Management of acute type B aortic dissection

INTRODUCTION — Aortic dissection is defined as a tear in the innermost layer of the aortic wall (ie, intima), which results in high-pressure blood flow between the layers of the aorta, creating a true and false lumen (between the intima and adventitia). With type B aortic dissection, the intimal tear originates in the aorta distal to the subclavian artery (figure 1), and because treatment differs, type B dissection must be distinguished from type A aortic dissection. Acute type B aortic dissection is usually suspected clinically based on history and physical examination when a patient presents with severe, sharp, or "tearing" chest or back pain. A diagnosis of acute type B aortic dissection can easily be overlooked among patients with acute chest pain, and a high index of suspicion is needed to make a timely diagnosis and initiate appropriate therapy. Better awareness and advances in imaging have improved the diagnosis.

The goals of initial medical management of acute type B aortic dissection are to control pain and limit the extension of the dissection using anti-impulse therapy. We agree with major interdisciplinary guidelines that generally suggest reserving intervention (surgical or endovascular) for those who develop complications related to the dissection (eg, dissection extension, malperfusion, aneurysm formation, persistent pain [1-3]). (See "Surgical and endovascular management of acute type B aortic dissection".)

Acute type B aortic dissection is distinguished from chronic type B aortic dissection based on the duration from initial onset of symptoms. The management of acute (hyperacute, acute, subacute) type B aortic dissection is reviewed. The management of chronic type B aortic dissection is discussed separately. (See "Management of chronic type B aortic dissection".)

The management of type A aortic dissection and other acute aortic syndromes are discussed separately. (See "Overview of acute aortic dissection and other acute aortic syndromes" and "Management of acute type A aortic dissection" and "Surgical and endovascular management of acute type A aortic dissection".)

EXTENT AND ETIOLOGY OF DISSECTION — Aortic dissection is defined as a tear in the innermost layer of the aortic wall (ie, intima) that results in high-pressure flow of blood between the layers of the aorta, creating a true and false lumen. Determining the location of the aortic dissection, duration since onset of symptoms/occurrence, severity of symptoms, and etiology are important, as these impact prognosis and management.

Classification — Aortic dissection is classified based upon the anatomic location of the entry tear, the clinical severity of the dissection (uncomplicated, complicated), and the duration of symptoms (hyperacute, acute, subacute, chronic) [4]. These all impact the options for and timing of treatment.

The anatomic location and extent of the aortic dissection are determined using cardiovascular imaging. When the diagnosis is suspected, clinically, the diagnostic evaluation should be accomplished as promptly as possible. For hemodynamically stable patients, computed tomographic (CT) angiography is chosen because of its high sensitivity and availability in most emergency departments where most patients initially present. Gated CT is preferred to eliminate motion artifacts. For patients who are hemodynamically unstable, bedside transesophageal echocardiography can be used with high sensitivity but is often not immediately available. Diagnostic imaging is reviewed separately. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Cardiovascular imaging'.)

●Location of entry tear – The DeBakey and Stanford (Daily) systems were commonly used to classify aortic dissection (figure 1). The Stanford system, which has been more widely used, classifies dissections that involve the ascending aorta as type A, regardless of the site of the primary intimal tear; all other dissections are classified as type B. Approximately one-third of aortic dissections present as type B, and two-thirds are type A [5]. The DeBakey and the Stanford aortic dissection classification systems have limitations [6,7]. Both are relatively nonspecific regarding the precise extent of the dissection and are ambiguous regarding the involvement of the aortic arch. A task force commissioned by the Society for Vascular Surgery (SVS) and Society for Thoracic Surgery (STS) has addressed these issues with the distinction between type A and type B aortic dissection predicated based on entry tear location alone (figure 2) [4]. Type B aortic dissection is defined as an entry tear in a zone >1, and the proximal and distal extent are noted. Therefore, in the SVS/STS system, dissections that originate in the arch (zone 2, 3) can be considered type B dissections and are managed surgically and medically, depending on presentation and clinical course. Type A aortic dissection is classified as an entry tear in zone 0, and the distal extent can range from zone 1 to 12.

●Duration from onset – Acute type B aortic dissection is distinguished from chronic type B aortic dissection based on the duration from the onset of symptoms [4]. In the past, type B aortic dissection was classified simply as acute (<14 days) or chronic (>14 days), which was based on the timing of death in the era of open surgery. The SVS/STS reporting guidelines have provided additional classifications based on the timing from the onset of symptoms as follows [4]:

•Hyperacute: <24 hours

•Acute: 1 to 14 days

•Subacute: 15 to 90 days

•Chronic: >90 days

For the purposes of our discussion, we will use the term "acute" type B aortic dissection to refer to the period ≤14 days encompassing the hyperacute and acute periods.

