Aortic Dissection: What You Need to Understand

What It Is

The aorta is the largest artery in the body. It leaves the left ventricle, arches over the heart, and descends through the chest and abdomen before dividing at the pelvis into the iliac arteries. Its wall has three layers. The intima is a thin, smooth inner lining. The media is a thick middle layer of smooth muscle and elastin that gives the aorta its mechanical strength. The adventitia is the tough outer coat.

Aortic dissection begins when a tear forms in the intima. Blood under arterial pressure then forces its way through that tear into the media, splitting the wall longitudinally. This propagates, often at extraordinary speed, creating a false lumen that runs parallel to the true lumen. In some cases the dissection propagates proximally, toward the heart. In others it runs distally, down the descending aorta and into the abdominal branches.

The clinical consequences of this propagation depend entirely on which structures the false lumen compresses or obstructs. When it reaches the coronary ostia, it causes myocardial infarction. When it extends to the aortic valve annulus, it causes acute aortic regurgitation, sometimes severe enough to cause acute pulmonary edema within hours. When it reaches the pericardial space, it causes cardiac tamponade. When it blocks the carotid arteries, it causes stroke. When it occludes the mesenteric vessels, it causes bowel ischemia. When it compresses the spinal arteries, it causes paraplegia.

The Stanford Classification

The most widely used classification system divides dissections into two types based on whether the ascending aorta is involved.

Type A: Involves the ascending aorta (regardless of where the tear originates). This is the immediately life-threatening category. Approximately 60 to 70 percent of acute aortic dissections are Type A. Without surgery, hourly mortality in the first 48 hours approaches 1 to 2 percent per hour.

Type B: Does not involve the ascending aorta. The tear is typically in the descending thoracic aorta, distal to the left subclavian artery. Most uncomplicated Type B dissections are managed medically. Complicated Type B dissections (those with malperfusion, persistent pain, rupture, or rapid expansion) require intervention.

The older DeBakey classification divides dissections into Types I (involves the entire aorta), II (ascending only), and III (descending only). DeBakey I and II correspond to Stanford A; DeBakey III corresponds to Stanford B. The Stanford system has largely replaced DeBakey in clinical practice because the management decision hinges on ascending versus non-ascending involvement.

Acute Versus Chronic

Aortic dissection is acute when presentation occurs within 14 days of symptom onset. It is subacute between 15 and 90 days. It is chronic beyond 90 days. Approximately 5 to 15 percent of patients with chronic Type B dissections develop late aortic expansion requiring intervention.

The Mechanism

Why the Aortic Wall Fails

The primary failure is mechanical. The media, subjected to decades of pulsatile stress, develops cystic medial degeneration: fragmentation of the elastin fibers and replacement by pools of mucoid material. This is not a disease of lifestyle in the way coronary artery disease is. It is a structural deterioration that hypertension accelerates dramatically.

Hypertension is present in approximately 75 percent of patients with Type B dissection and 60 percent of those with Type A 5 / Solid . The mechanism is straightforward: raised systolic pressure produces higher peak wall stress with each heartbeat. Over decades, this cycles the aortic wall through mechanical fatigue that healthy architecture can tolerate but degenerated media cannot.

Several conditions accelerate medial degeneration:

Marfan syndrome. An autosomal dominant disorder of fibrillin-1 (FBN1 gene) that weakens elastic tissue throughout the body. The aortic root dilates progressively, and dissection risk is substantially raised. Patients with Marfan syndrome tend to dissect at younger ages and at smaller aortic diameters than those without connective tissue disorders. About 5 percent of Type A dissections occur in patients with Marfan syndrome 5 / Solid .

Bicuspid aortic valve. Present in approximately 1 to 2 percent of the population. Bicuspid valves are associated with aortopathy regardless of valvular function. The ascending aorta dilates faster and dissects at lower diameters than in tricuspid valve patients. The reason is partly hemodynamic and partly intrinsic medial disease related to the developmental abnormality.

Loeys-Dietz syndrome, vascular Ehlers-Danlos syndrome, Turner syndrome. Each of these heritable conditions carries raised dissection risk through distinct molecular mechanisms. Vascular Ehlers-Danlos (caused by COL3A1 mutations) carries particularly high mortality from arterial rupture; prophylactic repair has a worse risk-benefit profile than in Marfan syndrome.

Cocaine and methamphetamine. These catecholamine-surge drugs cause abrupt hypertensive spikes and have a well-documented association with aortic dissection in younger patients, often without underlying aortopathy.

Iatrogenic dissection. A small fraction of dissections are caused by cardiac catheterization, aortic cannulation during cardiac surgery, or intra-aortic balloon pump placement. These are Type A dissections that present in a monitored setting, which paradoxically can improve outcomes because the diagnosis is not delayed.

The Propagation Cascade

Once the intimal tear forms, blood enters the media under systemic arterial pressure. The false lumen expands with each systolic ejection. The rate of propagation depends on blood pressure, heart rate, and the integrity of the remaining medial tissue. This is why the first principle of medical management is “anti-impulse therapy”: lower the systolic pressure below 120 mmHg and reduce the heart rate to below 60 beats per minute. Both maneuvers reduce aortic wall stress and slow or stop false lumen propagation.

The aortic valve may be pulled apart by the expanding dissection plane. As the false lumen extends proximally and dilates the aortic root, the valve commissures detach and the leaflets prolapse into the left ventricular outflow tract. Acute aortic regurgitation of this severity cannot be tolerated hemodynamically for long. The left ventricle, unprepared for the sudden volume load, dilates acutely and fails.

How We Diagnose

Who Should Raise Suspicion

The classic presentation is sudden-onset, maximal-at-onset, tearing or ripping chest pain radiating to the back. But only about half of patients describe “tearing.” Many describe “ripping.” Many describe “the worst pain of my life.” Some describe only back pain, without chest pain. A subset presents with syncope, stroke symptoms, or acute limb ischemia, with pain playing a secondary role.

The 2010 American Heart Association/American College of Cardiology guidelines introduced the Aortic Dissection Detection Risk Score (ADD-RS), which assigns points for three categories: predisposing conditions (hypertension with medial degeneration, known aortic disease, Marfan syndrome, family history), pain features (abrupt onset, tearing/ripping quality, radiating to back), and examination findings (pulse deficit, blood pressure differential >20 mmHg, focal neurological deficit, new aortic regurgitation murmur, hypotension or shock). A score of zero requires supplemental biomarker evidence before imaging; a score of one or higher warrants urgent CT angiography.

