Aortic Dissection
A tear in the aortic intima allows blood to dissect between the intimal and adventitial layers, creating a false lumen that propagates along the aorta, compresses branch vessels, and ruptures into the pericardium or pleural space — Stanford type A involves the ascending aorta and is a surgical emergency, while type B is restricted to the descending aorta and is generally managed medically unless complicated.
Typical presentation
A patient with poorly controlled hypertension or a connective-tissue diathesis presents with sudden severe anterior chest or interscapular pain that is maximal at the moment of onset, often described as tearing or ripping, with migration of the pain across territories as the dissection flap propagates.
Clinical Pattern
A patient with poorly controlled hypertension or a connective-tissue diathesis presents with sudden severe anterior chest or interscapular pain that is maximal at the moment of onset, often described as tearing or ripping, with migration of the pain across territories as the dissection flap propagates. Pulse asymmetry, a new aortic regurgitation murmur, or hypotension after presenting hypertension redirect the differential toward dissection in any chest-pain patient with the demographic profile. Painless dissection occurs in approximately 5-10% of cases in registry series, more often in older patients and in those with diabetes, a known aneurysm, or prior cardiac surgery, who tend to present instead with syncope, heart failure, or stroke, so the absence of tearing pain does not exclude the diagnosis when other dissection features are present.
An elevated troponin can reflect coronary ostial compromise or systemic hypoperfusion from dissection. Acute ostial involvement is coronary pathology and is not automatically secondary myocardial infarction; dissection alone does not establish primary myocardial infarction. When dissection is suspected, urgent aortic imaging precedes antithrombotic treatment, and type A dissection requires emergency surgery.
Pathophysiology and Clinical Expression
Chronic hypertension, connective tissue disease, or aging weakens the elastic and collagen scaffolding of the aortic media — cystic medial necrosis is the classic histology in Marfan syndrome. Under shear stress the intima tears, most commonly at the sinotubular junction at the start of the ascending aorta (50–65% of tears) or just distal to the left subclavian artery at the aortic isthmus (20–30%); approximately 90% of intimal tears occur within 10 cm of the aortic valve. Pulsatile blood enters the media and dissects between the intimal and adventitial layers, propagating distally (most often), proximally, or both, to form a false lumen. As the false lumen advances it compresses or shears off the origins of the great vessels, coronaries, spinal arteries, renal arteries, mesenteric arteries, or iliac arteries, producing malperfusion syndromes. Rupture through the adventitia is rapidly fatal; retrograde extension into the pericardium produces tamponade; disruption of the aortic root commissures produces acute aortic regurgitation; and coronary occlusion produces acute myocardial infarction.
This mechanism maps directly onto the bedside picture. The migrating, multi-territory pain pattern reflects the false lumen advancing along the aorta — pain that begins substernal, becomes interscapular, then epigastric, then flank, is dissection until proven otherwise. Pain is maximal at the moment of onset because the tear is a discrete mechanical event, in contrast to ACS, in which pain crescendos over minutes as ischemia evolves. The branch-vessel ischemic findings — stroke, paraplegia, limb ischemia, mesenteric ischemia, AMI — explain why dissection masquerades as so many other diagnoses; locking onto the first explanation misses the unifying diagnosis. An aortic regurgitation murmur with chest pain redirects the differential toward type A dissection involving the aortic root, and hypotension after presenting hypertension suggests rupture, tamponade, or acute severe AR — terminal events that demand immediate operative management. Empiric anticoagulation or thrombolysis is catastrophic in dissection because it expands hemorrhage into the false lumen — the rationale for excluding dissection before treating presumed ACS or stroke when high-risk features coexist.
Epidemiology and Pretest Probability
Aortic dissection follows a bimodal age distribution: a younger peak in patients with connective tissue disorders or congenital aortopathies, and a larger peak after age 50 in patients with chronic hypertension — mean age at presentation is approximately 63 years. Male predominance is approximately 65%; women present at older ages, more often with intramural hematoma, and carry higher in-hospital mortality. The pooled incidence is 2.9 to 4.7 cases per 100,000 persons per year. Acute aortic syndromes — classic dissection, intramural hematoma, and penetrating atherosclerotic ulcer — are uncommon overall, but each missed case carries high mortality. In pregnancy, dissection clusters in the third trimester and early postpartum period and is rare overall but disproportionately fatal. The demographic profile that most often defeats the classic older-hypertensive-male picture is young (<40) patients with Marfan, Ehlers-Danlos, Loeys-Dietz, bicuspid aortic valve, or familial thoracic aortic disease; pregnant or early-postpartum women with connective-tissue disease; recent cocaine or amphetamine use; and deceleration trauma at any age. Chronic hypertension is the single most important risk factor, present in approximately 72% of cases, with systolic blood pressure above 200 mmHg observed in approximately 50% of patients at presentation — the fuller list of predisposing conditions (connective tissue disease, bicuspid aortic valve, family history, prior aortic surgery or dissection, cocaine use, pregnancy, syphilis, trauma) is detailed in the illness script core below.