●Clinical severity – Clinical features of acute type B aortic dissection include severe, sharp, or "tearing" chest or back pain that may or may not be associated with evidence of end-organ ischemia. Clinical features of acute aortic dissection and the features that may distinguish between type A and type B aortic dissection are reviewed separately. (See "Clinical features and diagnosis of acute aortic dissection".)

Type B aortic dissection is considered complicated if there is evidence of malperfusion, rapid expansion or aneurysmal degeneration of the aortic wall, impending or frank rupture, uncontrolled pain, or refractory hypertension (persisting despite ≥3 classes of antihypertensives at max doses) [1-3]. Approximately 30 percent of patients presenting with type B aortic dissection are acutely complicated [1,5,8]. Complicated acute type B aortic dissection requires urgent intervention. (See 'Complicated type B dissection' below and 'Intervention' below.)

All other type B aortic dissections are considered uncomplicated. Uncomplicated type B aortic dissection is generally managed with optimal medical therapy, which includes pain control and strict blood pressure and heart rate control (also referred to as "anti-impulse therapy") [1]. (See 'Uncomplicated type B dissection' below.)

Etiology — The etiology of type B aortic dissection has a bearing on management and in particular the nature of intervention (open surgical, hybrid repair) and potentially its timing. The etiology of type B aortic dissection differs for older compared with younger patients. Older patients are more likely to have atherosclerosis, prior aortic aneurysm, iatrogenic dissection, or intramural hematoma [9]. Younger patients are more likely to have genetically mediated or familial conditions [10].

High-risk conditions associated with thoracic aortic dissection are reviewed in detail separately. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Incidence and associated conditions'.)

●Severe acute hypertension (eg, uncontrolled, high-intensity resistance training, drug use [eg, cocaine, methamphetamine])

●Genetically mediated connective tissue disorder (eg, Marfan syndrome, Ehlers-Danlos syndrome)

●Preexisting aortic aneurysm

●Bicuspid aortic valve

●Aortic instrumentation or surgery

●Aortic coarctation

●Familial thoracic aortic aneurysm/dissection

●Turner syndrome

●Inflammatory vasculitis (eg, giant cell arteritis, Takayasu arteritis)

●Blunt aortic trauma

●Pregnancy and delivery

MEDICAL MANAGEMENT — For patients diagnosed with acute type B aortic dissection, acute management priorities include resuscitation for hypotensive patients, initiation of anti-impulse therapy, pain control (table 1), and identification of malperfusion syndromes or other complications that indicate the need for repair. (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Acute medical management' and 'Complicated type B dissection' below.)

Subsequent medical management consists of ongoing pain control, titration of medications to maintain heart rate and blood pressure at the desired targets (table 1 and table 2), transition from intravenous to oral medications, patient and family counseling, and lifelong imaging surveillance. (See 'Anti-impulse therapy' below and 'Identifying associated genetic conditions' below and 'Surveillance imaging' below.)

For patients who develop a complicated course, intervention is required, and interfacility transfer is appropriate if vascular resources are not available. Despite intensive medical therapy, 20 to 40 percent of patients may progress to require surgical or endovascular intervention. (See 'Referral or transfer' below.)

Supportive care and monitoring — Blood pressure management typically requires intensive care monitoring with an arterial line for strict heart rate and blood pressure control and may also include monitoring central venous pressure and cardiac indices, depending upon the patient's clinical and hemodynamic status. Routine laboratories are obtained and trended and include complete blood count, electrolytes, coagulation parameters, and D-dimer, as well as markers of malperfusion, including liver function tests (alanine aminotransferase [ALT], aspartate aminotransferase [AST], alkaline phosphatase [ALP], bilirubin), renal function tests (blood urea nitrogen, creatinine), and lactate.