The problem with ADD-RS is that it performs better in academic retrospective series than in real emergency departments. Missing this diagnosis is catastrophic. In clinical practice, a low threshold for CT angiography in any patient with severe, sudden chest or back pain is defensible and widely practiced.

The Diagnostic Workup

Chest radiograph. A widened mediastinum (>8 cm at the aortic knob) is present in approximately 60 percent of dissections but its absence does not exclude the diagnosis. An irregular aortic contour, displacement of aortic wall calcification inward from the outer wall (the “calcium sign”), and pleural effusion (especially left-sided, representing hemothorax) are supportive findings. The chest radiograph buys time for resource mobilization but is never diagnostic.

CT angiography. The standard of care for diagnosis. Sensitivity exceeds 98 percent and specificity exceeds 95 percent. It identifies the entry tear, the extent of the false lumen, the involvement of branch vessels, and the presence of pericardial effusion or hemothorax. The scan takes minutes in a modern facility. The contrast load is a real concern in patients with renal insufficiency, but the risk of contrast nephropathy is acceptable when the alternative is missing a lethal diagnosis.

Transesophageal echocardiography (TEE). Sensitivity for Type A dissection approaches 98 to 99 percent in experienced hands. It has the advantage of portability: it can be performed in the operating room immediately before surgery, avoiding the time cost of transfer to CT. It also provides detailed assessment of the aortic valve, coronary ostia, and pericardial space. The limitation is that it requires conscious sedation or general anesthesia and is operator-dependent. In a stable patient in an institution with 24/7 CT availability, CT angiography is typically faster.

MRI. Excellent sensitivity and specificity, no radiation. Not useful in the acute setting because scan times are long, the patient is not monitored adequately during the scan, and hemodynamically unstable patients cannot tolerate the protocol. MRI is valuable for surveillance of chronic dissections and for characterizing aortic anatomy in patients with renal failure where CT contrast is contraindicated.

Biomarkers. D-dimer, if negative (<500 ng/mL), has a high negative predictive value for aortic dissection in low-risk patients. However, it cannot be used to rule out dissection in intermediate or high-risk presentations. Smooth muscle myosin heavy chain, soluble elastin fragments, and calponin have been studied as aortic dissection biomarkers but none has achieved clinical adoption. As of 2026, there is no blood test that rules out dissection in a high-risk presentation. CT angiography remains the definitive answer.

The Blood Pressure Differential

A blood pressure differential greater than 20 mmHg between arms is present in approximately 20 percent of Type A dissections and suggests involvement of the innominate artery or left subclavian artery. Measure both arms in every patient with suspected dissection. When only one arm can be measured, the number must be interpreted knowing you have incomplete information.

The Evidence

Medical Management: The Anti-Impulse Foundation

The goal of medical management is to stop false lumen propagation by reducing aortic wall stress. This means two things simultaneously: lower the systolic blood pressure and lower the heart rate.

Beta-blockers first. Intravenous labetalol (a combined alpha and beta blocker) or esmolol (a short-acting beta-1 selective agent) is the initial agent of choice. Esmolol is preferred when tight titration is needed because its half-life is approximately nine minutes. The target is a heart rate below 60 beats per minute and a systolic pressure below 120 mmHg.

Calcium channel blockers as alternatives. In patients with asthma, reactive airway disease, or significant bradycardia, intravenous diltiazem or verapamil can be used. These agents reduce heart rate and blood pressure through distinct mechanisms from beta-blockers.

Vasodilators require caution. Nitroprusside is an effective vasodilator for acute hypertension but can cause reflex tachycardia, which worsens aortic wall stress. It should never be used as monotherapy. If additional blood pressure reduction is needed after adequate beta-blockade, nitroprusside can be added.

What not to do. Do not give dihydropyridine calcium channel blockers (amlodipine, nifedipine) as initial therapy. They cause reflex tachycardia. Do not give nicardipine as a solo agent for the same reason.

Type A Dissection: The Surgical Evidence

Surgery for Type A dissection is not based on a randomized trial. No randomized trial exists and none will ever exist, for the same reason we do not randomize gunshot wounds to observation versus surgery. The evidence comes from large registries.

In IRAD, in-hospital mortality for Type A dissection was 57.9 percent with medical management and 26.1 percent with surgical management 5 / Solid . The gap is large enough that the recommendation for urgent surgery is considered a Class I indication in every major guideline without the qualifier “unless strongly contraindicated.”

Outcomes have improved with surgical technique and center experience. Contemporary high-volume centers report operative mortality for Type A dissection in the 10 to 15 percent range for elective repairs and 15 to 25 percent for truly acute presentations in patients without major comorbidities. Patients presenting with malperfusion, tamponade, stroke, or shock have substantially higher operative mortality.

The operative approach involves replacing the ascending aorta with a Dacron graft. When the aortic root is involved, root replacement is performed (the Bentall procedure if the valve is diseased or the aortic sinuses are dilated; a valve-sparing root replacement such as the David procedure when the valve leaflets are structurally normal). When the arch is involved, total or hemi-arch replacement under deep hypothermic circulatory arrest is required. These are hours-long procedures performed at the interface of advanced perfusion management, circulatory arrest, and vascular reconstruction. Center volume matters enormously.

Type B Dissection: INSTEAD-XL and the Complicated vs. Uncomplicated Divide

The management of Type B dissection underwent substantial revision following the INSTEAD and INSTEAD-XL trials. INSTEAD enrolled 140 patients with stable (uncomplicated) Type B dissection randomized to guideline-directed medical therapy alone versus thoracic endovascular aortic repair (TEVAR) plus guideline-directed medical therapy. The original trial (2-year follow-up) showed no survival benefit for TEVAR. However, INSTEAD-XL at 5-year follow-up showed that TEVAR significantly improved aorta-specific survival (96.9 percent versus 82.4 percent, p=0.04) and all-cause mortality (88.9 percent versus 79.3 percent, p=0.04) 5 / Solid 61836-3).

The INSTEAD-XL result introduced an important nuance: TEVAR may not save lives in the first two years of uncomplicated Type B dissection, but it appears to improve remodeling of the false lumen in a way that reduces late mortality. This has shifted practice toward earlier TEVAR in select patients with uncomplicated Type B dissection, particularly those with large false lumen diameter, patent false lumen, and high-risk imaging features.

Complicated Type B dissection (defined as rupture, impending rupture, malperfusion of visceral or limb vessels, refractory pain or hypertension despite medical therapy, rapid expansion) requires intervention, and TEVAR has largely supplanted open surgical repair in this setting because it avoids thoracotomy and aortic clamping.