The base rate of aortic dissection in undifferentiated chest pain is low — far rarer than ACS, GERD, or musculoskeletal pain — but the consequence of a missed diagnosis is catastrophic, so the threshold to consider it stays low; approximately 22% of cases remain undiagnosed prior to death. Pretest probability is anchored to the Aortic Dissection Detection Risk Score (ADD-RS), which stratifies patients with suspected acute aortic syndrome into a 0–3 point score across three categories — high-risk predisposing conditions (Marfan syndrome, family history of aortic disease, known aortic valve disease, recent aortic manipulation, known thoracic aortic aneurysm), high-risk pain features (abrupt onset, severe intensity, ripping or tearing quality), and high-risk exam findings (pulse deficit or limb-to-limb systolic blood pressure differential, focal neurologic deficit with chest/back/abdominal pain, new aortic insufficiency murmur with pain, shock or hypotension) — with one point awarded per category in which any listed feature is present. ADD-RS ≥1 has a pooled sensitivity of approximately 94% for acute aortic syndrome (95% CI 90–96% in a 26,598-patient meta-analysis); the combination of ADD-RS ≤1 plus a negative D-dimer (<500 ng/mL) carries a missed-diagnosis rate of approximately 0.3% in prospective validation and pooled meta-analyses, with combined sensitivity approaching 99–100%. For ADD-RS ≥2, definitive imaging proceeds without reliance on D-dimer. Pretest probability modifies the interpretation of every downstream finding: a "good story" for ACS does not exclude dissection, because the two share risk profiles (older, hypertensive, male) and can coexist when retrograde dissection occludes a coronary ostium.
Illness Script Core
Predisposing Conditions
- Chronic hypertension — the single most important risk factor, present in approximately 72% of cases; systolic blood pressure >200 mmHg is observed in approximately 50% of patients at presentation.
- Connective tissue disease: Marfan syndrome, Ehlers-Danlos syndrome (vascular type), and Loeys-Dietz syndrome.
- Bicuspid aortic valve independently weakens the ascending aortic wall; calcification typically appears in the fourth decade with symptoms by the sixth.
- Family history of aortic dissection or thoracic aortic aneurysm.
- Pre-existing thoracic aortic aneurysm.
- Prior cardiac or aortic surgery is reported in approximately 22% of dissections; iatrogenic intimal injury and chronic shear at suture lines are mechanisms.
- Prior aortic dissection is an independent risk factor for recurrence.
- Cocaine or amphetamine use produces an acute hypertensive surge superimposed on accelerated medial degeneration.
- Pregnancy, particularly third trimester and early postpartum; the dissection rate in Marfan pregnancies is approximately 4.4%.
- Tertiary syphilis with atherosclerosis of the vasa vasorum.
- Trauma, particularly deceleration injury.
- Cystic medial necrosis is the underlying histologic substrate, present in connective tissue disease and aging.
- Atypical demographics raising suspicion outside the classic profile: young (<40) with Marfan, Ehlers-Danlos, Loeys-Dietz, bicuspid aortic valve, or familial thoracic aortic disease; pregnant or early-postpartum women with connective-tissue disease; recent cocaine or amphetamine use; deceleration trauma in any age.
Temporal Profile
- Pain is maximal at the moment of onset because the tear is a discrete mechanical event — the tempo that separates dissection from ACS, in which pain crescendos over minutes as ischemia evolves.
- Abrupt onset, maximal at the moment of onset, is present in approximately 84% of cases; its absence lowers but does not exclude probability.
- Migration of pain across chest, back, and abdomen tracks the propagating dissection flap and carries a strongly elevated likelihood ratio.
- Progressive dissection can continue after symptoms ease — cessation of pain does not equal resolution, since blood may re-enter the true lumen and create a falsely reassuring clinical picture.