For patients with uncomplicated disease, medical therapies are continued until pain abates and heart rate and blood pressure are well controlled. Any increase in pain or recurrence of pain should raise suspicion that the dissection has propagated, prompting repeat cardiovascular imaging. Other clinical features that may indicate the development of malperfusion syndromes include abdominal findings consistent with intestinal ischemia (eg, abdominal pain), renal ischemia (worsened renal function), peripheral ischemia (eg, pain, pallor, diminished/absent pulses) and spinal cord ischemia (eg, paraparesis/paraplegia, which is rare). Also rare are symptoms consistent with involvement of the proximal aorta due to retrograde dissection (eg, aortic regurgitation, cardiac tamponade). (See "Clinical features and diagnosis of acute aortic dissection", section on 'Symptoms and signs' and "Clinical features and diagnosis of acute aortic dissection", section on 'Ascending versus descending aortic involvement'.)

Anti-impulse therapy — Anti-impulse therapy consists of heart rate (<60 beats per minute) and blood pressure (<120/80) control to decrease aortic wall shear stress and to minimize the tendency for the dissection to propagate and the development of complications (eg, aneurysmal degeneration, rupture). Combination antihypertensive drug therapy is usually required. Medications and dosing used to treat acute aortic dissection are provided in the table (table 2). The initiation of acute medical therapies should not interfere with timely transfer when immediate intervention is indicated. (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Acute medical management'.)

Decreasing the force of myocardial contraction has been shown to slow aortic expansion and possibly rupture after aortic dissection, and this has been the basis for prescribing beta-blockers as first-line antihypertensive therapy for patients with thoracic aortic dissection [11-14]. Although not evaluated in controlled trials, we suggest a target heart rate <60 beats per minute and target blood pressure of less than 120/80 mmHg [13]. Patients with optimal heart rate (<60 beats per minute) and systolic blood pressure (SBP; <120 mmHg) control have better outcomes with reduced rates of aortic expansion and rupture [2,15]. In addition to beta-blockers, aortic expansion and survival are improved for patients who receive calcium channel blockers for maintenance therapy [16,17]. In a review of 18 studies that evaluated factors associated with aortic expansion over a median time period of 51.6 months in patients with uncomplicated type B aortic dissection, the use of calcium channel blockers was among several factors including tight heart rate control (<60 beats/min) associated with negative or limited aortic expansion [15].

Once control of heart rate has been achieved and the patient is tolerating an oral diet, intravenous beta blockers (or other antihypertensive) therapy can be transitioned to an oral route. All patients should be maintained on lifelong therapy to maintain heart rate and systemic blood pressure goals [13].

While approximately 71 percent of patients who sustain type B aortic dissection have a SBP >150 mmHg on initial presentation [2], about 90 percent of patients are normotensive with anti-impulsive therapy at discharge, achieving recommended values for SBP of between 100 and 120 mmHg [17,18].

Exercise limitation — Though unproven, avoidance of strenuous physical activity that would lead to a spike in blood pressure (eg, dynamic resistance training, isometric exercise) is also recommended for all patients who have had aortic dissection as another method to minimize aortic shear stress. (See "Management of Marfan syndrome and related disorders", section on 'Restriction of strenuous activity'.)

Identifying associated genetic conditions — Similar with thoracic aortic aneurysm, patients with thoracic aortic dissection, particularly younger patients or those with clinical features or a family history of connective tissue disorders, and others without an identifiable etiology for aortic dissection (eg, severe hypertension, pregnancy/delivery, aortic trauma) should be evaluated (algorithm 1) for possible underlying genetic or familial disorders known to be related. These may increase the patient's individual risk of progression or complications [2,3,19].

Genetically mediated conditions for aortic dissection are listed below and discussed in more detail separately. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Incidence and associated conditions'.)

●Syndromic – Marfan syndrome, Loeys-Dietz syndrome, Vascular Ehlers-Danlos syndrome, Turner syndrome, familial aneurysm-osteoarthritis syndrome (SMAD3 mutations).

●Nonsyndromic – Familial aortic aneurysm/dissection, bicuspid aortic valve, aortic coarctation.

Screening first-degree family members for aortic aneurysm (or bicuspid aortic valve) should also be considered [2,3,20,21]. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Incidence and associated conditions' and "Management of thoracic aortic aneurysm in adults", section on 'Identifying associated genetic conditions'.)

Surveillance imaging — For patients with type B aortic dissection who continue to be managed medically, we generally perform a baseline thoracic magnetic resonance (MR) or computed tomographic (CT) angiography prior to discharge, with follow-up examinations at 3, 6, and 12 months and annually thereafter, even if the patient remains asymptomatic (and presuming the patient is a candidate for an intervention) given the natural history of type B aortic dissection and the risk for future aortic events. (See "Management of chronic type B aortic dissection", section on 'Natural history' and "Management of chronic type B aortic dissection", section on 'Predictors of adverse aortic events'.)