The ADSORB trial randomized 61 patients with uncomplicated Type B dissection to best medical therapy alone versus TEVAR. At one year, TEVAR patients had significantly better false lumen thrombosis (91 percent versus 19 percent) and less aortic expansion 4 / Promising . Aortic remodeling, while not the same as mortality, is a meaningful intermediate endpoint because a thrombosed false lumen is associated with substantially lower risk of late aortic rupture.

The JCS/JSCS 2020 Guidelines

The Japanese Circulation Society and Japanese Society for Cardiovascular Surgery 2020 guidelines on aortic aneurysm and dissection provide a well-developed evidence-based framework that aligns with the European and American guidelines on most major points. The key additions are: explicit risk stratification tools for Type B dissection based on false lumen patency status, strict blood pressure targets (systolic <120 mmHg in the acute phase), and detailed protocols for endovascular intervention timing 5 / Solid .

The Patient Experience

What the Pain Feels Like

Patients use a limited vocabulary for the worst pain of their lives. “Torn.” “Ripped.” “Something exploded.” “Like being stabbed through the chest into the back simultaneously.” The onset is instantaneous. Patients who have had previous severe pain (kidney stones, prior heart attacks) uniformly rank the dissection pain as categorically different.

The pain typically localizes to the anterior chest, the back between the shoulder blades, or both simultaneously. As the dissection propagates, the pain can migrate: it follows the path of the false lumen. A patient who initially reports midsternal pain who then develops flank pain or abdominal pain may be experiencing expansion of the dissection into the abdominal aorta. This migration of pain is an important clinical sign.

Some patients faint at onset, not from pain but from a vagal response or from acute disruption of cerebral perfusion. Some patients develop stroke symptoms. Some present in hemorrhagic shock from aortic rupture. A minority of patients, especially with Type B dissection, describe pain that is severe but tolerates position changes and is not immediately incapacitating. These patients are at risk for delayed diagnosis because their presentation is less typical.

The Hospital Experience

For a Type A dissection, the timeline from emergency department arrival to operating room is measured in hours, ideally less than two. What the patient and family experience in that window is a controlled but intense convergence of multiple teams: emergency medicine, cardiology, cardiothoracic surgery, anesthesia, perfusion, and nursing. Consent for a high-risk procedure must be obtained from a patient who is typically in extreme pain, frightened, and may have received opioid analgesia that affects their processing.

The surgery itself typically takes four to eight hours. The patient emerges intubated, in an intensive care unit, with a chest tube, a urinary catheter, arterial line, central venous line, and Swan-Ganz catheter in place. The first 24 to 48 hours require intensive monitoring for complications: bleeding, stroke, acute kidney injury, mesenteric ischemia, and arrhythmia.

For a Type B dissection managed medically, the first three to seven days require an intensive care unit with continuous arterial pressure monitoring. The blood pressure targets are strict and maintained with intravenous infusions that are titrated to hemodynamic response. The patient lies in bed, attached to monitors, in pain that is managed with intravenous opioids that are tapered as the acute phase resolves.

The Question Families Ask First

“Is he going to make it?”

The honest answer depends on type, extent, time from onset to diagnosis, presence of malperfusion, and surgical center capability. For a Type A dissection caught within six hours in a center that performs more than 30 aortic repairs per year, survival probability is in the 75 to 90 percent range. For a Type A dissection presenting with stroke and shock after 24 hours, operative mortality exceeds 50 percent at any center.

Families should know that the surviving patient will require lifelong surveillance. Aortic dissection is a chronic disease once the acute event is survived. The false lumen does not disappear. It persists, and it can expand over years. Surveillance CT or MRI imaging is required every six to twelve months for the first two years and annually thereafter.

Life After Dissection

Blood pressure control becomes, permanently, the single most important health variable in the life of a dissection survivor. Every major guideline recommends a target systolic blood pressure below 120 to 130 mmHg. Beta-blockers are the preferred first agent. ACE inhibitors and ARBs are used extensively in Marfan syndrome. The patient typically goes from having mildly raised blood pressure managed with one pill to tight control with two or three agents and twice-daily home monitoring.

Physical activity restrictions are real and permanent. Heavy weight lifting, isometric exercise, and contact sports are contraindicated because the abrupt pressure spikes they generate stress the residual dissected aorta. Walking, swimming, and cycling at moderate intensity are generally well tolerated.

Decisions and Trade-Offs

The Imaging-to-OR Pipeline: How Hospitals Should Function

The time from hospital arrival to skin incision for Type A aortic dissection is, in some ways, the cardiovascular equivalent of door-to-balloon time for STEMI. Data from IRAD and from high-volume aortic centers consistently show that shorter time to surgery is associated with better outcomes, and that every hour of delay adds mortality risk.

The critical bottleneck in most institutions is not the OR itself but the pre-operative workup: confirming the diagnosis, obtaining additional imaging of the arch and visceral vessels, waiting for cardiac surgery availability, and completing the consent process with an anxious family in a frightened patient.

The hospitals that perform best have protocolized aortic dissection pathways: a single phone call activates the cardiac surgery team simultaneously with the imaging team; CT angiography acquisition and reading is performed immediately, not in the sequence after initial triage stabilization; an established OR time commitment is made by the operating team within minutes of diagnosis; and the consent process is led by the cardiac surgeon who will perform the operation, not delegated to a house officer.

In Illinois, the highest-volume aortic programs are at Northwestern Medicine in Chicago, Rush University Medical Center, the University of Illinois at Chicago, and Carle Foundation Hospital in Urbana. For patients presenting to community hospitals without on-site cardiac surgery, the transport decision should be made within minutes of diagnosis, not hours.

Long-Term Surveillance After Aortic Dissection Repair

Survival of the acute Type A dissection event does not end the aortic disease. The repaired ascending aorta is stable, but the dissection frequently extends beyond the repair into the arch and descending thoracic aorta, leaving a persistent false lumen in the residual native aorta distal to the surgical repair. This residual dissected segment can expand over years. The five-year rate of requiring a second aortic operation after Type A repair is approximately 20 to 30 percent; many of these are for progressive aneurysmal dilation of the residual false lumen.

Surveillance imaging protocol after Type A repair: CT angiography of the entire aorta (chest, abdomen, pelvis) at 1 month, 6 months, 12 months, and annually thereafter. Any growth of the residual false lumen exceeding 5 mm per year, or total aortic diameter exceeding 55 to 60 mm, triggers reassessment for prophylactic intervention on the descending thoracic aorta.

