present in 30-40%)
  • Pulse deficits: absent or diminished peripheral pulses from branch vessel involvement
  • Aortic regurgitation murmur: diastolic decrescendo murmur in Type A (40-75%)
  • Neurologic deficits: stroke, paraplegia, or altered mental status from vascular compromise
  • Hypotension or shock: suggests rupture, tamponade, or severe aortic regurgitation
  • Pericardial rub or muffled heart sounds: hemopericardium
  • Superior vena cava syndrome: from mediastinal compression

Organ-specific manifestations

  • Cardiac: myocardial infarction (coronary ostial involvement), acute heart failure (severe AR), tamponade
  • Neurologic: stroke (15%), syncope (10-15%), paraplegia (spinal artery), Horner syndrome (sympathetic chain)
  • Renal: acute kidney injury, flank pain, hematuria
  • Gastrointestinal: mesenteric ischemia with abdominal pain
  • Limb ischemia: pain, pallor, pulselessness, paresthesias

High-risk patient profiles that should trigger immediate consideration: hypertensive emergency, Marfan syndrome, known thoracic aortic aneurysm, recent aortic manipulation, cocaine use.

Diagnosis

Rapid diagnosis is critical. Clinical suspicion based on history and physical examination should prompt immediate imaging.

Initial evaluation

ECG: performed to exclude ST-elevation myocardial infarction but cannot rule out dissection. May show:

  • Left ventricular hypertrophy (chronic hypertension)
  • ST-segment changes if coronary ostia are involved
  • Normal ECG does not exclude dissection

Chest X-ray: may show widened mediastinum (>8 cm), abnormal aortic contour, pleural effusion (hemothorax), or displacement of calcified aortic wall. However, chest X-ray is normal in 10-20% of cases and cannot exclude dissection.

Laboratory tests:

  • D-dimer: negative result (<500 ng/mL) has high negative predictive value within 24 hours of symptom onset, but low specificity limits utility
  • Troponin, CBC, metabolic panel, coagulation studies, type and cross-match

Definitive imaging

One of three modalities is used based on availability and patient stability:

CT angiography (CTA) of the chest, abdomen, and pelvis:

  • First-line test in most centers
  • Sensitivity >95%, specificity >95%
  • Shows intimal flap, true and false lumens, entry and re-entry tears, branch vessel involvement
  • Rapid acquisition suitable for unstable patients

Transesophageal echocardiography (TEE):

  • Sensitivity 95-98%, specificity 90-95%
  • Excellent for Type A dissection, ascending aorta, and aortic valve assessment
  • Can be performed at bedside or in OR
  • Limited visualization of distal ascending aorta and arch due to tracheal air artifact
  • Operator-dependent

MRI/MRA:

  • Sensitivity and specificity >95%
  • Best for chronic dissection follow-up
  • Not suitable for unstable patients due to time required and limited monitoring capability

Transthoracic echocardiography (TTE): low sensitivity (60-70%) for dissection but useful for detecting aortic regurgitation, pericardial effusion, and wall motion abnormalities.

Diagnostic criteria on imaging

Direct signs: intimal flap separating true and false lumens, differential flow velocities between lumens.

Indirect signs: aortic dilation, pericardial or pleural effusion, branch vessel compromise.

Type A dissection is a surgical emergency; diagnosis should lead to immediate cardiothoracic surgery consultation. Type B dissection is typically managed medically unless complicated by rupture, malperfusion, refractory pain, or uncontrolled hypertension.

Differential diagnosis

Aortic dissection must be distinguished from other causes of acute severe chest pain:

Cardiovascular

  • Acute coronary syndrome: crescendo pain, ECG changes, elevated troponin; however, coronary involvement by dissection can cause true MI
  • Pulmonary embolism: dyspnea, hypoxemia, D-dimer elevation; may coexist with dissection
  • Acute pericarditis: positional pain, diffuse ST elevation, pericardial rub
  • Thoracic aortic aneurysm without dissection: chronic symptoms, no acute intimal tear

Non-cardiovascular

  • Esophageal rupture (Boerhaave syndrome): severe pain after vomiting, subcutaneous emphysema, pleural effusion
  • Pneumothorax: sudden dyspnea, absent breath sounds, hyperresonance
  • Musculoskeletal pain: reproducible on palpation, positional, less severe
  • Mediastinal mass or tumor: subacute presentation, systemic symptoms

Key discriminators for dissection: maximal pain at onset, migratory pain, pulse or blood pressure differentials, history of hypertension or connective tissue disorder.

Clinicians must maintain high suspicion because misdiagnosis as ACS with subsequent thrombolytic administration can be catastrophic.

Management

Management depends on dissection type and is focused on blood pressure and heart rate control to limit propagation, along with definitive repair when indicated.