Symptom Clusters
- The prototypical vignette: a 60-year-old man with poorly controlled hypertension, often with a smoking history, presents with abrupt severe anterior chest pain that began moments ago at maximum intensity and radiates between the shoulder blades, described as tearing; he is hypertensive on arrival, the right radial pulse is weaker than the left, a soft early diastolic murmur is appreciable at the right upper sternal border, and the chest radiograph demonstrates a widened mediastinum.
- No chest pain at all occurs in approximately 10% of cases — painless dissection is a recognized symptom cluster in its own right and is detailed further under Atypical Variants.
Physical Exam Patterns
- Unilateral carotid, radial, or femoral pulse deficit (pooled LR+ roughly 5.7, with a wide confidence interval) — one of the highest-LR exam findings; present in approximately 15% of cases and predicts increased Type A mortality.
- Inter-arm systolic blood pressure differential >20 mmHg (elevated LR+) — useful when present; also occurs in healthy elderly patients with subclavian atherosclerosis.
- New aortic insufficiency (early diastolic) murmur with chest pain (LR+ ~5 for type A) — present in approximately 32% of cases; implies type A involvement of the aortic root.
- Focal neurologic deficit with chest, back, or abdominal pain (LR+ 4.4) — present in approximately 20% of type A cases, from carotid extension (stroke) or spinal artery occlusion (paraplegia).
- Hypotension or shock (LR+ 2.9) — present in 18–25% of cases; implies rupture, tamponade, severe acute AR, or massive blood loss.
- Systolic blood pressure <100 mmHg (LR+ ~5 for type A) — discriminates type A from type B dissection.
- Hoarseness, dysphagia, or Horner syndrome — suggestive of mass effect from a dilated proximal aorta on adjacent structures.
Rule-In Features
- All three von Kodolitsch predictors present (tearing/ripping pain + pulse deficit + mediastinal widening) — LR+ 65.8; virtually pathognomonic.
- Two of three von Kodolitsch predictors — LR+ 5.3; a strong positive shift.
- Migrating pain across chest, back, and abdomen — strongly elevated LR+; tracks the propagating dissection flap.
- Tearing or ripping pain quality — elevated LR+; approximately half of patients describe pain this way, the remainder describe sharp or pressure pain.
- Anterior chest pain — elevated LR+; approximately 60% of cases, more common with type A involvement.
- Radiation to interscapular back — elevated LR+; more common with descending (type B) involvement.
- Syncope at onset — elevated LR+; occurs in approximately 10% of type A presentations, suggesting tamponade, severe AR, or stroke from arch involvement.
Rule-Out Features
- Absence of all three von Kodolitsch predictors (tearing/ripping pain, pulse deficit, mediastinal widening) — LR- 0.1; a strong negative shift in a low-pretest patient.
Atypical Variants
Painless dissection. A meaningful subset of confirmed dissections present without chest, back, or abdominal pain (approximately 5-10% in registry series, more often in older patients and in those with diabetes, a known aneurysm, or prior cardiac surgery). The presenting complaint is one of the dissection's complications: stroke (carotid involvement), syncope (tamponade or aortic-arch propagation), acute limb ischemia, paraplegia (spinal artery occlusion), or new aortic regurgitation murmur. Substitutes for the classic ripping/tearing-pain feature: a focal neurologic or limb-ischemic deficit dominates the presentation.
Stroke-presenting dissection. Frank stroke complicates roughly 5-15% of type A dissections (hemiparesis, dysphasia) when the dissection extends into the carotid arteries — large registries report the lower end and single-center series the higher — part of the broader ~20-30% that present with some neurologic finding (syncope, transient or focal deficit, or coma); type A extension into the carotid producing a focal neurologic deficit specifically is reported in approximately 20% of cases. The temptation is to start tPA — which is catastrophic in a dissection. Substitutes for the classic chest-pain feature: pain may be absent or minor, and the stroke team's tempo can fast-track the patient past the pulse-deficit / blood-pressure-asymmetry findings — or the chest or back pain itself — that would have raised dissection suspicion.
Syncope-only dissection. Pericardial tamponade from a type-A dissection rupturing into the pericardial sac, or cerebral malperfusion from arch-vessel involvement, produces transient hypotension and syncope as the dominant complaint, with chest pain often described after the fact or absent. Substitutes for the classic acute-pain feature: syncope is the entry signal; the pulse deficit, mediastinal widening, and JVD findings are the diagnostic pivots.