For Type B dissection survivors, the same surveillance protocol applies. The goal is to detect aneurysmal enlargement before rupture, which is silent in its early phases. Patients and their families should understand that aortic dissection is a lifelong diagnosis: the acute event is survived, but the aorta requires monitoring for the remainder of the patient’s life.

Type A: The Surgical Consent Conversation

The surgeon’s conversation with the family of a patient with Type A aortic dissection is one of the most difficult in all of medicine. The procedure is urgent. The risks are substantial. The alternative is near-certain death.

Several specific decisions must be made in the operating room or immediately before it:

Aortic root management. If the dissection extends to the aortic root and the patient has Marfan syndrome or a dilated root, root replacement (Bentall or David procedure) reduces the risk of future root-related reoperation but adds time and complexity to an already complex procedure. In an elderly patient in shock, the surgeon may elect a more limited resection to reduce cross-clamp time.

Arch management. Extending the repair to the arch (hemi-arch or total arch replacement) under hypothermic circulatory arrest reduces the risk of future arch-related complications but significantly increases operative complexity. The frozen elephant trunk technique, which places a stent graft in the descending aorta simultaneously with arch replacement, has advantages for staged repair of the descending component but is not universally available.

Coronary involvement. If the dissection has compromised the coronary ostia and caused myocardial infarction, the surgeon faces the decision of whether to address the coronary disease at the same time. Typically, after aortic repair, coronary perfusion is restored and revascularization is deferred unless there is clear ongoing ischemia.

Type B: The TEVAR vs. Medical Therapy Decision

For uncomplicated Type B dissection, INSTEAD-XL provides the strongest argument for TEVAR: better 5-year aortic remodeling, with a trend toward improved survival. But the operative mortality of TEVAR for Type B dissection in elective settings ranges from 0 to 3 percent in high-volume centers and up to 10 percent in lower-volume centers. The decision is genuinely patient-specific.

Factors favoring TEVAR in uncomplicated Type B:

• Age below 60 (longer life expectancy means more time to benefit from false lumen remodeling)
• Patent false lumen on imaging (poor spontaneous remodeling probability)
• False lumen diameter above 40 mm at presentation
• Entry tear in the proximal descending aorta amenable to endovascular coverage

Factors favoring continued medical management:

• Age above 75 with significant comorbidities
• False lumen already thrombosed on initial CT
• Patient preference after informed discussion
• Anatomy unfavorable for TEVAR (inadequate landing zone)

The Malperfusion Question

Malperfusion is the most feared complication after Type A repair and the most urgent indication for TEVAR in Type B. When the false lumen compresses the true lumen, branch vessels fed by the true lumen lose flow. This produces ischemia in the organs supplied by those branches.

In Type A dissection, the management sequence for malperfusion before surgery remains debated. Some centers proceed directly to aortic repair, believing that restoring antegrade true lumen flow resolves the malperfusion. Other centers first perform percutaneous fenestration (creating a hole between the true and false lumen to equalize pressure) or stenting of the obstructed branch vessel before aortic repair. The IRAD malperfusion data suggest that upfront aortic repair without pre-operative percutaneous intervention has outcomes similar to the staged approach in most scenarios 4 / Promising .

The Rural Access Problem

Aortic dissection surgery requires a cardiothoracic surgeon with aortic experience, a perfusionist, and a cardiac surgery operating room. These resources exist at approximately 400 to 500 hospitals in the United States. A patient presenting to a rural critical access hospital with a Type A dissection must be transferred. Transfer time is the enemy.

In rural Illinois, transfer from a critical access hospital to Carle Foundation Hospital in Urbana, OSF Saint Francis in Peoria, or Northwestern Medicine in Chicago can take 30 to 90 minutes by ground or 20 to 40 minutes by air. Every minute that the decision to transfer is delayed adds to that time. Emergency physicians in rural settings who maintain a high index of suspicion and initiate transfer before CT confirmation (when the pretest probability is high) save lives.

The SDE recommendation: if you are in a rural area and someone you love has sudden, severe, maximal-at-onset chest or back pain, do not drive to the local emergency department and wait. Call 911. The paramedics can initiate anti-impulse therapy en route, transmit the ECG to rule out STEMI, and activate the transfer system before the patient walks through the emergency department door.

The SDE Synthesis

Aortic dissection sits at the most acute end of the cardiovascular emergency spectrum. It is fast, it is catastrophic, and it has a narrow window for intervention.

From a prevention perspective, the Stop Dying Early framework addresses the dominant modifiable risk factor: uncontrolled hypertension. Seventy-five percent of Type B dissections occur in patients with hypertension. Many of those patients were walking around with systolic pressures in the 150s and 160s, without symptoms, without awareness of their risk. The SDE Audit identifies that gap. It does not require any specialized cardiac procedure. It requires knowing your blood pressure with the same precision you know your mortgage payment.

For patients with known connective tissue disorders (Marfan syndrome, bicuspid aortic valve with aortopathy), the SDE Audit includes aortic root measurement. An aortic root diameter of 4.5 cm in a Marfan patient is a surgical near-threshold. An aortic root of 5.0 cm in a patient with a bicuspid aortic valve is at the boundary of prophylactic intervention. Knowing that number changes everything. Not knowing it means waiting for the 2:47 AM phone call.

For dissection survivors, the SDE Executive tier provides structured surveillance coordination: confirming CT or MRI scheduling, ensuring blood pressure targets are met and documented, reviewing medications for agents that might blunt beta-blockade, and flagging any radiographic progression that warrants subspecialty re-evaluation.

The cardiothoracic surgeons who repair aortic dissections are among the most technically skilled physicians in medicine. They save lives in the middle of the night on patients who have hours left. What they cannot do is replace the preceding decade of blood pressure awareness that might have prevented the event entirely.

That is the SDE thesis, applied to the most acute emergency in this lane.

For patients and families seeking structured cardiovascular risk evaluation after a dissection event or in the presence of aortic disease risk factors: SDE Audit (screening tier), SDE Executive (ongoing management), or direct subspecialty referral through the SDE Cohort program.

Section 3a: The Genetics of Aortic Disease

Heritable Aortopathy: A Systematic Framework

The distinction between sporadic hypertension-driven dissection and heritable aortopathy has major implications for family members. When a 35-year-old dissects a morphologically normal-appearing aorta, the physician must ask whether a genetic explanation exists, not only for the patient’s management but because first-degree relatives may carry the same mutation and benefit from screening.