The following abnormalities can be detected on serial imaging:

●Extension or recurrence of the dissection

●Aneurysmal degeneration

●Malperfusion

MR angiography may be more acceptable for serial studies because it is noninvasive and does not expose patients to iodinated contrast and ionizing radiation as with CT angiography, which are important factors for younger patients who will likely have many years of serial monitoring. Although, due to concerns about long-term retained gadolinium, noncontrast MR angiography is an alternative that should be considered. Alternating CT and MR angiography is a reasonable option for patients with good renal function.

Imaging surveillance following endovascular or surgical repair of type B aortic dissection to detect complications is reviewed separately. (See "Endovascular repair of the thoracic aorta", section on 'Postoperative endograft surveillance' and "Overview of open surgical repair of the thoracic aorta", section on 'Follow-up imaging'.)

REFERRAL OR TRANSFER — Any decision for vascular intervention and its timing must be individualized, accounting for the patient's age, comorbidities (eg, prior stroke, renal failure, hypertension, coronary heart disease), and patient and family wishes. Experienced cardiovascular specialists and their team should be involved early in the care of the patient. Clinicians caring for the patient must be aware of the appropriate management of type B aortic dissection to determine if a need for transfer and/or intervention is present. If appropriate services are not available at the institution to which the patient presented, interfacility transfer to a tertiary aortic center should be initiated for any patient with complicated type B aortic dissection. Anti-impulse therapy should be continued during transfer.

Whether patients presenting with uncomplicated type B aortic dissection should be monitored and treated at an aortic center is unsettled. This would be the ideal situation, particularly since it cannot be known in advance whether an uncomplicated presentation will become complicated, and initial care at an aortic center would avoid delays in treatment for those who develop complications. Experienced teams at high-volume aortic centers are more likely to provide improved diagnostic capabilities and broader treatment options. In one series of 86 patients treated at an aortic center, 24 of 64 patients (38 percent) initially presenting as uncomplicated type B aortic dissection progressed to complicated dissection at a median interval of 7.1 days (95% CI 2-14), 10 patients had malperfusion, 3 had aortic rupture, 8 had early expansion >4 mm, 2 had refractory pain, and 1 had uncontrollable hypertension [22].

While there are few studies evaluating referral and outcomes, treatment at a tertiary aortic center is felt to be important to achieve optimal outcomes [23-27]. Operative and long-term mortality may be reduced by transferring patients to a high-volume facility experienced in the care of patients with acute aortic syndromes. In a systematic review, outcomes of endovascular intervention were much better at centers that had performed more than 20 endovascular procedures compared with fewer [24]. This included significantly lower rates of overall complications (7.7 versus 20.9 percent), neurologic complications (1 versus 5.7 percent), and 30-day mortality (3.2 versus 8.5 percent).

The time required for transfer does not appear to adversely impact outcomes. In a review of acute aortic syndromes, 183 patients were transferred (81 percent by ground, 19 percent by air; median transport time 42 minutes) [27]. The median time to operation for those with acute type B aortic dissection (for those with appropriate indications) was 45 hours. Distance traveled and transport mode and duration were not associated with increased risk of system-related mortality. On multivariate analysis, only Society for Vascular Surgery Comorbidity Severity Score >8 was independently associated with an increase in system-related mortality (odds ratio 7.73, 95% CI 2.32-25.8). Similarly, in a review of 306 patients admitted with acute aortic disease one year before and one year after initiation of an acute aortic treatment center pathway that included interfacility transfer, mean time to definitive therapy was reduced by 64 percent (from 526 versus 187 minutes) [26].

APPROACH TO INTERVENTION — The approach to intervention for type B aortic dissection is based upon the clinical severity of disease. Complicated acute type B aortic dissection requires urgent intervention, which can be lifesaving. Uncomplicated type B aortic dissection is predominantly managed medically. (See 'Complicated type B dissection' below and 'Uncomplicated type B dissection' below.)

In a review that included 1476 patients with type B dissection from the International Registry of Acute Aortic Dissection (IRAD), 63 percent of patients with type B acute aortic dissection were managed medically [5]. Overall, in-hospital mortality was 13 percent for type B aortic dissection, with most deaths occurring within the first week. Despite improvements in medical care and the introduction of endovascular management, overall in-hospital mortality for type B dissection did not change significantly over the 20-year period studied. However, the percentage of patients being medically managed fell (from 75 to 57 percent). This change in practice may be due to results of the INvestigation of STEnt grafts in patients with Aortic Dissection XL (INSTEAD-XL) trial, after which more and more centers moved towards a more aggressive thoracic endovascular aortic repair treatment paradigm, even though a mortality benefit was not demonstrated. (See 'Controversy over early intervention for uncomplicated disease' below.)

