Aortic Diseases


20
Aortic Diseases


I. Aortic dissection


A. Two types of aortic dissection



  • Type A dissection involves the ascending aorta, with or without any other part of the aorta. Type A dissection is the most common type of aortic dissection (>65% of aortic dissections), and generally requires emergent surgical correction.
  • Type B dissection involves the descending aorta and/or the aortic arch, without extension to the ascending aorta. Involvement of the aortic arch without the ascending aorta is labeled as type B dissection (ACC guidelines). Non-surgical treatment is generally recommended, with surgery reserved for vital branch compromise.

Aortic dissection, whether type A or B, can be acute (onset within the last 2 weeks) or chronic.


B. Causes


The media of the ascending aorta is rich in elastic fibers. Medial degeneration consists of a loss of elastic fibers and predisposes to ascending aortic aneurysm and dissection. Medial degeneration may be seen with repetitive injury (HTN) and aging; in fact, the combination of age and HTN is responsible for aortic dissection in most patients.


More severe medial degeneration, called cystic medial necrosis, may occur in the contexts of bicuspid aortic valve, Marfan syndrome, or coarctation of the aorta.


The aortic wall stress drastically increases with aortic size. Thus, the risk of aortic dissection and progressive aortic dilatation is drastically increased in patients whose aorta is already dilated. The yearly risk of aortic dissection or rupture is 2% if the aortic diameter is 4–5 cm, and ≥7% if the aortic diameter is >5.5–6 cm. However, since a normal-size aorta is much more common than a dilated aorta, only 40% of aortic dissections occur in patients with an aortic diameter of 5.5 cm or more, while 10–20% occur in patients with an aortic diameter of 4 cm or less.1


C. Mechanisms of acute and chronic aortic dissection


The typical aortic dissection consists of an intimal tear that allows blood to penetrate a diseased medial layer and cleave this media longitudinally. The blood-filled space within the media is the false lumen. Distention of the false lumen with blood may cause the intimal flap to bow into the true lumen and obstruct the lumen or the branches causing ischemia (e.g., carotid, mesenteric, or renal artery). The false lumen may also extend into the branches and cause ischemia. Most intimal tears occur in the ascending aorta, within a few centimeters of the aortic valve, or in the descending aorta just distal to the left subclavian artery.


In chronic aortic dissection, one or more spontaneous fenestrations occur in the intimal flap, which allows the false lumen to decompress and allows blood to flow through it. The false lumen becomes a functional lumen. Flow to vital branches supplied by the false lumen is improved, and organ ischemia improves (Figure 20.1). In fact, one of the endovascular therapies of aortic dissection consists of creating fenestrations in the intimal layer.


D. Other acute aortic syndromes: intramural hematoma and penetrating atherosclerotic ulcer


Intramural hematoma is characterized by bleeding within the media from rupture of vasa vasorum vessels without any obvious intimal tear, and thus without communication with the true lumen. This can usually be distinguished by CT: the intramural hematoma does not enhance with contrast. Invasive angiography misses intramural hematoma, owing to the lack of communication between the true and false lumens. However, the management is identical to the classical type A or B aortic dissection (intramural hematoma is more often distal, i.e., type B, than A). The prognosis and complications are similar to aortic dissection, and intramural hematoma often progresses to dissection, aneurysm, or rupture.2,3


Penetrating atherosclerotic ulcer is an ulceration of an atherosclerotic lesion of the aorta, usually the descending aorta, that penetrates into the media and results in a localized hematoma. There is a focal aortic outpouching rather than a false lumen. However, this ulcer may progress to a typical aortic dissection or aortic perforation, and, over time, it often leads to the late formation of aortic aneurysm or contained aortic perforation, i.e., pseudoaneurysm. Atherosclerotic ulcer is often seen in elderly patients with a heavily atherosclerotic and ulcerated descending aorta, many of whom already have a descending or abdominal aortic aneurysm. CT can distinguish it from a typical dissection. A penetrating ulcer is generally treated conservatively with surveillance. The treatment is surgical in case of transmural extension with pseudoaneurysm, or progressive aneurysmal dilatation.