The FBN1-Marfan Pathway. Fibrillin-1 mutations (FBN1 gene, chromosome 15) produce Marfan syndrome. The phenotype is variable: some patients have classic features (tall stature, arm span exceeding height, arachnodactyly, ectopia lentis, high-arched palate, pectus deformity, dural ectasia, stretch marks), while others present with only cardiovascular manifestations. In the cardiovascular system, the aortic root dilates over time in a characteristic fashion: the aortic sinuses of Valsalva expand while the sinotubular junction becomes proportionally smaller, producing the “inverted pear” root appearance. Beta-blocker therapy in Marfan syndrome reduces the rate of aortic root dilation 4 / Promising . Losartan was hypothesized to be superior through TGF-beta pathway modulation; the COMPARE trial showed no significant difference between losartan and beta-blocker for aortic root growth rate 5 / Solid .

Prophylactic aortic root replacement in Marfan syndrome is recommended when the sinus of Valsalva diameter reaches 5.0 cm (in most guidelines), or at smaller diameters (4.5 cm) in patients with rapid growth (>5 mm/year), family history of dissection, desire for pregnancy, or severe aortic regurgitation. The Bentall procedure (combined aortic root and valve replacement) and the valve-sparing David procedure achieve similar long-term survival in experienced hands. The David procedure preserves the native aortic valve and avoids lifelong anticoagulation, which is a meaningful quality-of-life advantage.

TGFBR1 and TGFBR2: Loeys-Dietz Syndrome. Mutations in the genes encoding transforming growth factor-beta receptors 1 and 2 produce Loeys-Dietz syndrome, which carries a higher risk of dissection at smaller aortic diameters and in arterial beds beyond the aorta. The bifid uvula, hypertelorism, craniosynostosis, and arterial tortuosity of the full phenotype are variable. Many cardiologists recommend earlier surgical thresholds (4.5 cm at the aortic root or less in some series) for Loeys-Dietz given the higher rupture-at-small-diameter risk compared to Marfan syndrome 4 / Promising .

COL3A1: Vascular Ehlers-Danlos Syndrome. Mutations in COL3A1 (encoding type III procollagen) produce vascular EDS, characterized by arterial fragility that affects medium-sized arteries throughout the body: the superior mesenteric artery, celiac artery, renal arteries, and iliac arteries, in addition to the aorta. The spontaneous rupture risk is high; surgical repair of vascular EDS carries high complication rates because the tissue tears easily. The traditional teaching that prophylactic repair reduces mortality has been challenged by studies showing high operative morbidity. Celiprolol (a cardioselective beta-blocker with vasodilatory properties) significantly reduced clinical events in a small RCT of vascular EDS patients 4 / Promising .

Bicuspid Aortic Valve Genetics. Bicuspid aortic valve has a genetic basis in approximately 80 to 90 percent of cases, though the specific genes responsible vary (NOTCH1 pathway mutations in a significant subset). First-degree relatives of patients with bicuspid aortic valve have a 5 to 10 percent risk of having the abnormality themselves, compared to 1 to 2 percent in the general population. Echocardiographic screening of first-degree relatives is a guideline-level recommendation 5 / Solid .

Genetic Testing in Clinical Practice

A patient presenting with aortic dissection under age 50 without long-standing hypertension as a clear cause should undergo genetic testing, regardless of whether external features of a connective tissue disorder are present. Genetic testing panels for heritable aortopathies are commercially available and cover FBN1, FBN2, TGFBR1, TGFBR2, SMAD3, COL3A1, ACTA2, MYH11, and other relevant genes.

Positive genetic testing changes the clinical approach substantially: it establishes the exact surgical threshold appropriate for the mutation, directs family screening, and identifies whether connective tissue involvement in other organ systems requires monitoring. A negative genetic panel does not exclude heritable aortopathy, as the field continues to identify new causative variants.

Genetic counseling is an integral part of managing families with heritable aortopathy. Not all family members want to know their genetic status, particularly for conditions (like vascular EDS) where the clinical management options are limited. This requires the kind of nuanced, non-coercive counseling that a genetics team or cardiologist experienced in inherited cardiovascular disease can provide.

Section 4a: Advanced Imaging in Aortic Dissection

CT Angiography Protocol Details

The diagnostic CT angiogram for suspected aortic dissection is not a standard chest CT. It requires specific protocol parameters: a non-contrast phase first (to identify intramural hematoma, which can be isoattenuating to contrast on enhanced images), a contrast-enhanced arterial phase with bolus triggering at the aortic root, and ideally a delayed venous phase to assess false lumen perfusion dynamics. The scan should extend from the thoracic inlet to the femoral arteries to fully define the dissection extent and identify branch vessel involvement.

Reconstruction must include coronal and sagittal reformats and maximum intensity projections to provide the surgical team a three-dimensional understanding of anatomy before skin incision. Experienced centers generate these reconstructions within minutes of scan completion.

Intramural Hematoma: A Related Entity

Intramural hematoma (IMH) is a variant of acute aortic syndrome in which blood accumulates within the aortic wall without a visible intimal tear on imaging. It is detected on non-contrast CT as a crescent of hyperdensity within the aortic wall. IMH is thought to arise from rupture of the vasa vasorum (small vessels that supply the aortic wall) with bleeding into the media.

IMH behavior is distinct from classic dissection: some cases stabilize and regress over weeks; others progress to frank dissection or aortic rupture. Type A IMH is managed surgically at most centers, following the same logic as Type A dissection. Type B IMH with thickness greater than 10 mm, periaortic hematoma, or focal intimal disruption has a higher risk of progression and typically warrants early TEVAR or careful monitoring in a high-volume center 4 / Promising .

Penetrating Aortic Ulcer

The third component of acute aortic syndrome is penetrating aortic ulcer (PAU): an atherosclerotic plaque that ulcerates through the intima and erodes into the media. PAU is most common in elderly patients with extensive atherosclerosis in the descending thoracic aorta. Many are incidental findings on CT; symptomatic PAU with a deep ulcer crater, surrounding hematoma, or rapid progression warrants intervention. Management parallels complicated Type B dissection: TEVAR in most cases when intervention is indicated 4 / Promising .

Understanding the full acute aortic syndrome triad (classic dissection, IMH, PAU) is important because they may coexist and because management decisions depend on correctly identifying which entity is present.