Complicated type B dissection — Endovascular or surgical intervention is required for all patients who develop complications at any time. Aortic dissection is frequently complicated by major aortic branch leading to end-organ ischemia (ie, malperfusion), rapid expansion or aneurysmal degeneration of the aortic wall, expanding hematoma, or impending or frank rupture. In an IRAD review, one-third of patients with acute type B dissection presented with complications [5]. Mortality associated with such complications can exceed 60 percent [28].

Endovascular or surgical intervention is also required for those who have uncontrolled pain, propagation of the dissection, or persistent severe hypertension (despite ≥3 classes of antihypertensives at max doses). (See 'Intervention' below.)

Uncomplicated type B dissection — In agreement with multidisciplinary cardiovascular guidelines, we suggest ongoing medical management for most patients with uncomplicated type B aortic dissection, rather than preemptive intervention [1-3,29]. The preference for ongoing medical management for uncomplicated acute type B aortic dissection is based upon observational data and two randomized trials that show similar long-term outcomes for medical therapy compared with intervention (endovascular, surgical) [30-37].

●The effectiveness of medical therapy was demonstrated in the INSTEAD trial, which compared conventional medical management with endovascular intervention [34]. The trial randomly assigned 140 patients who were clinically stable and free of malperfusion at the time of initial treatment (median of 12 days from randomization to stent-graft insertion) to continued medical therapy with a goal blood pressure of ≤120/80 mmHg, or to medical therapy and endovascular stent-grafting. At two-year follow-up, the small difference in overall survival for those receiving conventional medical therapy alone versus endovascular intervention was not statistically significant (96 versus 89 percent, respectively).

●In a meta-analysis that included observational and randomized trials comparing best medical therapy and endovascular repair for uncomplicated acute/subacute type B aortic dissection, inpatient mortality was similar [37]. Best medical therapy was associated with a statistically significant lower risk of early stroke, whereas intervention was associated with a lower risk of late all-cause and aorta-related mortality.

●In a review of six studies, short-, intermediate-, and midterm outcomes were similar for medical therapy and endovascular repair for acute, uncomplicated type B aortic dissection. Although the rate of aortic dilation was also similar, endovascular repair was associated with lower likelihood of aortic rupture at one year [31].

●In another review evaluating outcomes for endovascular repair for uncomplicated (8352 patients) versus complicated (7772 patients) type B aortic dissection (acute, chronic), overall one-year survival was higher in the uncomplicated group, but this difference was not observed in the five-year survival [33].

Controversy over early intervention for uncomplicated disease — Early endovascular intervention for uncomplicated type B aortic dissection is controversial. Some surgeons support individualized treatment that accounts for many patient factors (eg, life expectancy, extent and location of entry tear, size of aorta, technical complexity of thoracic endovascular repair). For patients who have stabilized on medical therapy (ie, subacute period) and without malperfusion or other complications, they suggest that early endovascular intervention can reduce or eliminate the false lumen, which may impact long-term outcomes, though this has yet to be definitively demonstrated [34,38-50].

Long-term survival with medical therapy is approximately 60 to 80 percent at four to five years [12,36,51,52] and approximately 40 to 45 percent at 10 years [51,52]. These less-than-desirable outcomes are in part related to issues of adherence with prescribed medical therapies and the natural history of type B aortic dissection. Spontaneous healing of the dissection, characterized by disappearance of the false lumen due to complete thrombosis, is overall uncommon in medically treated patients [53,54]. Continued flow through the false lumen (patent false lumen), either without thrombosis or partial thrombosis, has been postulated to prevent healing and lead to worse prognosis [54,55]. The relationship between false lumen patency and outcomes was evaluated in 201 hospital survivors of acute type B aortic dissection enrolled in IRAD [54]. Partial thrombosis was present in 34.9 percent, and complete patency of the false lumen occurred in 56.7 percent. Mortality at a median 2.8 years follow-up was 31.6 percent for patients with partial thrombosis and 13.7 for patients with a patent false lumen. In a later review of 11 cohort studies, a residual patent false lumen increased the risk for aortic events in patients with acute aortic dissection (hazard ratio [HR], 5.43, 95% CI 2.95-9.99) and was an independent predictor of long-term mortality in patients with type B aortic dissection (HR 2.79, 95% CI 1.80-4.32) [41]. Partial false lumen thrombosis was also associated with increased long-term mortality (HR 2.24, 95% CI 1.37-3.65).