Immediate medical management (all patients)

Initiate in the emergency department before diagnostic imaging if suspicion is high:

Blood pressure control:

  • Target systolic BP 100-120 mmHg (or lowest pressure maintaining organ perfusion)
  • IV beta-blockers first-line: reduce heart rate to 60 bpm and decrease aortic wall stress
  • Labetalol (alpha and beta blockade)
  • Esmolol (short-acting, titratable)
  • Metoprolol
  • Vasodilators after beta-blockade: calcium channel blockers or nitroprusside if BP target not met; never give vasodilators alone (reflex tachycardia worsens shear stress)

Pain control: IV opioids reduce sympathetic surge

Monitoring: ICU admission, continuous arterial line monitoring, telemetry

Type A dissection (ascending aorta)

Emergency surgical repair is the standard of care:

  • Median sternotomy, cardiopulmonary bypass
  • Resection of intimal tear, replacement of affected aorta with synthetic graft
  • Aortic valve resuspension or replacement if regurgitation present
  • Without surgery, mortality is 1-2% per hour

Surgery is contraindicated only in: profound neurologic injury, significant comorbidities precluding survival, or patient/family refusal.

Type B dissection (descending aorta)

Medical management is first-line for uncomplicated Type B:

  • Intensive BP and heart rate control as above
  • ICU monitoring for 24-48 hours, then step-down
  • Transition to oral antihypertensives (beta-blockers, ACE inhibitors, ARBs)
  • Imaging follow-up at discharge, 1 month, 6 months, then annually

Thoracic endovascular aortic repair (TEVAR) or open surgery indicated for:

  • Complicated Type B: rupture, malperfusion syndrome (visceral, renal, limb ischemia), refractory hypertension, persistent pain, rapid expansion
  • TEVAR involves endovascular stent-graft placement to cover the entry tear and promote false lumen thrombosis
  • Outcomes with TEVAR are superior to open surgery for Type B

Long-term management

All survivors require:

  • Lifelong antihypertensive therapy: beta-blockers are preferred; target BP <120/80 mmHg
  • Surveillance imaging: CT or MRI at 1, 3, 6, 12 months, then annually to detect aneurysm formation or redissection
  • Activity modification: avoid heavy lifting, Valsalva maneuvers, contact sports
  • Genetic counseling and family screening for patients with connective tissue disorders or FTAAD

Aortic diameter >5.5-6 cm warrants elective repair to prevent rupture.

Complications and prognosis

Acute complications

  • Aortic rupture: into pericardium (tamponade), pleural space, or mediastinum; rapidly fatal
  • Cardiac tamponade: from hemopericardium in Type A
  • Acute severe aortic regurgitation: heart failure and cardiogenic shock
  • Myocardial infarction: coronary ostial involvement
  • Stroke: carotid or vertebral artery involvement
  • Paraplegia: spinal cord ischemia from intercostal or spinal artery compromise (2-10% in Type B)
  • Mesenteric ischemia: superior mesenteric artery involvement
  • Renal failure: renal artery involvement
  • Limb ischemia: iliac or subclavian artery compromise

Prognosis

Type A dissection:

  • Without surgery: 50% mortality at 48 hours, 90% at 1 month
  • With emergency surgery: in-hospital mortality 15-30%
  • 5-year survival after successful repair: 60-80%

Type B dissection:

  • Uncomplicated, medical management: in-hospital mortality 10%
  • Complicated Type B requiring intervention: mortality 30-40%
  • 5-year survival with medical management: 60-80%

Long-term issues

  • Chronic dissection: false lumen may persist; 20-40% develop aneurysmal dilation requiring repair
  • Redissection: occurs in 10-15%, usually in the first year
  • Aortic regurgitation: may progress and require valve surgery
  • Chronic pain syndrome: from aortic wall stretching

Predictors of poor outcome: advanced age, hypotension/shock at presentation, cardiac tamponade, mesenteric ischemia, acute renal failure, coma or stroke, prior cardiac surgery.

Lifelong surveillance and strict blood pressure control are essential. Approximately 30% of long-term survivors require additional aortic surgery for aneurysm or redissection.

Mnemonic

DISSECT for risk factors: Drugs (cocaine), Iatrogenic, Syndromic (Marfan/Ehlers-Danlos), Syphilis (historical), Elevated BP, Coarctation, Trauma.

Practice questions

1. A 62-year-old man with a history of hypertension presents to the emergency department with sudden-onset severe tearing chest pain radiating to his back. His blood pressure is 180/100 mmHg in the right arm and 150/90 mmHg in the left arm. Physical examination reveals a diastolic murmur at the left sternal border and diminished right radial pulse. ECG shows left ventricular hypertrophy without acute ischemic changes. What is the most appropriate next step in management?

Answer: B. This patient has classic features of Type A aortic dissection: sudden tearing chest pain radiating to the back, blood pressure differential between arms, pulse deficit, and aortic regurgitation murmur. CT angiography is the first-line diagnostic test with >95% sensitivity. Immediate IV beta-blocker therapy should be initiated to lower blood pressure and heart rate to prevent propagation. Antiplatelet agents and thrombolytics would be dangerous and potentially fatal. While awaiting imaging, medical management should begin based on high clinical suspicion.