Section 5a: The Evidence Continued — Guideline-Directed Medical Therapy Targets

Blood Pressure Targets: The Evidence Base

The systolic blood pressure target of below 120 mmHg in the acute phase of aortic dissection is based on physiological reasoning (lower pressure equals lower aortic wall stress) and on retrospective data from IRAD showing that patients who achieved better blood pressure control had lower rates of aortic events during follow-up. The target is lower than the cardiovascular prevention target of below 130 mmHg used in general hypertension management, reflecting the added urgency in the diseased aorta.

Long-term blood pressure control matters beyond the acute phase. In a cohort study of Type B dissection survivors, every 10 mmHg increase in average systolic blood pressure was associated with a significantly higher hazard of aortic events over 5 years 4 / Promising . The precision required is not compatible with casual pharmacotherapy. These patients need twice-daily home blood pressure monitoring, frequent pharmacy check-ins for adherence, and periodic 24-hour ambulatory blood pressure monitoring to detect masked hypertension (adequate office readings but raised overnight pressures).

Beta-Blocker Selection and Dosing

Esmolol (short-acting IV beta-1 blocker, half-life 9 minutes) is preferred in the acute intensive care setting because it allows precise titration without the 2 to 4-hour offset time of oral agents. It is delivered by continuous infusion, typically starting at 50 to 200 mcg/kg/min, with close hemodynamic monitoring.

When transitioning from IV to oral therapy as the patient stabilizes, the preferred oral agents are metoprolol succinate (once daily, long-acting), atenolol, carvedilol (combined alpha-beta blocker that adds afterload reduction), or bisoprolol. The key is selecting an agent and a dose that achieves and maintains the systolic target in every measurement, not just the one taken in clinic. Amlodipine can be added as second-line if a calcium channel blocker is needed for additional blood pressure lowering without rate-lowering effect.

ACE inhibitors and ARBs are added in patients with Marfan syndrome (where losartan and perindopril have been studied) and in those with concomitant diabetes or chronic kidney disease where renin-angiotensin-aldosterone blockade provides organ protection. The combination of a beta-blocker plus ARB is commonly used and well-tolerated.

Diet, Lifestyle, and Non-Pharmacological Management

The anti-impulse principle extends beyond pharmacotherapy. Physical activity that generates acute blood pressure spikes is contraindicated in dissection survivors. This includes heavy weight lifting (squat max loads, deadlifts, overhead presses that involve Valsalva maneuver and produce systolic pressures of 200 to 250 mmHg transiently), contact sports, and competitive sports involving bursts of maximal exertion.

Acceptable exercise for dissection survivors: brisk walking, cycling at low to moderate intensity, swimming (freestyle at moderate pace), light resistance training using low loads and high repetitions without Valsalva maneuver. A structured cardiac rehabilitation program that teaches self-monitoring and defines exercise thresholds by heart rate and perceived exertion provides a safe re-entry to physical activity.

Dietary sodium reduction reduces the pharmacological dose burden needed to achieve blood pressure targets. In patients with poorly controlled hypertension, a reduction from typical Western dietary sodium intake (4,000 to 5,000 mg/day) to below 2,000 mg/day can lower systolic blood pressure by 5 to 8 mmHg: meaningful in a patient where every mmHg matters.

Section 6a: The Patient Experience Continued

The Cognitive Impact of the Acute Event

Aortic dissection survivors frequently report cognitive symptoms in the weeks and months following their event. These include memory difficulties, concentration impairment, word-finding problems, and emotional lability. In Type A dissection patients who underwent surgery with deep hypothermic circulatory arrest, there is a measurable incidence of neurocognitive dysfunction attributable to the period of circulatory arrest and the associated ischemic and reperfusion injury.

Cerebral oximetry monitoring during Type A repair has partially mitigated this, but not eliminated it. Patients should be counseled before discharge that cognitive symptoms are common and often improve over 3 to 6 months. Neuropsychological evaluation at 3 months provides a baseline for recovery tracking. Return-to-work decisions after Type A surgery should account for this cognitive dimension: a patient in a cognitively demanding profession may need a longer recovery period than a patient with less cognitively intensive work.

Pregnancy and Aortic Dissection Risk

The hemodynamic changes of pregnancy (30 to 50 percent increase in blood volume, increase in cardiac output, progesterone-mediated changes in aortic wall compliance) increase the risk of aortic dissection in women with underlying aortopathy. Approximately 50 percent of dissections in women under 40 occur during or immediately after pregnancy 4 / Promising .

Women with Marfan syndrome and aortic root diameters above 4.0 to 4.5 cm are advised against pregnancy until prophylactic surgery is performed. Women with root diameters below 4.0 cm who wish to become pregnant should have preconception genetic counseling, beta-blocker therapy (the safest beta-blocker in pregnancy is labetalol), and monthly aortic imaging during pregnancy, with delivery planned at a center with cardiac surgical capability.

This is a conversation that needs to happen proactively, not urgently. Cardiologists who manage young women with Marfan syndrome or bicuspid aortic valve aortopathy should initiate the pregnancy planning discussion well before conception, not in the third trimester.

Employment and Driving After Dissection

Patients often return to work within 6 to 12 weeks after Type A dissection repair, depending on occupation. Commercial vehicle operation is typically restricted for 6 to 12 months or permanently, depending on jurisdiction and the nature of residual aortic disease. Aviation careers are generally incompatible with a history of aortic dissection.

Patients must be counseled explicitly about what activities are safe and for how long restrictions apply. A patient who does not understand why heavy lifting is restricted will not comply with the restriction. The explanation should name the mechanism: a Valsalva-associated systolic pressure spike of 220 mmHg in a surgically repaired ascending aorta with a residual descending dissection is a real risk for false lumen expansion or rupture.

Financial and Logistical Implications

Open Type A dissection repair at a high-volume center costs $100,000 to $200,000 or more for the acute hospitalization alone. TEVAR for Type B dissection costs $30,000 to $80,000. The surveillance CTs or MRIs required every 6 to 12 months for the remainder of the patient’s life represent a recurring cost of $2,000 to $5,000 per scan with contrast, not counting the physician fee.

For uninsured or underinsured patients, this financial burden is staggering. Many patients defer surveillance imaging because of cost. In Illinois, the Medicaid expansion under the ACA has improved access for lower-income patients, but the deductibles and out-of-pocket maximums of marketplace plans can still produce four-to-five-figure annual costs. Carle Foundation Hospital has a financial counseling program that works with patients to access charity care and payment assistance. Northwestern Medicine and Rush University Medical Center have similar programs.