In the INSTEAD trial [34,56], while there were no statistically significant differences at two-year follow-up between the endovascular and medical groups for overall survival (89 versus 96 percent), favorable aortic remodeling was seen in 91.3 percent of the endovascular group compared with only 19.4 percent of the medically treated patients. With longer-term follow-up of five years (INSTEAD-XL), all-cause mortality was again not significant for endovascular versus medical treatment (11.1 versus 19.3 percent) [57]. However, aorta-specific mortality (6.9 versus 19.3 percent) and progression (27 versus 46.1 percent) were significantly lower for endovascular compared with optimal medical treatment alone. Another trial that assigned 61 patients to best medical therapy or best medical therapy plus endovascular stent-grafting reported significantly fewer events of the combined endpoint of incomplete/no false lumen thrombosis, aortic dilation, or aortic rupture for those who were treated with stent-grafts (per protocol results) [58]. Technical failures, loss to follow-up, and crossovers from the best medical therapy group limited the analysis. A later meta-analysis that included observational and randomized trials comparing best medical therapy and endovascular repair for acute/subacute uncomplicated type B aortic dissection reported similar rates for inpatient mortality and early reintervention [37]. Best medical therapy was associated with a significantly lower risk of early stroke, whereas endovascular repair was associated with a lower risk of late all-cause and aorta-related mortality.

The optimal timing for early intervention is not known for certain. However, aortic remodeling is more favorable for intervention performed for acute or subacute type B aortic dissection compared with chronic type B aortic dissection. In the VIRTUE registry, which followed a cohort of patients with complicated type B aortic dissection who underwent endovascular intervention, three-year all-cause mortality was 18 and 4 percent for acute and subacute dissection, respectively [59]. Analysis of aortic morphology observed that patients with subacute dissection demonstrated a similar degree of aortic remodeling to patients with acute dissection. Patients with acute and subacute dissection exhibited greater aortic plasticity than patients with chronic dissection.

High-risk features — With encouraging results of endovascular intervention, attempts have been made to identify a cohort of patients (ie, high-risk features) who may benefit from earlier, rather than later intervention. While various parameters have been identified, none have been validated prospectively.

The Society for Thoracic Surgery/American Association for Thoracic Surgery clinical guidelines for the management of type B aortic dissection have defined high risk as [60]:

●Refractory pain

●Refractory hypertension

●Bloody pleural effusion

●Aortic diameter > 40 mm

●Radiographic-only malperfusion

●Readmission

●Entry tear located on the lesser curve

●False lumen diameter > 22 mm

INTERVENTION — Intervention for acute type B aortic dissection is generally reserved for those who progress from uncomplicated to complicated disease (malperfusion, uncontrollable pain, hypertension, expansion, rupture, or impending rupture). The controversial role of intervention in the treatment of uncomplicated acute type B aortic dissection is discussed above. (See 'Controversy over early intervention for uncomplicated disease' above.)

The etiology of acute aortic dissection has a bearing on management, and in particular, the nature of intervention (surgical versus endovascular). In general, an open surgical approach is preferred for patients with genetically mediated type B aortic dissection due to the likelihood of further aortic degeneration, whereas patients with degenerative type B aortic dissection can generally be managed with endovascular techniques, provided anatomy is suitable for endovascular repair [61,62]. (See "Surgical and endovascular management of acute type B aortic dissection", section on 'Approach to repair'.)

Endovascular stent-grafting — With endovascular repair, the stent-graft is positioned to cover the intimal flap to seal the entry site of the dissection, resulting in thrombosis of the false lumen (figure 3 and image 1). (See "Surgical and endovascular management of acute type B aortic dissection", section on 'Endovascular repair'.)