2. A 35-year-old tall, thin man with known Marfan syndrome presents with acute onset substernal chest pain. His blood pressure is 90/60 mmHg, heart rate is 110/min, and he appears diaphoretic. Cardiac examination reveals muffled heart sounds and jugular venous distension. ECG shows sinus tachycardia with low voltage. What is the most likely complication?

Answer: C. This Marfan syndrome patient presents with classic findings of cardiac tamponade: hypotension, muffled heart sounds, jugular venous distension (Beck's triad), and low-voltage ECG. In a young patient with Marfan syndrome presenting with acute chest pain, Type A aortic dissection with rupture into the pericardium causing hemopericardium is the most likely diagnosis. Marfan patients develop dissection at younger ages due to cystic medial degeneration. Emergency pericardiocentesis and surgical repair are required.

3. A 68-year-old woman presents with sudden severe interscapular pain. CT angiography confirms a Stanford Type B aortic dissection involving the descending aorta distal to the left subclavian artery. Her blood pressure is controlled at 115/70 mmHg on IV esmolol and nicardipine. She has no evidence of end-organ ischemia, and pain is controlled. What is the most appropriate management?

Answer: C. This is an uncomplicated Type B aortic dissection, for which medical management is first-line therapy. Treatment includes aggressive blood pressure and heart rate control (target systolic BP 100-120 mmHg, HR <60 bpm), typically with IV beta-blockers followed by vasodilators. ICU monitoring for 24-48 hours is appropriate. Surgical or endovascular repair (TEVAR) is reserved for complicated Type B dissections with rupture, malperfusion, refractory pain, or uncontrolled hypertension. Discharge is premature at this stage, and maintaining hypertension would worsen outcomes.

Frequently asked questions

What causes aortic dissection?

Aortic dissection is caused by a tear in the intimal layer of the aorta that allows blood to dissect between the arterial wall layers. The primary underlying cause is degeneration of the aortic media, most commonly from chronic hypertension (present in 70-80%). Other causes include connective tissue disorders like Marfan syndrome and Ehlers-Danlos syndrome, bicuspid aortic valve, cocaine use, trauma, and iatrogenic injury during cardiac procedures. Advanced age and male sex are additional risk factors.

What are the first symptoms of aortic dissection?

The cardinal symptom is sudden-onset severe chest pain, described as tearing, ripping, or sharp, that is maximal at onset. The pain typically occurs in the anterior chest (Type A dissection) or between the shoulder blades (Type B dissection). The pain may migrate as the dissection propagates. Other early symptoms include syncope, pulse deficits, blood pressure differences between arms, and symptoms of end-organ ischemia such as stroke, limb pain, or abdominal pain. About 10-15% of patients present without pain, particularly the elderly.

How is aortic dissection diagnosed?

Diagnosis requires imaging, typically CT angiography of the chest, abdomen, and pelvis, which has >95% sensitivity and specificity and shows an intimal flap separating true and false lumens. Transesophageal echocardiography is an alternative, especially useful for Type A dissection and bedside evaluation in unstable patients. Initial tests include ECG to exclude MI and chest X-ray, which may show widened mediastinum but is normal in 10-20% of cases. D-dimer has high negative predictive value if negative within 24 hours but low specificity.

Is aortic dissection curable?

Aortic dissection is treatable but not truly curable. Type A dissection requires emergency surgery to replace the affected segment, with in-hospital survival of 70-85%. Type B dissection is typically managed medically with blood pressure control and has 90% in-hospital survival if uncomplicated. However, survivors require lifelong antihypertensive therapy and surveillance imaging because 30% develop late complications such as aneurysm formation or redissection requiring further surgery. With proper treatment and follow-up, 5-year survival is 60-80%.

Aortic dissection vs myocardial infarction — what is the difference?

Aortic dissection and MI both cause severe chest pain but differ in key ways. Dissection pain is sudden, maximal at onset, tearing/ripping in quality, and often radiates to the back, while MI pain typically builds gradually and is crushing or pressure-like. Dissection causes pulse or blood pressure differences between limbs, while MI does not. ECG in dissection is often normal or shows LVH, whereas MI shows ST-segment elevation or depression. Troponin may be elevated in both if dissection involves coronary arteries. This distinction is critical because thrombolytics given for presumed MI can be fatal in dissection.

Key drugs

LabetalolEsmololMetoprololNicardipineNitroprussideMorphineDiltiazemVerapamil
Thoracic aortic aneurysmMarfan syndromeEhlers-Danlos syndromeAcute coronary syndromeCardiac tamponadePulmonary embolismAortic regurgitationBicuspid aortic valve

Sources and further reading

StatPearls (NCBI Bookshelf)MedlinePlusWHO ICD-10: I71.0

Educational content for medical students, prepared by the WhiteCoat Pro editorial team with AI assistance; every page is reviewed by a second AI model for factual errors. It is not medical advice and does not replace the product label, local guidelines or a clinician.