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Management of aortic dissection

Management of aortic dissection

INTRODUCTION — Aortic dissection of the ascending or descending aorta is usually suspected clinically from the history and physical examination. Patients who survive the initial tear typically present with severe, sharp or “tearing” anterior chest pain (in ascending aortic dissection) or posterior chest or back pain (in dissection distal to the left subclavian). If the dissection leads to impaired or absent blood flow to peripheral vessels, the physical examination may reveal a pulse deficit, defined as a weak or absent carotid, brachial, or femoral pulse.

After the patient is stabilized, the diagnosis of aortic dissection is generally made noninvasively by computed tomography (CT), transesophageal echocardiography (TEE), or magnetic resonance imaging (MRI). (See ‘Acute management’ below and “Clinical manifestations and diagnosis of aortic dissection”.)

Two different anatomic systems – the DeBakey and Stanford (Daily) systems – have been used to classify aortic dissection [1,2]. The Stanford system, which is 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. In comparison, the DeBakey system is based upon the site of origin with type I originating in the ascending aorta and propagating to at least the aortic arch, type II originating in and confined to the ascending aorta, and type III originating in the descending aorta and extending distally or proximally.

There are several variants of aortic dissection, including intimal tear without hematoma and intramural hematoma. (See “Clinical manifestations and diagnosis of aortic dissection”, section on ‘Variants’ and “Aortic intramural hematoma”.)

The acute and chronic management of aortic dissection will be reviewed here. The recommendations are generally in agreement with guidelines published by a task force of the European Society of Cardiology in 2001 [3]. Management of a variant of aortic dissection, aortic intramural hematoma, is discussed separately. (See “Aortic intramural hematoma”.)

GENERAL PRINCIPLES — Acute dissections involving the ascending aorta are considered surgical emergencies. In contrast, dissections confined to the descending aorta are treated medically unless the patient demonstrates progressive dissection or continued hemorrhage into the pleural or retroperitoneal space.

In a review of 464 patients from the International Registry of Acute Aortic Dissection (IRAD) presenting with an aortic dissection, 72 percent of those with a type A dissection were treated surgically [4]. Reasons for no surgery included advanced age, comorbidity, patient refusal, intramural hematoma, or death prior to planned surgery. In contrast, only 20 percent of those with a type B dissection underwent surgery.

A similar difference in management of older patients was noted in another IRAD review of 550 patients with a type A dissection, 32 percent of whom were at least 70 years [5]. Elderly patients were significantly less likely than younger patients (mean age 55) to undergo surgery (64 versus 86 percent). Older patients also had a significantly higher mortality with either surgery or medical therapy (eg, in-hospital mortality 43 versus 28 percent).

The prognosis of patients requiring surgery improved dramatically in 1955 after DeBakey’s introduction of effective surgical techniques [6]. Surgical therapy involves:

  • Excision of the intimal tear
  • Obliteration of entry into the false lumen proximally
  • Reconstitution of the aorta with interposition of a synthetic vascular graft

In addition, restoration of aortic valve competence can be performed in patients who develop significant aortic regurgitation. This can be achieved by resuspension of the native aortic valve or by aortic valve replacement [7]. If the aortic valve is resuspended, intraoperative TEE should be used to document resolution of aortic regurgitation.

Medical therapy of aortic dissection involves lowering the blood pressure and decreasing the velocity of left ventricular contraction, both of which will decrease aortic shear stress and minimize the tendency for propagation of the dissection.

ACUTE MANAGEMENT — Patients with suspected aortic dissection should be admitted to an intensive care unit as rapidly as possible after confirmation of the diagnosis for pain control with morphine, and reduction of systolic blood pressure to 100 to 120 mmHg or the lowest level that is tolerated (table 1) [3,8]. Patients who are hemodynamically unstable or with airway compromise should be intubated (table 2).

For blood pressure control, initial treatment consists of an intravenous beta blocker to reduce the heart rate below 60 beats/min; the associated fall in both blood pressure and the rate of rise in systolic pressure will minimize aortic wall stress. Either propranolol (1 to 10 mg load, followed by 3 mg/h) or labetalol can be used in this setting. Labetalol can be given as a bolus (20 mg initially, followed by 20 to 80 mg every 10 minutes to a total dose of 300 mg) or as an infusion (0.5 to 2 mg/min). Esmolol may be preferable in the acute setting, due to its short half-life and ability to titrate to effect. It is also advantageous in patients who might be intolerant of beta blockers due, for example, to asthma, or heart failure [8]. Verapamil or diltiazem are alternatives in patients who cannot tolerate beta blockers [8].

The patient can be switched to oral beta blocker therapy after heart rate control has been achieved. (See “Drug treatment of hypertensive emergencies”.)