Stent-grafting has been evaluated for acute and subacute type B aortic dissection [5,24,63-65]. An early systematic review involving 609 patients who underwent stent-graft placement for type B dissection reported high rates of procedural success (98 percent) [24]. Complication rates compared favorably with previously reported surgical series. The complication rate (11.1 percent) was higher in later studies, which may have reflected the inclusion of higher-risk patients as experience with stent-grafting increased. In-hospital mortality was 5.2 percent. On Kaplan-Meier analysis, overall survival at one year was 90 percent and 89 percent at two years. At a mean follow-up of 19 months, aortic rupture occurred in 2.3 percent. In a meta-analysis of five trials (318 participants), endovascular repair for acute type B aortic dissection significantly reduced short-term mortality (Mantel-Haenszel fixed odds ratio [OR] 0.19, 95% CI 0.09-0.39) [43]. However, endovascular repair had no impact on postoperative complication rates or long-term mortality. Similarly, in a review of 18 studies including 12,789 patients, perioperative (30-day/in-hospital) mortality was significantly lower for patients with type B aortic dissection treated with endovascular compared with open surgical repair (pooled OR 0.54, 95% CI 0.43-0.68) [32]. However, long-term survival was similar.

Although initial repair of the dissection often results in resolution of peripheral ischemia, stenting and/or balloon fenestration of the dissecting membrane is a less invasive alternative for patients with mesenteric, renal, or peripheral ischemia after the initial repair [13,66]. (See "Surgical and endovascular management of acute type B aortic dissection", section on 'Fenestration of septum' and "Surgical and endovascular management of acute type B aortic dissection", section on 'Stenting visceral branch obstruction'.)

Open surgical repair — Although rarely necessary for complicated acute type B aortic dissection given the advances in thoracic aortic stent-graft designs (eg, fenestrated devices) and use of debranching procedures, open surgical repair may be needed for those whose anatomy will not support an endovascular stent-graft or for patients with high-risk genetically mediated conditions [5]. (See "Surgical and endovascular management of acute type B aortic dissection", section on 'Open surgery'.)

OUTCOMES

In-hospital mortality — In a review of nearly 1500 patients with type B aortic dissection from the International Registry of Acute Aortic Dissection, in-hospital mortality was 13 percent overall, with most deaths occurring within the first week, which did not change significantly over the 20 years prior to the study [5].

In-hospital mortality for those who require intervention is approximately double that of those managed medically, which is not surprising since patients who require intervention are primarily those with a complicated disease [1,5,12,36,51,63]. Among patients with uncomplicated type B aortic dissection who undergo intervention, mortality rates are similar to those managed medically [37].

For patients who undergo intervention, mortality is overall increased for open compared with endovascular repair. In a systematic review that included 9664 patients with type B aortic dissection, the risk of in-hospital mortality, acute renal failure, respiratory failure, and bleeding were increased for open compared with endovascular repair [42]. However, the risk of stroke, myocardial infarction, paraplegia, mesenteric ischemia/infarction, reinterventions, sepsis, and spinal cord ischemia were similar.

Long-term survival — The observed difference in mortality between those managed medically versus those requiring intervention tends to diminish over time [51]. Long-term outcomes may be similar [36,51]. The 10-year actuarial survival rate of patients with an acute aortic dissection who leave the hospital has ranged from 30 to 88 percent [36,51,52,67,68]. This variability may be explained by the natural history of the dissected aorta and occurrence of adverse events, such as recurrent dissection and aneurysm formation in the descending aorta [69]. The results from the INSTEAD trial and other studies have suggested that a lack of positive aortic remodeling (eg, false lumen thrombosis) may correlate with later complications and worse long-term survival, but this has not been proven [39-41]. Long-term survival is also impacted by preexisting medical comorbidities such as ongoing smoking, hypertension, and coronary and peripheral artery disease. (See "Management of chronic type B aortic dissection", section on 'Natural history'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Aortic dissection and other acute aortic syndromes".)

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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Aortic dissection (The Basics)" and "Patient education: Thoracic aortic aneurysm (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Type B aortic dissection – Aortic dissection is defined as a tear in the innermost layer of the aortic wall (ie, intima), which results in high-pressure blood flow between the layers of the aorta, creating a true and false lumen. With type B aortic dissection, the intimal tear originates in the aorta distal to the subclavian artery (figure 1). The time interval from the onset of symptoms differentiates acute type B aortic dissection (ie, hyperacute/acute; onset ≤14 days) from subacute (onset 14 to 90 days) and chronic (onset >90 days) dissection. (See 'Introduction' above and 'Extent and etiology of dissection' above.)

●Medical management – The main goals of initial medical management are to control pain and limit extension of the dissection using anti-impulse therapy, which consists of heart rate and blood pressure control (table 1 and table 2). We use a target heart rate <60 beats per minute and target blood pressure of less than 120/80 mmHg. Patients controlled to these parameters have better outcomes with reduced rates of aortic expansion and rupture. (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Acute medical management'.)

