62. Type A Aortic Dissection- Indications and Guidelines

Ke Xu MD, Ashraf Sabe MD
Brigham and Women’s Hospital
August 15th, 2024

Abbreviations & Definitions

AAS – Acute aortic syndromes
AATS – American Association for Thoracic Surgery
ATAAD – Acute type A aortic dissection
MRA – Magnetic resonance angiography
TEE – Transesophageal echocardiography

Indications & Guidelines for Management by Grade/Stage of Disease

Acute aortic dissection, intramural hematomas, and penetrating aortic ulcers are three clinical entities that belong to acute aortic syndromes (AAS).1 Acute aortic dissection accounts for 85-95% of AAS, and penetrating aortic ulcer about 2-7%.2 Aortic dissection is the separation of the layers of the media of the aortic wall through a tear in the aortic intima. The separation of the aorta creates a true and false lumen, where the dissection may be propagated either ante or retrograde. Intramural hematoma and penetrating aortic ulcers also result from intimal tears but are non-communicating aortic syndromes.

The incidence of AAS is low at 3.5-6.0 per 100,000 patients/year, but the mortality is high if untreated.3 The mortality of acute type A dissections (ATAAD) was often described as 1-2% per hour during the initial 48 hours.4 However, with advances in diagnostic testing and treatment, an updated study examined patients with ATAAD between 1996 and 2018 and concluded the overall mortality rate to be 5.8% in the first 48 hours. Among patients who were medically managed only, mortality was 0.5% per hour, and the mortality rate for those who were intended for surgical management, the mortality was 4.4% in the first 24 hours.5 It is important to note that ATAAD is underdiagnosed, as many acute mortalities are not subject to imaging or autopsy post-mortem. Moreover, sudden death, or unexplained sudden death, is often misdiagnosed and attributed to an acute coronary syndrome, stroke, or GI pathology.

Classification

The two common classification systems below are based on anatomical extent.

Stanford classification:

Type A: requires involvement of the ascending aorta (aorta proximal to the origin of the left subclavian artery)

Type B: all dissections not involving the ascending aorta (aorta distal to the left subclavian artery)

DeBakey classification:

Type I: involves the ascending and descending aorta

Type II: involves the ascending aorta only

Type III: involves the descending aorta only, commencing after the origin of the left subclavian artery

The chronicity of aortic dissections is classified based on the initial tear or symptom onset:

Acute: ≤14 days

Subacute: 15-90 days

Chronic: >90 days

Pathophysiology and clinical presentation

Aortic dissection is the result of surface tension exceeding the limit of the aorta, which is rendered by its three layers: intima, media, and adventitia. The adventitia is the strongest layer and is the main contributor to the aorta’s tensile strength. Therefore, mechanisms that increase intraluminal pressure and aortic radius (Laplace’s law: P x R = T) or decrease vessel wall strength will predispose the aorta to dissection. The underlying etiology of AAS is most often atherosclerotic disease, though it can also result from medial degeneration, trauma, or infection. Most dissections occur between the ages of 60 to 70 (mean age at diagnosis of 63 years) and have a 3:1 male predisposition. Chronic hypertension is the most common predisposing risk factor and is present in 75% of cases. Marfan, Loeys-Dietz, and Ehlers-Danlos syndrome are three connective tissue disorders that weaken the elastin or collagen layers within the media of the aortic wall, predisposing these patients to aortic aneurysms and dissections.

The presentation of ATAAD correlates with the extent of the dissection. Mid-sternal severe pain is the major symptom, which is often described as sudden in onset, reaching maximal severity quickly, and feeling a tearing sensation. Since early diagnosis of ATAAD is key to the outcome, and 30% of patients with dissection are initially thought to have another diagnosis, it is important to differentiate dissection from other pathologies presenting with chest pain. If the dissection propagates to cause coronary ischemia, the symptoms of ischemic cardiomyopathy may be less discernible from those of a dissection.

Diagnosis

Chest X-ray is usually the first test done in patients presenting with acute-onset chest pain. In ATAAD, 60-90% of CXRs are usually abnormal and show a widened mediastinum. Classic findings associated with ATAAD include a calcium sign (separation between calcification of the aortic intima and the lateral aortic wall of the aortic knob >10 mm), right tracheal deviation, obliteration of the aortic knob, and left main stem bronchus depression. However, these findings are not specific. Chest computed tomography angiography (CTA) is the imaging method of choice with 100% sensitivity and 98% specificity.6 Transesophageal echocardiography (TEE) and magnetic resonance angiography (MRA) can also identify ATAAD.1

CTA is fast and excellent in defining vascular anatomy and classifying AAS into Stanford types. However, it provides no information on aortic valve function and has a limited view of the coronary tree. The hallmark of an aortic dissection is a flap separating the aorta into a true and false lumen. TEE, on the other hand, while operator/interpreter dependent and requires sedation, is great at evaluating aortic valves and coronary arteries. MRA is excellent in assessing anatomy and end-organ ischemia, but it takes longer to perform and is not as readily available.