Type B dissection presenting as abdominal or flank pain. Descending dissections involving the abdominal aorta may present with epigastric, flank, or back pain that mimics renal colic, mesenteric ischemia, or AAA. Substitutes for the classic ripping-thoracic-pain feature: a more distal pain location with associated visceral findings (oliguria, lactate-elevated mesenteric ischemia).
Malperfusion-mimicking dissection (AMI, paraplegia, limb ischemia). Retrograde extension into the right coronary ostium produces an inferior STEMI pattern; giving aspirin, anticoagulation, and primary PCI without first obtaining aortic imaging is a known catastrophic error. Spinal artery occlusion from a descending dissection produces paraplegia, and limb ischemia — more common with type B dissection — can be the dominant complaint when a subclavian or iliac artery is occluded by the false lumen. Substitutes for the classic chest-pain-with-tearing-quality feature: the presenting complaint is the downstream ischemic event (STEMI, paraplegia, or a pulseless limb), and the unifying aortic process is found only by asking why a patient with a coronary, spinal, or limb occlusion also has chest or back pain.
Heart failure presentation. Acute severe aortic regurgitation from type A dissection produces flash pulmonary edema and a heart-failure-shaped presentation, particularly when the aortic root is involved. Substitutes for the classic tearing-pain feature: dyspnea and pulmonary edema dominate, and the aortic regurgitation murmur — not the pain history — is the pivot that redirects toward dissection.
Pregnancy and postpartum dissection. Dissection clusters in the third trimester and early postpartum period, particularly in women with Marfan syndrome, and is easily missed because the demographic — young, otherwise healthy, pregnant — does not fit the classic older-hypertensive profile. Substitutes for the classic older-hypertensive-male demographic: a young pregnant or postpartum woman, often with an unrecognized connective-tissue disorder, presenting with chest, back, or abdominal pain that is reflexively attributed to a pregnancy-related cause.
Walk-in presentation. Patients who walk in to triage rather than arrive by EMS experience delayed recognition and are at higher risk of misdiagnosis.
Differential Diagnosis
Life-Threatening Mimics
- Acute coronary syndrome — crescendo substernal pressure with an exertional pattern; ECG with territorial ST changes, a rise/fall troponin, and a coronary distribution on imaging distinguish it — but ACS and dissection coexist when the dissection occludes a coronary, so aortic imaging is indicated when the story is atypical.
- Pulmonary embolism — dyspnea predominant over pain, pleuritic quality, VTE risk factors. CT pulmonary angiography confirms it; a negative D-dimer excludes it only at low or intermediate pretest probability. Right heart strain appears on echo, and there is usually no pulse deficit or new AR murmur.
- Tension pneumothorax — sudden pleuritic pain with absent breath sounds and tracheal deviation; bedside ultrasound or chest radiograph confirms, and needle decompression is the immediate intervention.
- Esophageal rupture (Boerhaave) — severe pain after forceful vomiting with subcutaneous emphysema; pneumomediastinum on imaging, a left pleural effusion, the Mackler triad (vomiting, chest pain, subcutaneous emphysema), and a Hamman sign on auscultation distinguish it.
- Cardiac tamponade (other causes) — the Beck triad and pulsus paradoxus; echo confirms the effusion, and type A dissection can itself be the cause, so aortic imaging is indicated when tamponade is found in a chest-pain patient.
- Symptomatic abdominal aortic aneurysm — abdominal or back pain with a pulsatile abdominal mass; bedside abdominal ultrasound identifies it, rupture is the emergency, and CT is used if the patient is stable.
Common Mimics
- Pericarditis — positional pain, worse supine, better leaning forward; diffuse concave ST elevation with PR depression, a friction rub, and a preceding viral prodrome separate it from dissection.
- Musculoskeletal chest wall pain — reproducible with palpation, no risk profile, normal vitals; a diagnosis of exclusion in a low-pretest-probability patient — reproducible tenderness does not exclude dissection or ACS.
Subtle Look-Alikes
- Stroke / TIA — focal neurologic deficit without chest or back pain; time-sensitive, but chest or back pain in a stroke-appearing patient raises dissection, and pulse asymmetry on exam is informative.