•The initiation of acute medical therapies should not interfere with timely intervention when it is indicated.

•For patients who require intervention, expeditious treatment at an experienced aortic center is important for optimal outcomes, particularly among patients who require intervention.

•For patients who require interfacility transfer, anti-impulse therapy should be continued during transfer.

•All patients should be maintained on lifelong anti-impulse therapy.

●Approach to intervention – The approach to intervention for type B aortic dissection is based upon the clinical severity of disease (uncomplicated, complicated), as well as vascular anatomy and patient factors. The etiology of type B acute aortic dissection also has a bearing on management, and in particular, the nature of intervention (surgical versus endovascular), when it is indicated. Intervention is generally reserved for patients who present with or transition from uncomplicated to complicated disease. Open surgical management of type B aortic dissection is rarely necessary given the advances in endovascular techniques; however, open surgical repair may be needed if anatomy is unsuitable or for patients with high-risk genetically mediated conditions. With endovascular repair, the stent-graft is positioned to cover the intimal flap to seal the entry site of the dissection. Outcomes for endovascular repair of type B aortic dissection compared favorably with previously reported surgical series. While perioperative complication rates are lower, long-term survival and complication rates appear to be similar. (See 'Intervention' above and "Surgical and endovascular management of acute type B aortic dissection".)

•Complicated type B aortic dissection - Complicated acute type B aortic dissection requires urgent intervention, which can be lifesaving. Approximately 30 percent of patients presenting with type B aortic dissection are acutely complicated. Complications can also develop during a period of initial medical management. Complicated type B aortic dissection is present if there is a major aortic branch leading to end-organ ischemia (ie, malperfusion), rapid expansion or aneurysmal degeneration of the aortic wall, expanding hematoma, impending or frank rupture, propagation of the dissection (as may be manifested by persistent or recurrent pain), or refractory hypertension (persisting despite ≥3 classes of antihypertensives at max doses). (See 'Complicated type B dissection' above.)

•Uncomplicated type B aortic dissection – For most patients who are hemodynamically stable with uncomplicated type B aortic dissection, we suggest ongoing medical therapy, rather than early endovascular intervention (Grade 2C). However, the patient and clinician may reasonably choose endovascular intervention in addition to ongoing medical therapy to prevent malperfusion or other aortic complications, placing more value on potentially improved aortic outcomes in the long term over potential perioperative complications (eg, stroke, spinal cord ischemia). Factors that may influence decision making include the age of the patient, life expectancy, medical risk, and the presence of certain anatomic factors that may increase the risk for future aortic events. The optimal timing for early intervention when it is selected is unknown. (See 'Uncomplicated type B dissection' above.)

●Surveillance imaging – For patients with type B aortic dissection who are being managed medically, we generally perform a baseline thoracic magnetic resonance (MR) or computed tomographic (CT) angiography prior to discharge. Follow-up surveillance imaging is obtained at 3, 6, and 12 months and annually thereafter to detect complications. We generally prefer MR, particularly in younger patients, but CT angiography is an alternative. (See 'Surveillance imaging' above.)

●Identifying associated genetic conditions – Patients with thoracic aortic dissection, particularly younger patients and others without an identifiable etiology for aortic dissection (eg, severe hypertension, pregnancy/delivery, aortic trauma), should be evaluated (algorithm 1) for possible underlying genetic (Marfan syndrome, Loeys-Dietz syndrome, Vascular Ehlers Danlos syndrome, Turner syndrome) or familial disorders (SMAD3 mutations, familial thoracic aortic aneurysm and dissection) known to be related. These may increase the patient's individual risk of progression or complications. Screening first-degree family members for aortic aneurysm or bicuspid aortic valve should also be considered. (See 'Identifying associated genetic conditions' above.)

●Long-term outcomes – Mortality associated with complicated acute type B aortic dissection can exceed 60 percent. Short-term mortality is clearly higher among those who require intervention; however, long-term survival rates among patients who are discharged are similar regardless of management. Long-term survival is impacted by compliance with anti-impulse therapies, the natural history of the dissection, as well as preexisting medical comorbidities (eg, smoking, hypertension, atherosclerosis, underlying connective tissue disorders). (See 'Outcomes' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledges Emile R Mohler, III, MD, now deceased, who contributed to an earlier version of this topic review. UpToDate also wishes to acknowledge Dr. Mohler's work as our Section Editor for Vascular Medicine.