If, after beta blockade, the systolic blood pressure remains above 100 mmHg with good mentation and renal function, intravenous sodium nitroprusside should be added. The initial dose is 0.25 to 0.5 mcg/kg per minute. Nitroprusside should not be used without first controlling the heart rate with beta blockade since vasodilation alone induces reflex activation of the sympathetic nervous system leading to enhanced ventricular contraction and increased aortic wall shear stress. Patients receiving nitroprusside should be continuously monitored, preferably using an intraarterial cannula from the arm with the highest auscultatory pressure.

While nitroprusside is the preferred agent, angiotensin converting enzyme (ACE) inhibitors or intravenous nicardipine, verapamil or diltiazem may also be effective in lowering blood pressure [8]. Other direct vasodilators, such as hydralazine, should be avoided, since they increase aortic wall shear stress and provide less accurate and reversible control of the blood pressure.

Hypotensive patients should be evaluated to determine if the cause is blood loss, hemopericardium with tamponade, or cardiac failure before volume is administered. Inotropic agents should be avoided since they will increase aortic wall shear stress and worsen the dissection. In patients with cardiac tamponade, percutaneous pericardiocentesis can accelerate bleeding and shock [9].

Diagnostic evaluation should be accomplished as promptly as possible. In patients with severe hemodynamic instability, bedside TEE is the procedure of choice [8]. In more stable patients, chest computed tomography (CT), thoracic magnetic resonance imaging (MRI) or transesophageal echocardiography (TEE) are diagnostic options. (See “Clinical manifestations and diagnosis of aortic dissection”, section on ‘Imaging’.)


Descending (type B) aortic dissection

Medical therapy — Patients with uncomplicated aortic dissections confined to the descending thoracic aorta (Stanford type B or DeBakey type III) are best treated with medical therapy (table 3) [3,10,11]. In a series of 384 patients with type B dissections from the International Registry of Acute Aortic Dissection (IRAD), 73 percent were managed medically. In-hospital mortality for these patients was 10 percent [12].

The reported long-term survival rate with medical therapy is approximately 60 to 80 percent at four to five years [11,13-15] and approximately 40 to 45 percent at 10 years [13,14]. Survival is best in patients with noncommunicating and retrograde dissections [16].

Despite fair survival among patients treated medically, spontaneous healing of the dissection, characterized by disappearance of the false lumen due to complete thrombosis, is uncommon [3,16,17]. Continued flow through the false lumen (patent false lumen), which occurs with either partial thrombosis or no significant thrombosis, has been postulated to prevent healing.

The relationship between long-term prognosis and the degree of patency of the false lumen was evaluated in 201 hospital survivors of type B acute aortic dissection who were enrolled in the IRAD [17]. Complete false lumen patency or partial thrombosis was present in 57 and 34 percent of patients, respectively. The mean three-year mortality rate was significantly worse in patients with partial thrombosis compared to those with complete patency (32 versus 14 percent).

Surgery — Surgical intervention in descending aortic dissections is reserved for patients who have a complicated course. Indications for surgery include occlusion of a major aortic branch, dissection extension (as may be manifested by persistent or recurrent pain), presence within an aortic aneurysm, and evidence of aortic rupture (table 3) [8]. Acute distal dissections in patients with Marfan syndrome may also be best treated surgically [7]. (See “Management of Marfan syndrome and related disorders”.)

Because patients treated surgically are primarily those with a complicated course, it is not surprising that short-term mortality for these patients is higher than with medical therapy. In data from the IRAD, in-hospital mortality for surgical patients was 32 percent compared with 10 percent for those treated medically [12]. There were two independent predictors of surgical mortality: age ≥70 years and hypotension or shock on admission [18].

Although short-term outcomes are better for medically treated patients with type B dissections [11,13,15], the long-term outcomes may be similar [11,13]. This was illustrated in a report of 142 patients, 111 (78 percent) of whom were treated medically [13]. There was a trend toward lower mortality with medical therapy at one year (15 versus 33 percent); this difference tended to diminish over time. Both groups had similar survival at five and ten years (60 and 35 percent). (See ‘Long-term management’ below.)

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Endovascular stent-grafting has been employed as a less invasive alternative to surgery, particularly in stable patients with type B dissections. (See ‘Endovascular stent-grafts’ below.)

Ascending (type A) aortic dissection — Acute ascending aortic dissections (Stanford type A) should be treated as a surgical emergency since these patients are at high risk for a life-threatening complication such as aortic regurgitation, cardiac tamponade, or myocardial infarction, and the mortality rate is as high as 1 to 2 percent per hour early after symptom onset (table 4) [19].