Medical therapy

Once the diagnosis of ATAAD is made, medical therapy should begin immediately for anti-impulse control to prevent false lumen propagation, aortic rupture, and dynamic malperfusion. The first line of treatment is beta blockers. Esmolol is used in patients without contraindications to beta blockers, and it can be titrated to a goal systolic blood pressure of 100-120 mmHg and heart rate <60 bpm. Labetalol is a beta-blocker with intrinsic partial sympathomimetic activity, which lowers heart rate and blood pressure. In the setting of hypotension, volume resuscitation is reasonable to achieve a systolic blood pressure of 90 mmHg. However, if a patient were hypotensive, careful evaluation for hemorrhage is mandatory to rule out rupture, tamponade, or mesenteric malperfusion. Sodium nitroprusside and calcium channel blockers (verapamil or diltiazem) are potential alternatives.

In addition to immediate impulse control, medical management for ATAAD should include:

  • Early consultation for cardiac surgery
  • Pain control – fentanyl, morphine, hydromorphone
  • Lab acquisition for surgical planning and monitoring malperfusion
  • Consideration of Foley placement to monitor urine output for renal dysfunction

The AATS currently recommends transferring patients with ATAAD to a comprehensive aortic center if cardiac surgery is not readily available. The difference in operative mortality between low- and high-volume hospitals is 27% vs 16%, respectively.19

Surgical treatment

The goal of surgery in patients with ATAAD is to resolve malperfusion, acute aortic insufficiency, address tamponade, and/or prevent aortic rupture.48 The basic approach has been excision of the primary entry tear, reconstruction of the aorta with an interposition graft, and, depending on associated complications, intervention on the aortic valve, reimplantation of coronary arteries to prevent myocardial ischemia, as well as arch vessel reconstitution to maintain cerebral and upper body perfusion.

Several cannulation and perfusion strategies for ATAAD surgery can be utilized with the guiding principle to establish antegrade systemic perfusion whenever possible and to restore true lumen flow. Systemic temperature management, cardioplegia, and brain perfusion strategies are optimized during the operation. Femoral artery cannulation has been widely used previously due to its convenience and speed; however, it is limited by retrograde arterial flow, resulting in worsening of malperfusion. Right axillary artery cannulation is now most commonly performed for ATAAD; however, there has been a gain of momentum to directly cannulate the ascending aorta to provide physiologic antegrade perfusion.49 Epiaortic ultrasonography or TEE is required to confirm cannulation of the true lumen. Both axillary and central aortic cannulation have been shown to achieve a lower rate of stroke when compared to femoral artery cannulation.50

When the primary defect is isolated to the ascending aorta, both the aortic root and valve are normal in size and function, and the patient has no connective tissue disease, root- and valve-preserving surgery using a Dacron interposition graft can be performed. This operation can be modified with the addition of hemiarch replacement when the distal ascending aorta or proximal arch is involved with the intimal tear. Criteria for repair of a dissected aortic arch with transverse arch replacement only include no intimal tear at the arch, arch diameter <4 cm, and no malperfusion of the innominate or left common carotid artery. When cerebral malperfusion is present, the affected vessels should be repaired and reimplanted.

Criteria for direct aortic root repair include no intimal tear at the root, no suspected or known connective tissue disorder, and root diameter <4.5 cm. In direct aortic root repair, the false lumen created by the dissection can be addressed with the construction of a “neomedia” by placing felt, pericardium, adventitia, and/or Dacron between the dissected layers. The valve is resuspended by placing horizontal mattress transmural sutures at the tips of all three commissures. Patients who do not meet criteria for direct aortic root repair are treated with either valve-sparing aortic root replacement or total aortic root replacement. When ATAAD presents with a tear in the aortic root, aortic root dilation, aortic valve insufficiency, coronary artery involvement, and/or a connective tissue disorder is suspected (particularly in younger patients), direct aortic root replacement should be performed. The David and Yacoub procedures are two aortic valve-sparing techniques. The David procedure reimplants the aortic valve into a graft and is preferred for those with connective tissue disorder since it stabilizes the aortic annulus from further dilation. The Yacoub procedure, on the other hand, remodels the commissures to provide improved hemodynamics with the creation of three new aortic sinuses. When the aortic valve cannot be preserved, or in cases where surgeons judge that a shorter operation is safer, a Bentall procedure should be performed, where the valve is replaced with a tissue or mechanical valve, along with the aortic root. All three procedures require re-implantation of the coronary buttons onto the newly created aortic root.