The cardiologist managing a dissection survivor should explicitly ask about insurance status and financial barriers to surveillance imaging at every follow-up visit. Deferred imaging is not a minor inconvenience: it is a patient who may miss a 5.8 cm false lumen aneurysm that needs repair at 5.5 cm.

Section 7a: Technical Considerations in Aortic Surgery

The Frozen Elephant Trunk

For Type A dissection with significant arch involvement, the frozen elephant trunk (FET) technique combines open arch replacement with simultaneous deployment of a stent graft into the proximal descending thoracic aorta. The stent graft component is pre-loaded into the dacron graft and deployed in the descending aorta through the opened aortic arch, under circulatory arrest, during the arch reconstruction.

The FET technique creates a proximal landing zone for future TEVAR if the residual descending dissection requires subsequent intervention, eliminating the need for a thoracotomy for the second-stage procedure. Multiple FET devices are available (Jotec E-vita Open Plus, Terumo Thoraflex Hybrid), with differing deployment mechanisms and stent lengths. Published outcomes for FET in acute Type A dissection show spinal cord ischemia rates of 3 to 5 percent (from coverage of intercostal arteries) and early mortality in the 10 to 20 percent range in experienced centers 4 / Promising .

Spinal Cord Protection

Spinal cord ischemia is a devastating complication of both open aortic arch surgery and TEVAR for descending aortic disease. The anterior spinal artery receives critical supply from the artery of Adamkiewicz (typically originating from an intercostal artery at T8-T12). Coverage of this artery by a stent graft or sacrifice during open surgery can cause paraplegia or paraparesis.

Spinal cord protection strategies include: cerebrospinal fluid drainage (a lumbar drain is placed to reduce intrathecal pressure, improving spinal cord perfusion pressure), permissive hypertension in the post-operative period (maintaining mean arterial pressure above 90 mmHg), staged TEVAR deployment to minimize the length of aorta covered in a single session, and neuromonitoring (motor-evoked potentials and somatosensory-evoked potentials) during open surgery.

The rate of spinal cord ischemia after TEVAR for uncomplicated Type B dissection is approximately 2 to 4 percent with contemporary devices and protocols 5 / Solid . For emergency TEVAR in complicated Type B dissection, rates are higher because spinal cord protection strategies may not be fully deployable in a hemodynamically unstable patient.

Renal Protection During Aortic Surgery

Acute kidney injury after Type A dissection surgery is common, occurring in 15 to 25 percent of cases. Mechanisms include: renal malperfusion from the dissection itself (if the renal arteries are supplied by the compressed true lumen), renal ischemia from aortic cross-clamp during surgery, contrast nephropathy from pre-operative CT angiography, and low cardiac output in the post-operative period.

Renal protection strategies include adequate hydration, avoidance of nephrotoxic medications, cold renal perfusion during surgery (if the dissection extends to the renal arteries), and early consultation with nephrology if creatinine begins rising post-operatively. Patients with pre-existing renal insufficiency have a significantly higher risk of requiring temporary renal replacement therapy after Type A repair.

Section 7b: The Heart Team Discussion in Complex Dissection

The High-Risk Surgical Candidate

Not every patient with Type A dissection is an ideal surgical candidate. The cardiologist and cardiac surgeon must make explicit, documented decisions about operative risk in several categories of high-risk patients.

Patients with hemodynamic instability at presentation. The IRAD data show that patients presenting with shock or cardiac tamponade have operative mortality approaching 40 to 50 percent at even high-volume centers. The decision to operate on a patient in cardiogenic shock from Type A dissection is not automatic. The surgeon must weigh the possibility of a catastrophic intraoperative outcome against the near-certainty of death without surgery. In most circumstances, the calculus still favors surgery, but the family must be counseled about the operative mortality in this specific context.

Patients with prior stroke or neurological deficit from the dissection. Ascending aortic surgery under circulatory arrest carries inherent neurological risk. In a patient who already has a stroke from the dissection itself, the decision to operate is particularly difficult because: (a) the patient cannot meaningfully participate in the consent process, (b) the operative ischemic period adds to existing neurological injury, and (c) the post-operative neurological recovery may be incomplete regardless of hemodynamic success. Most centers still recommend surgery for Type A dissection with concurrent stroke because the alternative is death, but the prognostic context must be clearly established with the family.

Patients with severe biventricular failure from the dissection. When the dissection has caused massive aortic regurgitation with acute cardiogenic shock, the left ventricle has been subjected to sudden volume overload of extraordinary degree. The surgical team must decide whether to first place an intra-aortic balloon pump or Impella for partial hemodynamic support before chest opening, or whether to proceed directly to bypass because any delay risks further deterioration.

Octogenarians and patients with limited pre-morbid functional status. For an 84-year-old with Type A dissection and preserved cognitive function and functional independence, aggressive surgical repair is appropriate if the patient wishes it. For an 84-year-old with advanced dementia, nursing home residence, and multiple organ failure, the goals-of-care conversation with the family may lead to a decision for comfort-focused management rather than emergency surgery. This is not a failure of the medical system; it is an appropriate application of patient-centered care.

Pre-Operative Workup Efficiency

In a patient with confirmed Type A dissection, the question is not whether to operate but how quickly the surgery can begin. The pre-operative workup should be limited to what is absolutely necessary and performed in parallel, not sequentially.

Required before surgery:

• CT angiography of chest, abdomen, and pelvis (already obtained at diagnosis)
• Type and crossmatch for 6 to 10 units packed red cells and appropriate blood products
• Baseline CBC, BMP, coagulation panel
• ECG (primarily to assess for coronary involvement, not for cardiac risk stratification)
• Consent process with patient or family

What should not delay surgery:

• Routine echocardiography (the TEE can be performed in the operating room during anesthesia induction)
• Cardiology consult for “clearance” (the cardiologist should be physically present as a collaborative partner, not a gatekeeper)
• Coronary angiography (rarely changes operative strategy and wastes 30 to 60 minutes that are critical)
• Waiting for all laboratory values to return before proceeding to OR

In institutions with established aortic dissection protocols, the time from diagnosis to skin incision can be reduced to under 2 hours. Every additional hour of delay adds to the 1 to 2 percent per hour mortality of untreated Type A dissection.

Section 8b: Prevention and Screening

Who Should Be Screened for Aortic Disease

The primary prevention of aortic dissection addresses the two major modifiable contributors: uncontrolled hypertension and unrecognized genetic aortopathy in high-risk individuals.