The use of and survival benefit from surgery were illustrated in an IRAD review of 547 patients with a type A dissection [20]:

  • 80 percent of patients were treated surgically. The main cited reasons for medical therapy were comorbid conditions, advanced age (mean 80 years), and patient refusal.
  • The in-hospital mortality was 27 and 56 percent for surgical and medical therapy, a difference that was due in part to increased comorbidity in medically treated patients. A similar in-hospital mortality with surgical therapy (22 percent) was noted in a series of 487 patients [21].
  • Not surprisingly, the patients who died had a higher rate of in-hospital complications such as neurologic deficits, coronary or mesenteric ischemia, acute renal failure, and limb ischemia.

Even the presence of acute myocardial infarction, which may be due to the dissection involving a coronary ostium (particularly the right coronary artery), should not entirely exclude the option of rapid surgical intervention. However, patients with stroke in progress are at increased risk for hemorrhagic cerebral infarction due to intraoperative heparinization and restoration of cerebral blood flow. Thus, hemorrhagic stroke is a relative contraindication to urgent surgical intervention.

Patients ≥70 years of age are less likely to be treated surgically (64 versus 86 percent in younger patients [mean age 55 years]) in the IRAD registry [5]. However, older age alone should not preclude surgery [5,22]. In the registry report, in-hospital mortality was significantly higher in the older patients (38 versus 23 percent) but lower than in older patients treated medically (38 versus 53 percent) [5]. Thus, surgery should be considered in selected elderly patients, even some octogenarians.

Women are also less likely to be treated surgically (71 versus 87 percent) in the IRAD registry [23]. As with elderly patients, women have a higher in-hospital mortality with surgical treatment than men (32 versus 22 percent), but a lower mortality than with medical therapy (32 versus 54 percent).

Operative mortality for ascending aortic dissections at experienced centers varies from 7 to 36 percent, well below the more than 50 percent mortality with medical therapy [4,11,20,22,24-29]. An aggressive surgical approach, including a full root or hemiarch replacement when the aortic valve, sinuses, or arch are involved, may not be associated with an increased operative risk [30,31]. Hypothermic circulatory arrest has been used, especially in repairs involving the aortic arch, although a retrospective analysis of 307 patients failed to find a benefit in terms of survival, complications, or need for late reoperation [29].

Poor prognostic factors which mitigate against surgical success include [4,5,20,21,24-26,28,32-35]:

  • Age over 70 years
  • Abrupt onset of chest pain
  • Hypotension, shock, or tamponade at presentation
  • Renal failure at presentation and before surgery
  • Pulse deficit
  • Abnormal ECG, particularly ST segment elevation
  • Prior myocardial infarction
  • Previous aortic valve replacement
  • Renal and/ or visceral ischemia
  • Underlying pulmonary disease
  • Preoperative neurologic impairment
  • Perioperative bleeding and massive blood transfusion
  • Prolonged clamping time

The first six factors were the most important predictors of in-hospital mortality in the IRAD review [20]. Using a complicated predictive score that incorporated these parameters, patients could be identified with subsequent in-hospital mortality rates that ranged from 2 to over 80 percent.

Evaluation for CAD and aortic valve disease — In addition to the imaging necessary to secure the diagnosis of type A aortic dissection, CT coronary angiography, percutaneous coronary angiography and transesophageal echocardiography (TEE) may be considered to evaluate the patient for concomitant coronary artery disease (CT) or aortic valve disease (TEE, MRI, transthoracic echocardiography) prior to urgent surgical repair of the ascending aorta. (See “Clinical manifestations and diagnosis of aortic dissection”, section on ‘Imaging’.)

Patients with acute aortic dissection have a significant incidence of CAD. As a result, it has been suggested that coronary angiography be performed prior to surgery so that bypass surgery on critical stenoses can be performed while the patient is under cardiopulmonary bypass. There has been concern that the presence of undiagnosed critical coronary stenoses may make weaning from cardiopulmonary bypass more difficult and can increase the risk of perioperative myocardial infarction or death. However, the resulting delay of surgery increases the risk of cardiac tamponade or aortic rupture, which are important causes of preoperative mortality in aortic dissection.

The role of percutaneous coronary angiography was evaluated in a study that retrospectively analyzed the outcome of 122 patients who underwent emergency aortic surgery, primarily for a type A aortic dissection [33]. There was no difference in the in-hospital mortality between those who did or did not undergo coronary angiography (22 versus 16 percent), including those who had a prior myocardial infarction which was the only predictor of in-hospital mortality. Coronary angiography had no impact on the incidence of coronary artery bypass grafting (17 versus 25 percent), three-quarters of which were performed because of coronary artery dissection not atherosclerotic disease. These observations suggest limited value from coronary angiography and support the recommendation of proceeding to surgery as rapidly as possible [33].