For distal anastomosis of the ascending aorta, meticulous suturing is important to avoid new intimal tears, minimize bleeding, and provide late durability. A few common techniques for the distal anastomosis include simple suturing, intussuscepting the graft into the distal aorta to decrease pressure along the suture line, multilayer reconstruction with felt/pericardium or Dacron, and buttressing with folded redundant adventitia or graft.

In 13-32% of ATAAD patients, the primary entry tear occurs in the aortic arch or proximal descending thoracic aorta; therefore, an extended aortic arch replacement may be warranted and should be performed by experienced surgeons. Aortic arch replacement with reconstruction of arch branch vessels and a classic or frozen elephant trunk are some techniques for extended aortic arch replacement. A hybrid arch procedure with TEVAR have been useful in addressing complex ATAAD.

Delayed surgical repair

End-organ failure due to malperfusion syndrome may represent a more imminent life-threatening problem, as operative mortality with central aortic repair can be up to 60-70%. Malperfusion can be diagnosed via clinical exam or radiographic evidence. “Malperfusion syndrome” is the consequence of prolonged malperfusion that can be diagnosed by clinical symptoms (abdominal pain, low urine output), physical exam (peritoneal signs), and lab tests (lactate, LFTs, and ABG). When patients are otherwise hemodynamically stable (no rupture, no tamponade) but present with severe malperfusion, they may benefit from upfront endovascular reperfusion with descending TEVAR, aortic fenestration, and branch vessel stenting prior to definitive treatment of the ATAAD repair.36 The hypothesis is such that the risk of dying from organ failure due to malperfusion is higher than the risk of dying from aortic rupture. For patients with malperfusion syndrome initially treated with fenestration/stenting and delayed repair, observed mortality was significantly lower than the calculated rates from various models that include upfront repairs for all patients. In contrast, patients with neuro-malperfusion and coronary malperfusion were shown to represent a high-risk subgroup who may benefit from immediate surgical intervention.51

Postoperative considerations

Postoperative management includes controlling blood pressure, surveillance imaging, screening of first-degree relatives, and genetic testing. Beta-blocker, but not angiotensin-converting enzyme inhibitor, has been shown to lower the mortality rate postoperatively.52 Fluoroquinolones have been shown to exacerbate aortic wall damage and should be avoided postoperatively. Follow-up imaging with CTA or MRI should be performed at regular intervals. Genetic testing can be offered if a patient has a family history of aortic aneurysm or a diagnosis at an early age (younger than 50 years of age or age 50-60 years without hypertension). Lastly, all first-degree relatives of patients with ATAAD should be considered for screening studies.

The 2021 AATS recommendations regarding ATAAD are summarized in Table 1.7 The 2022 ACC/AHA Class I recommendations for the diagnosis and management of AAS are in Table 2.8

Table 1. 2021 AATS recommendations regarding ATAAD treatment.

Recommendation Class of Recommendation References
Initial medical therapy
Beta blockers are recommended in the initial management of ATAAD without severe aortic regurgitation. I 9, 10
Pain relief is recommended in patients with ATAAD. I 11, 12
Calcium channel blockers are a potential alternative to beta blockers. IIa 10, 13
When multiple agents are required, it is reasonable to start vasodilators after initial rate control. IIa 9, 10
In the setting of hypotension, volume resuscitation is reasonable to achieve a systolic blood pressure of 90 mmHg. IIa 14, 15
Interhospital transfer
When cardiac surgery is not immediately available, it is reasonable to transfer patients with ATAAD to a Comprehensive Aortic Center. IIa 16, 17
Surgical triage
Emergency surgery is recommended for patients with ATAAD. I 18, 19
Surgery is recommended in patients with type A intramural hematoma and one or more high-risk features. I 20, 21
Surgery can be effective in patients with ATAAD and brain malperfusion. IIa 22, 23
Nonoperative management is reasonable in catheter-induced ATAAD, if limited to the aortic root. IIa 24, 25
Cannulation and perfusion strategy
Right axillary artery cannulation is reasonable for stable patients undergoing ATAAD repair. IIa 26
Direct aortic cannulation with imaging guidance is reasonable for ATAAD repair. IIa 27
The addition of either antegrade or retrograde cerebral perfusion is reasonable for ATAAD repair. IIa 28
Circulatory arrest with antegrade cerebral perfusion and moderate or deep hypothermia is reasonable for ATAAD repair during extended arch reconstruction. IIa 29
Management of aortic root recommendations
Aortic valve resuspension is recommended for most patients with ATAAD. I 30
Aortic root replacement is recommended in ATAAD with root aneurysm or primary entry tear in the root. I 30
Expeditious coronary artery bypass grafting should be performed in patients with ATAAD and persistent coronary malperfusion after repair. I 31
Aortic root replacement is reasonable in patients with ATAAD and Marfan syndrome or other hereditary thoracic aortic disorders. IIa 32
Management of ascending aorta and distal anastomosis
Circulatory arrest with open distal anastomosis is preferred in ATAAD. I 33
The extent of aortic resection should include the entire ascending aorta and primary entry tear. I 34
Management of aortic arch
Extended aortic arch replacement is reasonable in patients with ATAAD and: primary entry tear in the arch or proximal descending thoracic aorta, brain and peripheral malperfusion, or arch or descending thoracic aortic aneurysm or rupture. IIa 35
Management of malperfusion
It is reasonable to delay proximal aortic repair until after definitive treatment of mesenteric malperfusion. IIa 36
Descending TEVAR, aortic fenestration, and branch vessel stenting are reasonable treatment options for mesenteric malperfusion. IIa 36, 37