Schematic illustration of acute aortic dissection, the false lumen (F) is tense with sluggish flow and becomes larger than the true lumen (dashed arrow).

Figure 20.1 In acute aortic dissection, the false lumen (F) is tense with sluggish flow and becomes larger than the true lumen (dashed arrow). In chronic dissection, multiple tears occur in the intimal flap and allow the false lumen to decompress and blood to flow through it (arrows).


In this illustration, the dissection extends into the left renal artery rather than around it. Thus, the left renal artery is now practically supplied by the false lumen. There is no flow through the renal artery acutely, but once the false lumen decompresses, some flow is re-established through the false lumen of the renal artery, which becomes a functional lumen.


E. Clinical suspicion


Three clinical features suggest the possibility of aortic dissection:4



  • Predisposing condition (aortic valve disease, known aortic aneurysm, Marfan, or family history of dissection).
  • Suggestive symptoms: chest, back, or abdominal pain that is very abrupt (within seconds), severe, or tearing. Contrary to common belief, the pain of aortic dissection is commonly sharp rather than tearing.
  • Suggestive exam findings: AI murmur (in 25–45%), pulse deficit or blood pressure differential between both arms (~20%), neurologic deficit concomitant to chest pain (5%).

The presence of two or three features makes aortic dissection highly probable. In the presence of one feature, the probability is intermediate and aortic imaging is warranted if the patient’s symptoms are not clearly explained on chest X-ray or ECG. Up to 5% of aortic dissections have none of these features, but may be suspected by a widened mediastinum on chest X-ray.4


F. Diagnosis


Chest X-ray shows widening of the aorta and mediastinal silhouette and widening of the aortic knob in 80–90% of patients (Figures 20.2, 20.3). The “calcium sign” may be seen (outer displacement of the aortic knob calcium by more than 1 cm).


Perform any of the following three gold-standard studies to establish the diagnosis and define the type of dissection:



  • CT angiogram.
  • MR angiogram.
  • TEE. This has the additional potential of assessing acute AI and the coronary ostia. It is also advantageous if the patient is unstable, because TEE can be performed at the bedside.
  • Invasive aortography used to be the gold standard. It is still useful if the ECG shows acute STEMI but the clinical picture suggests aortic dissection. In the latter case, aortography may be performed, followed by coronary angiography once dissection is ruled out.

Typically, the false lumen is larger than the true lumen because of its slower emptying (or lack of emptying). On a TEE short-axis cut: (i) the true lumen is compressed and crescentic, while the false lumen is oval; (ii) the false lumen has “smoke” and no flow, or less flow, on Doppler imaging (Figure 20.4).

Schematic illustration of chest X-ray in aortic dissection or dilatation.

Figure 20.2 Chest X-ray in aortic dissection or dilatation.

Image described by caption.

Figure 20.3 (a) Widening of aortic knob (arrow) indicative of descending aortic dissection or aneurysm. (b) Widening of the ascending aortic shadow (right arrow) and the descending aortic knob (left arrow). This patient has ascending and descending aortic dilatation and dissection.

Schematic illustration of axial cut across aortic dissection.

Figure 20.4 Axial cut across aortic dissection. True lumen (T) and false lumen (F) are shown.

Schematic illustration of mechanisms of aortic insufficiency (AI) with aortic dissection.

Figure 20.5 Mechanisms of aortic insufficiency (AI) with aortic dissection: (i) dissection dilates the sinotubular junction, preventing leaflet coaptation; (ii) dissection extends into the sinotubular junction, where the sinuses of Valsalva insert, resulting in leaflet prolapse and eccentric AI; (iii) dissection flap prolapses through the aortic orifice and prevents leaflet coaptation. AI may also be pre-existent, secondary to a bicuspid aortic valve. Note that the valvular leaflets (cusps) are attached to the sinuses of Valsalva.