In addition to its important role in the diagnosis of aortic dissection, TEE can define the severity and mechanism of aortic regurgitation and involvement of the coronary ostia that complicates acute type A aortic dissection [36]. This information is useful when considering aortic valve repair versus replacement. Patients with an intrinsically normal valve who have aortic regurgitation due to a correctable aortic lesion (incomplete leaflet closure, leaflet prolapse, or dissection flap prolapse) can undergo aortic valve repair; in comparison, abnormalities that cannot be repaired (Marfan, bicuspid valve, aortitis) require valve replacement. (See “Transesophageal echocardiography in the evaluation of aortic valve disease”.)

Survival after surgical repair — Long-term survival after surgical repair of type A dissections is relatively good. This was illustrated in an IRAD report of 303 patients with type A dissection who were seen between 1996 and 2003, 90 percent of whom were managed surgically [37]. Survival at one and three years was 96 and 91 percent, respectively.

Longer term follow-up was provided in a series of 208 patients presenting between 1978 and 1995 [27] Patient survival at 5 and 10 years was 68 and 52 percent, respectively; residual distal dissected aorta did not affect late survival and had a low risk for aneurysmal change and reoperation. Whether improvements in surgical and medical care have led to better long-term outcomes over time is not known.

The natural history of the distal aorta was evaluated in an observational study of surgical survivors of Type A dissection. Serial computed tomography in 89 patients identified a median expansion rate of approximately 1 mm/year. Male gender, an initial descending aorta diameter of greater than 4 cm, or an initial diameter of less than 4 cm with a patent false lumen were identified as predictive of more rapid descending aorta growth [38]. The overall risk of reoperation was 16 percent at 10 years.

Endovascular stent-grafts — Endovascular stent-grafting, which has been used successfully in patients with thoracic and abdominal aortic aneurysms, has been employed as a less invasive alternative to surgery, primarily in stable patients with type B dissections [8]. The stent graft is positioned to cover the intimal flap and seal the entry site of the dissection, resulting in thrombosis of the false lumen (table 5). (See “Endovascular repair of abdominal aortic aneurysms”.)

Type B dissections — In the IRAD series of 384 type B dissections, 46 (12 percent) were managed with endovascular stent grafting [12]. This technique was reserved for patients who had undergone at least eight weeks of medical management. Only three (6.5 percent) died during the initial hospitalization.

The outcome of stent grafting was compared with surgery in a nonrandomized evaluation of 24 consecutive patients with a subacute or chronic thoracic type B dissection who had at least one indication for surgery [39]. There was no morbidity (paraplegia, stroke, embolization, side-branch occlusion or infection) or mortality with stent grafting, while surgery was associated with a 33 percent mortality and a 42 percent incidence of adverse events within 12 months. At three months, thrombosis of the false lumen had occurred in all patients undergoing stent grafting.

Stent grafting has also been evaluated for acute and, in some cases, life-threatening dissections, but the outcomes are not as good [40-42]. One report evaluated 19 patients with an acute dissection (four type A) and an indication for surgery [40]. This included involvement of aortic branches in 14, which led to symptomatic compromise of multiple branch vessels in seven. Complete thrombosis was achieved in 79 percent, and revascularization of ischemic branch vessels with relief of symptoms occurred in 76 percent of obstructed branches. However, the morbidity rate was 21 percent (small bowel and renal infarction and lower extremity gangrene) and 30-day mortality was 16 percent. Among patients who survived this period, there were no deaths or instances of aneurysm or aortic rupture during the subsequent 13 month follow-up period.

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Longer term follow-up was described in a series of 49 patients with acute and chronic aortic dissection who were treated with stent grafts [43]. Serial CT studies in the 34 patients with descending aortic dissections, showed that, at two years, total occlusion of the false lumen was more often achieved with acute compared to chronic dissections (76 versus 36 percent). The chronic dissections had similar reductions in false lumen diameter, but had larger false lumens prior to treatment (eg, 25.2 versus 16.2 mm in the middle descending aorta).

In an attempt to overcome the small number of patients in most published series, a meta-analysis was performed of 39 studies involving a total of 609 patients who underwent stent-graft placement for a type B dissection [42]. The following findings were noted:

  • Procedure success was achieved in 98 percent of patients.
  • Major complications occurred in 11.1 percent; neurologic complications, the most serious, occurred in 2.9 percent, mostly periprocedural stroke and paraplegia (1.9 and 0.8 percent, respectively). The major complication rate was significantly higher with acute compared to chronic dissections (21.7 versus 9.1 percent). Minor complications occurred in 2.5 percent. The rate of complications compared favorably to previously reported surgical series. The rate was higher in more recent studies, which may reflect inclusion of higher risk patients with increasing experience with the procedure.
  • The false lumen was not abolished in about 25 percent of patients and, at a mean follow-up of 19 months, aortic rupture occurred in 2.3 percent.
  • The mortality rate was 5.2 percent in-hospital and 5.3 percent at 30 days, being significantly higher with acute dissections (9.8 versus 3.2 percent). Kaplan-Meier analysis revealed overall survival rates of 90 percent at one year and 89 percent at two years.
  • The outcomes were much better in centers that had performed more than 20 endovascular procedures compared to less experienced centers. This included significantly lower rates of overall complications (7.7 versus 20.9 percent), neurologic complications (1.0 versus 5.7 percent), and 30-day mortality (3.2 versus 8.5 percent).

