Aortic dissection

Aortic dissection - the penetration of blood through cracks in the inner shell of the aorta with the separation of the inner, middle shells and the creation of a false lumen.

Cracks in the intima may be primary or secondary - occurring as a result of hemorrhage within the middle shell. Stratification can occur anywhere in the aorta and spread proximally and distally to other arteries. Arterial hypertension is an important etiologic factor. Symptoms of aortic dissection include sudden sudden pain in the chest or lower back. Stratification can lead to aortic regurgitation and impaired circulation in the branches of the artery. The diagnosis of aortic dissection is established using visualization studies (eg, transesophageal echocardiography, computed tomography with angiography, MRI, contrast aortography). Treatment of aortic dissection always involves strict control of blood pressure and periodic research to monitor the dynamics of separation. Surgical treatment of aortic aneurysm and prosthetics with the use of a synthetic implant is necessary for the dissection of the ascending aorta and certain delaminations of the descending section. A fifth of patients die before admission to the hospital, and about a third - from operational and perioperative complications.

Signs of stratification are found in approximately 1-3% of all autopsies. Representatives of the Negroid race, men, the elderly and people with hypertension are in the category of special risk. The peak incidence is 50-65 years, and in patients with congenital anomalies of connective tissue (for example, Marfan's syndrome) - for 20-40 years.

The aortic dissection is classified anatomically. The Debakey classification system, which is most widely used, distinguishes the following types:

• the bundles beginning in the ascending part of the aorta and extending at least to the arch of the aorta are sometimes lower (type I, 50%);
• bundles that begin and are limited to the ascending aorta (type II, 35%);
• bundles that begin in the descending section of the thoracic aorta below the left subclavian artery and extend distally or (more rarely) proximally (type III, 15%).

In the simpler Stanford classification, the ascending aortic dissection (type A) is distinguished from the stratification of the descending part of the aorta (type B).

Although a stratification can occur anywhere in the aorta, it often occurs in the distal part of the ascending aorta (within 5 cm from the aortic valve) or the descending thoracic aorta (immediately after the left subclavian artery). Sometimes the bundle is limited to specific single arteries (for example, coronary or carotid), usually this happens in pregnant women or after childbirth.

[1], [2], [3], [4], [5], [6], [7]

What causes aortic dissection?

Aortic dissection always occurs against the background of pre-existing degeneration of the middle aortic membrane. The causes include connective tissue diseases and injuries. Atherosclerotic risk factors, especially arterial hypertension, contribute more than two-thirds of patients. After the rupture of the inner membrane, which becomes the primary event in some patients and secondary to hemorrhage in the middle shell in others, the blood penetrates into the middle layer, creating a false channel that widens the distal or (more rarely) proximal portion of the artery.

The bundles can once again communicate with the lumen of the vessel through the disruption of the intima at a remote site from the center, supporting the systemic blood flow. However, in such cases, severe consequences usually develop: violation of the blood supply of the dependent arteries (including coronary arteries), dilatation of the aortic valve and regurgitation, cardiac failure and fatal aortic rupture through the adventitial membrane into the pericardium or the left pleural cavity. Acute stratification and bundles with a prescription of less than 2 weeks are most likely to cause these complications; the risk decreases after 2 weeks or more if there is convincing evidence in favor of thrombosis of false lumen and loss of communication between the true and false vessels.

Variants of aortic dissection include the separation of the inner and middle membranes by an internal hematoma without an obvious intimal tear, an internal lining and swelling without a hematoma or false lumen, delaminations or bruises caused by ulceration of the atherosclerotic plaque. It is believed that these variants are the precursors of classical aortic dissection.

Symptoms of aortic dissection

As a rule, suddenly there is painful pain in the precordial or interscapular area, often described as "tearing" or "tearing." Pain often migrates from the initial location, as the bundle spreads over the aorta. Up to 20% of patients faint due to intense pain, irritation of the aortic baroreceptors, extracranial obstruction of the cerebral artery or cardiac tamponade.