Screening for uncontrolled hypertension does not require any specialized imaging. It requires knowing the blood pressure with the same precision that the healthcare system expects patients to know their cholesterol level. Blood pressure screening is available at every pharmacy, at every emergency department visit, at every primary care encounter. The failure is not a failure of opportunity; it is a failure of action when the opportunity presents. A systolic blood pressure of 158/94 documented at a pharmacy kiosk that is not followed up with pharmacological management is a missed prevention opportunity.

Genetic aortopathy screening is indicated in:

• First-degree relatives of patients with aortic dissection under age 55 (particularly if the index patient has Marfan syndrome, bicuspid aortic valve, or any other known heritable aortopathy)
• Any patient with physical features of Marfan syndrome (height above 97th percentile for age, arachnodactyly, pectus deformity, arm span greater than height, lens dislocation)
• Patients with bicuspid aortic valve (who need annual echocardiographic measurement of the aortic root and ascending aorta)
• Patients with known connective tissue disorders (Loeys-Dietz, vascular EDS, Turner syndrome)

Screening echocardiography for aortic root size is the entry-level test: inexpensive, no radiation, no contrast. An aortic root diameter above 4.0 cm warrants further evaluation; above 4.5 cm in a non-Marfan patient or above 4.0 cm in a Marfan patient warrants subspecialty cardiology evaluation.

The family cascade. When a patient is diagnosed with heritable aortopathy, the physician has an obligation to ensure family members are screened. This is not a simple ask. Some families have excellent communication and self-organize screening immediately. Others require the physician’s office to facilitate by providing guidance letters, contacting family member physicians directly, and following up to confirm that screening occurred.

In Illinois, genetic cardiology programs at Northwestern Medicine, the University of Chicago, and Carle Foundation Hospital have established family cascade protocols for heritable aortopathy that include mailing screening letters directly to identified first-degree relatives, coordinating with primary care physicians, and tracking completion of the screening recommendation.

The Cost-Effectiveness Argument

Prophylactic aortic root replacement in a Marfan patient with a 4.8 cm root diameter, performed electively at a high-volume center, has an operative mortality of approximately 1 to 2 percent. The same patient who dissects has a mortality of 15 to 30 percent at surgery. The cost of the prophylactic replacement, including hospitalization, is approximately $60,000 to $100,000. The cost of an acute dissection hospitalization, including the emergency surgery, ICU stay, complications, and rehabilitation, is commonly $200,000 to $500,000 or more, with a worse functional outcome.

The argument for aggressive surveillance and prophylactic intervention in heritable aortopathy is both clinically and economically compelling. The barrier is identification: these patients must be recognized as high-risk before they dissect.

The SDE Audit, applied to patients with known connective tissue disorders, bicuspid aortic valve, or family history of aortic dissection, performs this identification function. The audit flags the aortic root measurement, the genetic testing status, and the current surgical threshold recommendation, and places the patient in a structured follow-up program that will not lose track of the surveillance imaging schedule.

Clinical Pearls and Common Pitfalls

The Interarm Blood Pressure Difference — Measuring It Correctly

The arm-to-arm systolic blood pressure difference greater than 20 mmHg is one of the most specific physical findings in aortic dissection involving the subclavian or innominate arteries. But this finding requires both arms to be measured simultaneously or in rapid sequence by two operators, because sequential single-operator measurement introduces enough time delay that spontaneous blood pressure variability can mimic or mask a real difference.

In busy emergency departments, both arms are not routinely measured simultaneously. The standard practice is sequential arm measurement, which introduces a measurement gap of 2 to 5 minutes. During that time, blood pressure fluctuates by 5 to 15 mmHg normally. A real 20+ mmHg difference is still detectable through sequential measurement, but a borderline 15 to 20 mmHg difference may be missed or misattributed.

In a patient with tearing chest pain where aortic dissection is on the differential, both arms should be measured simultaneously if two operators are available. If only one operator is present, the two arms should be measured in the shortest possible sequence, and any difference of 15 mmHg or more should be considered significant until proven otherwise.

The absence of an arm-to-arm difference does not exclude dissection. In IRAD, only 20 percent of Type A dissections showed this sign. The ADD-RS scoring accounts for this: pulse deficit or arm-to-arm difference are one component, not the sole determinant.

Distinguishing Dissection Pain from Other Chest Pain

The single most useful discriminating feature between aortic dissection and other causes of acute chest pain is the time course of pain onset. Dissection pain reaches maximum intensity at onset, within the first second. Myocardial infarction pain typically builds over minutes. Pericarditis pain is positional and reaches its maximum over minutes to hours.

The word choices patients use matter. “Tearing” and “ripping” are highly specific for dissection when they occur in the context of maximal-at-onset pain. “Squeezing” and “pressure” favor MI. “Sharp” and “pleuritic” (worse with breathing) favor pericarditis or PE.

Atypical presentations are the diagnostic trap. A Type A dissection that initially presents as syncope, without prominent chest pain, will trigger a neurological workup, not a cardiac workup, until someone measures the arms and finds a 28 mmHg difference and the patient is transferred. This exact sequence (syncope, neurological concern, missed arm blood pressure measurement, delayed diagnosis) is documented in IRAD and in malpractice literature.

The emergency physician who adds “check both arm blood pressures simultaneously” to every syncope workup in patients over 50 will prevent some of these delays. It takes 90 seconds. The consequences of missing the diagnosis are permanent.

Anticoagulation in Confirmed Type A Dissection

Type A aortic dissection is a condition where anticoagulation, in most circumstances, should not be administered. The risk of worsening hemopericardium, of precipitating bleeding into the false lumen, and of complicating the surgical field with anticoagulation outweighs any theoretical benefit.

The clinical trap: a patient with Type A dissection involving the coronary ostia presents with ST elevation on the ECG. The STEMI protocol activates. Heparin is administered, aspirin is given. Then the CT angiogram shows a long dissection flap extending from the aortic root into the descending aorta. Now the patient is anticoagulated and heading to the operating room for aortic surgery.

This scenario is prevented by one decision point: when ST elevation appears in the context of a hypertensive patient with tearing chest pain and a BP differential, a non-contrast CT chest to look for mediastinal widening should precede any anticoagulation decision. CT takes less than 5 minutes. Administering heparin to a patient with Type A dissection and subsequent hemopericardium carries consequences that outlast the scan.

The 2022 AHA/ACC Aortic Disease Guidelines explicitly address this: in patients with suspected aortic dissection, anticoagulation should be withheld until dissection is excluded 5 / Solid .

Dr. Job Mogire, MD FACP FACC. Carle Foundation Hospital; Carle Illinois College of Medicine. Stop Dying Early.