Table 2. 2022 ACC/AHA Class I recommendations regarding diagnosis and management for aortic disease.

Recommendation Class of Recommendation References
Diagnostic evaluation (imaging, laboratory testing)
In patients with suspected AAS, CT is recommended for initial diagnostic imaging, given its wide availability, accuracy, and speed, as well as the extent of anatomic detail it provides. I 38
Medical management of AAS
In patients presenting to the hospital with AAS, prompt treatment with anti-impulse therapy and invasive monitoring of BP via an arterial line in an ICU setting is recommended as initial treatment to decrease aortic wall stress. I 10
Patients with AAS should be treated to a SBP <120 mmHg or to lowest BP that maintains adequate end-organ perfusion, as well as to a target heart rate of 60-80 bpm. I 39
In patients with AAS, initial management should include beta blockers, except in patients with contraindications. I 40
In patients with AAS, initial management should include intravenous vasodilators if the BP is not well controlled after initiation of intravenous beta-blocker therapy. I 41
Patients with AAS should be treated with pain control to help with hemodynamic management. I 11
In patients with AAS, it is recommended to treat with long-term beta blockers (unless contraindicated) to control heart rate and BP to reduce late aortic-related adverse events. Additional antihypertensive agents (particular ARBs and ACEIs) should be added, as necessary, to adequately control BP I 10
ATAAD surgical management
In patients presenting with suspected or confirmed ATAAD, emergent surgical consultation and evaluation followed by immediate surgical intervention is recommended due to the high risk of associated life-threatening complications. I 19
In patients with ATAAD presenting with renal, mesenteric, or lower extremity malperfusion, it is recommended to proceed to immediate operative repair of the ascending aorta. I 43
In patients with ATAAD and a partially dissected aortic root but no significant aortic valve leaflet pathology, aortic valve resuspension is recommended over valve replacement. I 44
In patients with ATAAD who have extensive destruction of the aortic root, a root aneurysm, or a known genetic disorder, aortic root replacement is recommended with a mechanical or biological valved conduit. I 45
In patients with ATAAD undergoing aortic repair, an open distal anastomosis is recommended to improve survival and increase false-lumen thrombosis rates. I 46
In patients with ATAAD without an intimal tear in the arch or a significant arch aneurysm, hemiarch repair is recommended over more extensive arch replacement. I 47

become life-long medical problems that require a thoughtful multidisciplinary approach acutely, and long-term care to improve overall survival and quality of life for the patient, their family, and the community at large.

Supporting Evidence for Current Indications & Guidelines

Pape et al. examined 17-year trends in the presentation, diagnosis, and hospital outcomes of acute aortic dissection from the International Registry of Acute Aortic Dissection (IRAD).19 Of the 2952 patients included in the analysis, in-hospital mortality for ATAAD patients has decreased significantly to around 20% in 2010-2013, as compared to 25-33% prior to 2005. This mortality rate is in line with other studies.53, 54 The 10-year actuarial survival rate, including in-hospital mortality, was between 46 and 70%.54, 55 Using multivariable logistic regression analysis, variables associated with operative outcome were age, malperfusion, LVEF, prior cardiac surgery, preoperative mechanical ventilation, preoperative resuscitation, and concomitant coronary artery bypass grafting.56

Ongoing Trials/Recent Publications

Up to 20% of patients with ATAAD are not surgical candidates due to comorbidities. No devices are commercially approved for ascending TEVAR. There are trials assessing ascending stent grafts in these patients, but long-term outcomes are pending.57

Expert Commentary

While ATAAD is a surgical emergency with high mortality, several comorbidities have been identified to correlate with increased risk in ATAAD repair,58 including malperfusion syndromes, frailty, advanced age, previous cardiac surgery, and use of novel anticoagulant medications. Therefore, improvement in risk stratification should guide appropriate delay or permanent deferral of surgery in select individuals. Patient-centered decision making is extremely important in these cases. Aortic syndromes become life-long medical problems that require a thoughtful multidisciplinary approach acutely, and long-term care to improve overall survival and quality of life for the patient, their family, and the community at large.

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