G. Complications



  • Aortic regurgitation (Figure 20.5).
  • Aortic rupture into the pericardium, leading to tamponade.
  • Stroke is seen in 6% of type A aortic dissections. It is due to carotid obstruction by an aortic flap or extension of the dissection into a carotid artery.
  • STEMI is seen in 4% of type A aortic dissections. It is easier for the dissection to extend on the outer curve of the aorta into the RCA, explaining why two-thirds of MIs are inferior MIs (IRAD registry).2 MI may be due to the false lumen compressing the coronary ostium or extending into it. In addition, ST depression or T inversion occurs in up to 50% of patients with type A aortic dissection, as a result of demand/supply mismatch or catecholamine-induced ST–T abnormalities.5 Those ST–T abnormalities may mimic ACS and delay the diagnosis of aortic dissection.
  • Hemorrhagic, large pleural effusion may be seen with descending aortic dissection. It results from aortic leakage into the mediastinal pleural space.
  • Peripheral and mesenteric ischemia.

H. Treatment


1. Administer IV β -blockers to decrease the aortic wall stress dP/dt


  • Aggressively control blood pressure with β-blockers ± vasodilators. IV labetalol or the combination of IV esmolol + IV nitroprusside may be used. β-Blockers reduce the stroke volume and thus reduce the pulse pressure (dP), the slope of aortic pressure rise in systole (dP/dt), and the frequency of aortic exposure to the pulse pressure. The aortic pressure rises gradually rather than sharply (↓ dP/dt). Diltiazem IV may be used if β-blockers are contraindicated. Morphine may be used for pain control.
  • Goal: Mean BP 60–70 mm Hg, SBP <120 mm Hg, heart rate <60 bpm.6

2. Type A aortic dissection

Emergent surgery should be performed and consists of excising the dissected segment of the aorta and interposing a prosthetic graft. If the sinuses of Valsalva are dilated, the graft needs to extend to the aortic valve. If moderate or severe AI is present, the aortic valve is repaired (resuspend the leaflets); it may need to be replaced if severe intrinsic valvular disease is present. A composite graft consisting of an aortic graft and valvular prosthesis is used whenever the aortic valve needs replacement.


3. Type B aortic dissection

Aggressive blood pressure control is the initial therapy. Surgery is indicated for: (i) impending aortic rupture, such as aneurysmal dilatation of the false lumen; or (ii) peripheral ischemia, such as carotid, mesenteric, renal (renovascular HTN), spinal cord, or lower extremity ischemia.


Surgery may simply involve revascularization of the ischemic territories rather than extensive, laborious aortic repair.


Surgery is not typically indicated solely for persistent pain (pain being secondary to a distended false lumen).Data from IRAD registry suggests that extension to the aortic arch does not change the prognosis of type B dissection.


4. If surgery is not performed , the mortality risk with type A dissection is 1% per hour for the first 48 hours (~50% at 48 hours) and 85% at 2 weeks.


5. In survivors, there is a long-term risk of AI, recurrence of dissection, and secondary aneurysm formation, especially during the first 2 years. This mandates frequent CT/MRI monitoring every 3–6 months for the first 2 years then every 6–12 months afterward.


6. Chronic dissection (= dissection that occurred >2 weeks prior)

Whether it is type A or B, chronic medical therapy without surgical intervention is the initial treatment of choice at this point. Medical therapy consists of aggressive BP control (SBP <130 mmHg) with regular monitoring for aneurysm formation and size, extension of the dissection, and development of severe AI. Aneurysmal dilatation of the aorta, particularly the false lumen, occurs frequently and dictates surgery.


I. Notes on surgical techniques


1. Ascending aortic dissection

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Related posts:

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  2. Atrial Flutter and Atrial Tachycardia
  3. Congenital Heart Disease
  4. Valvular Disorders

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Nov 27, 2022 | Posted by in CARDIOLOGY | Comments Off on Aortic Diseases

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