Type A dissections — A possible alternative to surgery in patients with type A dissections who have ischemic complications is endovascular stent-grafting [8]. There is only a limited experience in patients with acute type A dissections. In one series, the false lumen was completely obliterated in 14 of 15 patients with a type A dissection within three months [43]. Further study is required to determine the role for this approach in such patients.

A hybrid approach to the repair of type A aortic dissection, sometimes referred to as the “frozen elephant trunk repair,” uses an open approach to surgically repair the ascending aorta while using a stent-graft to manage the descending aorta. Several case series have compared this technique with conventional open repair [44-58].

In one case series, a triple-branched stent graft was placed into the three arch vessels and descending aorta in 30 patients with acute type A dissection. The procedure was technically successful in all patients and aortic cross clamp and lower body arrest times were 84 and 31 minutes, respectively, which is generally much lower than with conventional treatment [44].

Fenestration and other stents — Aortic dissection frequently causes life-threatening ischemia of distal organs, and the mortality associated with such complications can exceed 60 percent. Although surgical repair of the dissection often results in resolution of peripheral ischemia, stenting and/or balloon fenestration of the dissecting membrane may be noninvasive alternatives for patients with a type A dissection in whom mesenteric, renal, or peripheral ischemia persists after surgical repair or for patients with a type B dissection treated medically in whom mesenteric, renal, or peripheral ischemic complications arise (table 5) [8,41,59].

The efficacy of these approaches was evaluated in a series of 40 patients who were treated with percutaneous revascularization of the aortic branch artery using a stent placed in either the true or false lumen, with or without balloon fenestration of the intimal flap to restore flow to the involved organ [59]. Revascularization was successful in 93 percent of patients, but the 30 day mortality rate was 25 percent, primarily related to irreversible organ ischemia present before the procedure. Among the 30 patients who survived the first 30 days, the mortality at 29 months was 17 percent.

PROGNOSIS — The 10-year actuarial survival rate of patients with an aortic dissection who leave the hospital has ranged from 30 to 88 percent in different studies; survival appears similar whether the patient has had a type A or a type B dissection [11,13,14,21,25-27,60]. This may be explained by the fact that adverse events, such as recurrent dissection or complications of aneurysm formation in the descending aorta, occur in both type A and type B dissection (DeBakey type 1) patients [61].

Late aneurysm formation as well as adverse outcomes including death are related to the initial diameter of the false lumen in the upper thoracic aorta. This was illustrated in a study of 100 patients (51 type I and 49 type III) who survived initial hospitalization for aortic dissection in whom contrast-enhanced computed tomography was performed during the acute phase [62]. The following findings were noted at a mean CT follow-up of 31 months and a mean clinical follow-up of 53 months:

  • Aneurysm (diameter ≥60 mm) formation occurred in 15 of the 53 patients who had follow-up CT, most often in the upper thoracic descending aorta.
  • Patients with an initial false lumen diameter of ≥22 mm at the upper thoracic aorta, compared with those with a smaller diameter, were significantly more likely to develop late aneurysm formation (42 versus 5 percent) or death.

The causes of death were illustrated in a report of 380 survivors of an initial type A dissection in which there were 31 late deaths [21]. The causes were stroke (12 patients), aortic reoperation for re-dissection or progressive dilatation of the false lumen (seven patients), malignancy (five patients), myocardial infarction (four patients), and heart failure (three patients).

LONG-TERM MANAGEMENT — There are three main management issues in patients who have survived the initial dissection: medical therapy to minimize aortic wall shear stress; serial imaging to detect signs of dissection progression, redissection, or aneurysm formation; and reoperation when indicated.

Medical therapy — All patients should receive life-long therapy with an oral beta blocker to reduce systemic blood pressure and the rate of rise in systolic pressure, both of which will minimize aortic wall stress [8]. Although not evaluated in controlled trials, we suggest a target blood pressure of less than 120/80 mmHg [8]. Combination antihypertensive drug therapy is usually required.

Avoidance of strenuous physical activity is also recommended as another method to minimize aortic shear stress. (See “Management of Marfan syndrome and related disorders”, section on ‘Restriction of strenuous activity’.)