- Pre-eruptive herpes zoster — dermatomal chest or back pain that precedes the vesicular eruption by days can convincingly mimic the pain of dissection; the pain stays within a single dermatomal band rather than migrating across territories, the vesicular rash later declares itself along that same band, and there is no pulse deficit, new aortic regurgitation murmur, or mediastinal widening to accompany it.
Diagnostic Strategy
Initial Approach
- No formal scoring criteria diagnose aortic dissection the way criteria exist for other conditions, so the diagnosis is made only on imaging.
- The first branch point is risk stratification via the Aortic Dissection Detection Risk Score (ADD-RS) (0–3 points across predisposing conditions, high-risk pain, and high-risk exam categories), not any single test.
- Bilateral blood pressures and a pulse exam are obtained early in any chest-pain patient where dissection is being considered, both because they are high-yield findings and because they shape the ADD-RS score that routes the rest of the workup.
- Two related entities — intramural hematoma and penetrating atherosclerotic ulcer — are part of the acute aortic syndrome family, share imaging modalities and initial management principles with classic dissection, though natural history differs.
Targeted Testing
- Confirmatory study. Computed tomography angiography of the chest, extended to the abdomen and pelvis when feasible, confirms dissection when an intimal flap separates a true from a false lumen. Gating the scan to the electrocardiogram sharpens the root and ascending aorta. When the patient is unstable, contrast cannot be given or the scan is non-diagnostic, transesophageal echocardiography shows the same flap. Magnetic resonance angiography is a slower alternative in a stable patient.
- CT angiography of the chest, abdomen, and pelvis with intravenous contrast. Contrast fills the flowing true lumen briskly and the false lumen more slowly or not at all, so the intimal flap appears as a thin line dividing the aorta into two channels, which often opacify at different densities. Pooled sensitivity is approximately 95–100% and specificity approximately 98–100%. CTA also defines proximal and distal extent (Stanford classification), identifies branch vessel involvement, detects pericardial or pleural blood, and screens for end-organ malperfusion.
- Transesophageal echocardiography (TEE) is the bedside alternative in hemodynamically unstable patients, in patients with severe contrast allergy or renal failure where CTA is not feasible, or when CTA is non-diagnostic. Pooled sensitivity and specificity are approximately 95–98%; it visualizes the ascending aorta and aortic root well and can be performed at the bedside, but accuracy is operator-dependent and the descending thoracic aorta is harder to fully image.
- MR angiography can confirm the diagnosis in stable patients (sensitivity and specificity approximately 95–98%, comparable to CTA) but is generally too slow for an acutely unstable presentation; its role is limited to stable or follow-up imaging.
- Chest radiograph shows a widened mediastinum in approximately 50–60% of cases (LR+ ~2.0) and is otherwise of moderate specificity when abnormal (LR- ~0.3); it is a useful clue but a normal CXR does not exclude dissection — the film is completely normal in 12–40% of proven dissections.
- ECG is nonspecific — abnormal in 69–81% of cases (ST depression 15–22%, nonspecific ST/T changes 41–62%, ST elevation 3–4%) — and mainly serves to exclude an obvious alternative STEMI cause; ischemic changes can occur from coronary involvement by the dissection itself.
- D-dimer (<500 ng/mL cutoff) has sensitivity of approximately 94.5–98% but low specificity (~41–69%); it is useful only paired with the ADD-RS as a probability-shifter, not as a stand-alone rule-out.
- Bedside transthoracic echo / POCUS has low sensitivity for dissection itself and is not a confirmatory study, but it detects tamponade, aortic root dilation, or new AR — clues that warrant CTA.
- ADD-RS + D-dimer algorithm (prospective validation and subsequent meta-analyses): an ADD-RS of 0 or 1 with a D-dimer <500 ng/mL effectively rules out acute aortic syndrome, with a failure rate of approximately 0.3%; an ADD-RS of 0 or 1 with a D-dimer ≥500 ng/mL proceeds to CTA; an ADD-RS of ≥2 proceeds directly to CTA regardless of D-dimer result.
- Additional workup runs in parallel with imaging: two large-bore IVs and type and crossmatch for possible transfusion, continuous arterial blood pressure monitoring in both arms when feasible, and bedside echocardiography to evaluate for pericardial effusion, ascending aortic dilation, and new aortic insufficiency. Full-dose anticoagulation, antiplatelet therapy, and thrombolytics are withheld until dissection has been excluded, since laboratory studies do not delay imaging or operative consultation.