Serial imaging — We generally perform a baseline thoracic MRI scan prior to discharge with follow-up examinations at three, six, and twelve months, even if the patient remains asymptomatic (table 6) [3,8]. Subsequent screening studies are then performed every one to two years if there is no evidence of progression.

The following abnormalities can be detected on serial imaging:

  • Extension or recurrence of the dissection
  • Aneurysm formation
  • Leakage at anastomoses or stent sites

MRI is as accurate as TEE and, because it is noninvasive, and is more acceptable for serial studies. CT scanning is an alternative, but exposes the patient to considerable ionizing radiation and requires iodinated contrast, which may cause nephrotoxicity. (See “Pathogenesis, clinical features, and diagnosis of contrast-induced nephropathy”.)

Alternating chest CT and thoracic MRI is another option for patients with good renal function. Non-contrast MRI can be used for patients with impaired renal function to avoid the risk of nephrogenic systemic fibrosis. (See “Nephrogenic systemic fibrosis/nephrogenic fibrosing dermopathy in advanced renal failure”.)

Reoperation — Repeat surgery is required in approximately 12 to 30 percent of patients, usually because of extension or recurrence of dissection at the previous site of intervention, localized aneurysm formation remote from the site of repair, graft dehiscence or infection, or aortic regurgitation (table 7 and table 8) [3,16,25,26,60,63]. The reoperation rate is higher in patients with Marfan syndrome [3]. (See “Management of Marfan syndrome and related disorders”.)

The evolution of a type A aortic dissection after surgical repair was evaluated in a report of 58 patients who were discharged from the hospital and then followed with serial MR scans [63]. Residual distal dissection was present in 45 (78 percent). The yearly aortic growth rate of this segment was 0.37 cm overall and significantly higher at 0.56 cm in the absence of thrombus in the false lumen. During a seven year follow-up, 16 patients (28 percent) underwent reoperation because of progressive dilation of the untreated aortic segment. Residual dissection was present in all but one and 13 had no thrombosis in the false lumen.


  2. Daily PO, Trueblood HW, Stinson EB, et al. Management of acute aortic dissections. Ann Thorac Surg 1970; 10:237.
  3. Erbel R, Alfonso F, Boileau C, et al. Diagnosis and management of aortic dissection. Eur Heart J 2001; 22:1642.
  4. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 2000; 283:897.
  5. Mehta RH, O’Gara PT, Bossone E, et al. Acute type A aortic dissection in the elderly: clinical characteristics, management, and outcomes in the current era. J Am Coll Cardiol 2002; 40:685.
  6. DE BAKEY ME, COOLEY DA, CREECH O Jr. Surgical considerations of dissecting aneurysm of the aorta. Ann Surg 1955; 142:586.
  7. DeSanctis RW, Doroghazi RM, Austen WG, Buckley MJ. Aortic dissection. N Engl J Med 1987; 317:1060.
  8. Tsai TT, Nienaber CA, Eagle KA. Acute aortic syndromes. Circulation 2005; 112:3802.
  9. Isselbacher EM, Cigarroa JE, Eagle KA. Cardiac tamponade complicating proximal aortic dissection. Is pericardiocentesis harmful? Circulation 1994; 90:2375.
  10. Crawford ES. The diagnosis and management of aortic dissection. JAMA 1990; 264:2537.
  11. Doroghazi RM, Slater EE, DeSanctis RW, et al. Long-term survival of patients with treated aortic dissection. J Am Coll Cardiol 1984; 3:1026.
  12. Suzuki T, Mehta RH, Ince H, et al. Clinical profiles and outcomes of acute type B aortic dissection in the current era: lessons from the International Registry of Aortic Dissection (IRAD). Circulation 2003; 108 Suppl 1:II312.
  13. Umaña JP, Lai DT, Mitchell RS, et al. Is medical therapy still the optimal treatment strategy for patients with acute type B aortic dissections? J Thorac Cardiovasc Surg 2002; 124:896.
  14. Bernard Y, Zimmermann H, Chocron S, et al. False lumen patency as a predictor of late outcome in aortic dissection. Am J Cardiol 2001; 87:1378.
  15. Estrera AL, Miller CC 3rd, Safi HJ, et al. Outcomes of medical management of acute type B aortic dissection. Circulation 2006; 114:I384.
  16. Erbel R, Oelert H, Meyer J, et al. Effect of medical and surgical therapy on aortic dissection evaluated by transesophageal echocardiography. Implications for prognosis and therapy. The European Cooperative Study Group on Echocardiography. Circulation 1993; 87:1604.
  17. Tsai TT, Evangelista A, Nienaber CA, et al. Partial thrombosis of the false lumen in patients with acute type B aortic dissection. N Engl J Med 2007; 357:349.
  18. Trimarchi S, Nienaber CA, Rampoldi V, et al. Role and results of surgery in acute type B aortic dissection: insights from the International Registry of Acute Aortic Dissection (IRAD). Circulation 2006; 114:I357.
  19. Nienaber CA, Eagle KA. Aortic dissection: new frontiers in diagnosis and management: Part I: from etiology to diagnostic strategies. Circulation 2003; 108:628.
  20. Mehta RH, Suzuki T, Hagan PG, et al. Predicting death in patients with acute type a aortic dissection. Circulation 2002; 105:200.
  21. Chiappini B, Schepens M, Tan E, et al. Early and late outcomes of acute type A aortic dissection: analysis of risk factors in 487 consecutive patients. Eur Heart J 2005; 26:180.
  22. Kawahito K, Adachi H, Yamaguchi A, Ino T. Early and late surgical outcomes of acute type A aortic dissection in patients aged 75 years and older. Ann Thorac Surg 2000; 70:1455.
  23. Nienaber CA, Fattori R, Mehta RH, et al. Gender-related differences in acute aortic dissection. Circulation 2004; 109:3014.
  24. Miller DC, Mitchell RS, Oyer PE, et al. Independent determinants of operative mortality for patients with aortic dissections. Circulation 1984; 70:I153.
  25. Haverich A, Miller DC, Scott WC, et al. Acute and chronic aortic dissections–determinants of long-term outcome for operative survivors. Circulation 1985; 72:II22.
  26. Pansini S, Gagliardotto PV, Pompei E, et al. Early and late risk factors in surgical treatment of acute type A aortic dissection. Ann Thorac Surg 1998; 66:779.
  27. Sabik JF, Lytle BW, Blackstone EH, et al. Long-term effectiveness of operations for ascending aortic dissections. J Thorac Cardiovasc Surg 2000; 119:946.
  28. Kawahito K, Adachi H, Yamaguchi A, Ino T. Preoperative risk factors for hospital mortality in acute type A aortic dissection. Ann Thorac Surg 2001; 71:1239.
  29. Lai DT, Robbins RC, Mitchell RS, et al. Does profound hypothermic circulatory arrest improve survival in patients with acute type a aortic dissection? Circulation 2002; 106:I218.
  30. Moon MR, Sundt TM 3rd, Pasque MK, et al. Does the extent of proximal or distal resection influence outcome for type A dissections? Ann Thorac Surg 2001; 71:1244.
  31. Kazui T, Washiyama N, Muhammad BA, et al. Extended total arch replacement for acute type a aortic dissection: experience with seventy patients. J Thorac Cardiovasc Surg 2000; 119:558.
  32. Bossone E, Rampoldi V, Nienaber CA, et al. Usefulness of pulse deficit to predict in-hospital complications and mortality in patients with acute type A aortic dissection. Am J Cardiol 2002; 89:851.
  33. Penn MS, Smedira N, Lytle B, Brener SJ. Does coronary angiography before emergency aortic surgery affect in-hospital mortality? J Am Coll Cardiol 2000; 35:889.
  34. Ehrlich MP, Schillinger M, Grabenwöger M, et al. Predictors of adverse outcome and transient neurological dysfunction following surgical treatment of acute type A dissections. Circulation 2003; 108 Suppl 1:II318.
  35. Collins JS, Evangelista A, Nienaber CA, et al. Differences in clinical presentation, management, and outcomes of acute type a aortic dissection in patients with and without previous cardiac surgery. Circulation 2004; 110:II237.