Decision Points
- If ADD-RS is 0 or 1 and D-dimer is negative (<500 ng/mL), acute aortic syndrome is effectively ruled out (failure rate approximately 0.3%) and definitive imaging can be deferred.
- If ADD-RS is ≥2, CTA is pursued directly regardless of the D-dimer result.
- If CTA cannot be performed — hemodynamic instability, severe contrast allergy, or renal failure — or is non-diagnostic, TEE becomes the confirmatory study of choice.
- If the chest radiograph is normal, imaging decisions still follow the ADD-RS rather than the film, since the CXR is normal in 12–40% of proven dissections.
- If a patient presents with an inferior STEMI pattern alongside features suggesting dissection (tearing pain, pulse deficit, blood pressure differential), aortic imaging precedes cath lab activation and empiric anticoagulation.
Complications and Natural History
The natural history of an untreated type A dissection is dominated by aortic rupture, most often into the pericardium (tamponade) or the left pleural space (massive hemothorax), and almost always rapidly fatal: cardiac tamponade, acute severe aortic regurgitation, and coronary occlusion, usually inferior from right coronary involvement; these terminal events account for the steeply rising hour-by-hour mortality. Cardiac tamponade presents with the Beck triad of hypotension, jugular venous distension, and muffled heart sounds, though pulsus paradoxus may be absent when concurrent acute aortic regurgitation neutralizes the inspiratory pressure swing. Acute severe aortic regurgitation from aortic root disruption produces a physiology distinct from chronic AR: a shorter diastolic murmur, tachycardia, a pulse pressure that does not widen, a lower systolic blood pressure, and a faint or absent S1 from premature mitral valve closure, with flash pulmonary edema and cardiogenic shock following. Mortality for type A is far higher with medical management alone than with surgery, which carries approximately 18% mortality in contemporary registry data; the gap widens with each hour of delay. Branch-vessel malperfusion produces stroke from carotid involvement (approximately 20% of type A cases), paraplegia from spinal artery occlusion, and limb or visceral ischemia from subclavian, iliac, mesenteric, or renal artery compromise.
Type B dissections follow a milder acute course but a chronic-disease trajectory. Pooled medical mortality is approximately 10.7% for uncomplicated type B; complicated type B (refractory pain, refractory hypertension, malperfusion, aneurysmal dilation, or rupture) carries pooled surgical mortality of approximately 29% and is the primary indication for thoracic endovascular aortic repair (TEVAR). Long-term, residual false-lumen patency drives ongoing aortic remodeling and progressive dilation; lifelong tight blood pressure control with beta-blockade is the cornerstone of secondary prevention, and surveillance imaging of the residual aorta is required.
Iatrogenic complications dominate when the diagnosis is missed in its mimicked form. Aspirin, full-dose heparin, or thrombolysis given for a presumed AMI or stroke expands hemorrhage from the false lumen and is rapidly fatal — the rationale for excluding dissection before treating a high-suspicion ACS or stroke when atypical features (pulse deficit, blood-pressure differential, migrating pain, new aortic regurgitation murmur) coexist. Cessation of symptoms in a patient with suspected dissection does not indicate resolution; the false lumen may have re-entered the true lumen, falsely reassuring the clinician while propagation continues.
Cognitive Pitfalls
- Anchoring on STEMI. Inferior ECG changes from coronary involvement trigger reflexive anticoagulation before aortic imaging.
- Anchoring on stroke. A focal neurologic deficit from carotid involvement is worked up as primary stroke; chest or back pain is dismissed as anxiety; the dissection is missed.
- Anchoring on musculoskeletal back pain. A patient with poorly controlled hypertension and abrupt severe interscapular pain is discharged with NSAIDs.
- Treating a normal CXR as exclusion. A non-widened mediastinum on a portable supine film is reassuring to the eye but means little statistically; the CXR is normal in a substantial proportion of dissections.
- Treating absence of tearing-quality pain as exclusion. Approximately half of patients describe pain as tearing; the remainder describe sharp or pressure pain identical to ACS.
- Treating a normal D-dimer as a stand-alone rule-out. D-dimer sensitivity is high but imperfect; the only cohort in which a negative D-dimer can reasonably defer imaging is the ADD-RS ≤1 group.
- Premature closure on the first explanation. Identifying ACS, stroke, or limb ischemia and stopping there before asking whether dissection is the unifying upstream cause.
- Cutting pressure before rate. Administering a vasodilator without prior beta-blockade increases shear and propagates the dissection.
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