  36. Movsowitz HD, Levine RA, Hilgenberg AD, Isselbacher EM. Transesophageal echocardiographic description of the mechanisms of aortic regurgitation in acute type A aortic dissection: implications for aortic valve repair. J Am Coll Cardiol 2000; 36:884.
  37. Tsai TT, Evangelista A, Nienaber CA, et al. Long-term survival in patients presenting with type A acute aortic dissection: insights from the International Registry of Acute Aortic Dissection (IRAD). Circulation 2006; 114:I350.
  38. Halstead JC, Meier M, Etz C, et al. The fate of the distal aorta after repair of acute type A aortic dissection. J Thorac Cardiovasc Surg 2007; 133:127.
  39. Nienaber CA, Fattori R, Lund G, et al. Nonsurgical reconstruction of thoracic aortic dissection by stent-graft placement. N Engl J Med 1999; 340:1539.
  40. Dake MD, Kato N, Mitchell RS, et al. Endovascular stent-graft placement for the treatment of acute aortic dissection. N Engl J Med 1999; 340:1546.
  41. Duebener LF, Lorenzen P, Richardt G, et al. Emergency endovascular stent-grafting for life-threatening acute type B aortic dissections. Ann Thorac Surg 2004; 78:1261.
  42. Eggebrecht H, Nienaber CA, Neuhäuser M, et al. Endovascular stent-graft placement in aortic dissection: a meta-analysis. Eur Heart J 2006; 27:489.
  43. Kusagawa H, Shimono T, Ishida M, et al. Changes in false lumen after transluminal stent-graft placement in aortic dissections: six years’ experience. Circulation 2005; 111:2951.
  44. Chen LW, Dai XF, Lu L, et al. Extensive primary repair of the thoracic aorta in acute type a aortic dissection by means of ascending aorta replacement combined with open placement of triple-branched stent graft: early results. Circulation 2010; 122:1373.
  45. Uchida N, Shibamura H, Katayama A, et al. Operative strategy for acute type a aortic dissection: ascending aortic or hemiarch versus total arch replacement with frozen elephant trunk. Ann Thorac Surg 2009; 87:773.
  46. Murzi M, Tiwari KK, Farneti PA, Glauber M. Might type A acute dissection repair with the addition of a frozen elephant trunk improve long-term survival compared to standard repair? Interact Cardiovasc Thorac Surg 2010; 11:98.
  47. Uchida N, Katayama A, Tamura K, et al. Long-term results of the frozen elephant trunk technique for extended aortic arch disease. Eur J Cardiothorac Surg 2010; 37:1338.
  48. Gorlitzer M, Weiss G, Meinhart J, et al. Fate of the false lumen after combined surgical and endovascular repair treating Stanford type A aortic dissections. Ann Thorac Surg 2010; 89:794.
  49. Pichlmaier MA, Teebken OE, Khaladj N, et al. Distal aortic surgery following arch replacement with a frozen elephant trunk. Eur J Cardiothorac Surg 2008; 34:600.
  50. Mestres CA, Fernández C, Josa M, Mulet J. Hybrid antegrade repair of the arch and descending thoracic aorta with a new integrated stent-Dacron graft in acute type A aortic dissection: a look into the future with new devices. Interact Cardiovasc Thorac Surg 2007; 6:257.
  51. Baraki H, Hagl C, Khaladj N, et al. The frozen elephant trunk technique for treatment of thoracic aortic aneurysms. Ann Thorac Surg 2007; 83:S819.
  52. Schoenhoff FS, Schmidli J, Eckstein FS, et al. The frozen elephant trunk: an interesting hybrid endovascular-surgical technique to treat complex pathologies of the thoracic aorta. J Vasc Surg 2007; 45:597.
  53. Karck M, Kamiya H. Progress of the treatment for extended aortic aneurysms; is the frozen elephant trunk technique the next standard in the treatment of complex aortic disease including the arch? Eur J Cardiothorac Surg 2008; 33:1007.
  54. Roselli EE, Soltesz EG, Mastracci T, et al. Antegrade delivery of stent grafts to treat complex thoracic aortic disease. Ann Thorac Surg 2010; 90:539.
  55. Baraki H, Al Ahmad A, Sarikouch S, et al. The first fifty consecutive Bentall operations with a prefabricated tissue-valved aortic conduit: a single-center experience. J Heart Valve Dis 2010; 19:286.
  56. Karck M, Chavan A, Khaladj N, et al. The frozen elephant trunk technique for the treatment of extensive thoracic aortic aneurysms: operative results and follow-up. Eur J Cardiothorac Surg 2005; 28:286.
  57. Karck M, Chavan A, Hagl C, et al. The frozen elephant trunk technique: a new treatment for thoracic aortic aneurysms. J Thorac Cardiovasc Surg 2003; 125:1550.
  58. Usui A, Fujimoto K, Ishiguchi T, et al. Cerebrospinal dysfunction after endovascular stent-grafting via a median sternotomy: the frozen elephant trunk procedure. Ann Thorac Surg 2002; 74:S1821.
  59. Slonim SM, Miller DC, Mitchell RS, et al. Percutaneous balloon fenestration and stenting for life-threatening ischemic complications in patients with acute aortic dissection. J Thorac Cardiovasc Surg 1999; 117:1118.
  60. Glower DD, Speier RH, White WD, et al. Management and long-term outcome of aortic dissection. Ann Surg 1991; 214:31.
  61. Isselbacher EM. Dissection of the descending thoracic aorta: looking into the future. J Am Coll Cardiol 2007; 50:805.
  62. Song JM, Kim SD, Kim JH, et al. Long-term predictors of descending aorta aneurysmal change in patients with aortic dissection. J Am Coll Cardiol 2007; 50:799.
  63. Fattori R, Bacchi-Reggiani L, Bertaccini P, et al. Evolution of aortic dissection after surgical repair. Am J Cardiol 2000; 86:868.
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