Sometimes patients develop signs of stroke, myocardial infarction, intestinal infarction, paraparesis, or paraplegia due to impaired blood flow to the spinal cord, as well as limb ischemia due to acute distal arterial occlusion.

Approximately 20% of patients have a partial or complete deficiency of the central arterial pulse, which can weaken and decrease. BP on the limbs may differ, sometimes more than 30 mm Hg. Which reflects a poor prognosis. Noise of aortic regurgitation is heard in approximately 50% of patients with proximal stratification. There may be peripheral signs of aortic regurgitation. Sometimes, due to severe aortic regurgitation, heart failure develops. Penetration of blood or inflammatory serous fluid into the left pleural cavity can lead to symptoms of pleural effusion. Occlusion of the artery of the limb can cause signs of peripheral ischemia or neuropathy. Occlusion of the renal artery can cause oliguria or anuria. With cardiac tamponade pulsus paradoxus and tension of the jugular veins are possible .

Diagnosis of aortic dissection

Aortic dissection should be suspected in any patient with pain, chest pain, chest pain, inexplicable fainting ), syncope or abdominal pain, stroke or acute heart failure, especially when the pulse or BP on the limbs differ . Such patients need chest radiograph : 60-90% expanded mediastinum shadow is usually limited convexity showing a portion of the aneurysm. Often find a left-sided pleural effusion.

If the roentgenogram of the chest causes suspicion of stratification, immediately after stabilization of the patient's condition, transesophageal echocardiography (CTE), CT angiography (CTA) or magnetic resonance angiography (MRA) are performed. The data obtained on the tearing of the inner shell and double lumen confirm the stratification.

Volumetric polyposition TSE has 97-99% sensitivity and together with M-mode echocardiography becomes almost 100% diagnostic. The study can be performed at the patient's bed in less than 20 minutes, and there is no need to use contrast. If TSE is not available, the CTA is recommended; its diagnostic value is 100% for a positive result and 86% for a negative result.

MRA has almost 100% sensitivity and specificity for aortic dissection, however it is time consuming and not suitable for critical conditions. Probably, this study is better used in stable patients with subacute or chronic chest pain with suspicion of stratification.

Contrast angiography is the method of choice in preparation for surgical treatment. In addition to detecting the presence and extent of stratification, the severity of aortic regurgitation and the degree of involvement of the major branches of the aorta are assessed. Aortography helps determine if simultaneous aortocoronary bypass surgery is necessary. Echocardiography is also necessary to detect aortic regurgitation and determine the need for simultaneous plasty or replacement of the aortic valve.

ECG appoint almost always. However, the range of data obtained varies from the norm to marked pathological changes (with acute occlusion of the coronary artery or aortic regurgitation), so the study has no diagnostic significance. The study of the content of soluble fragments of elastin and heavy chains of myosin smooth muscle cells is at the stage of study; it looks promising, but usually unavailable. CFC-MB serum and troponin can help distinguish aortic dissection from myocardial infarction, except when the bundle causes myocardial infarction.

In routine laboratory tests, a small leukocytosis and anemia can be detected if blood seeps out of the aorta. Increased LDH activity may be a nonspecific sign of involvement of the mesenteric or iliac artery.

At the stage of early diagnostic search, a cardiothoracic surgeon is needed.

[8], [9], [10]

Treatment of aortic dissection

If the patient does not die immediately after the dissection of the aorta, it must be hospitalized in the ICU with monitoring of intra-arterial pressure. To monitor the amount of urine released, use a permanent urinary catheter. It is necessary to determine the blood group: during the surgical intervention, probably from 4 to 6 packets of erythrocyte mass. Hemodynamically unstable patients must be intubated.

Immediately begin the introduction of drugs to reduce blood pressure, arterial wall tension, ventricular contractility and pain. It is necessary to maintain systolic blood pressure <110 mm Hg. Art. Or at a lower level, capable of supporting the necessary cerebral, coronary and renal blood flow. First, a b-blocker is usually used. Propranolol 0.5 mg is administered intravenously 1-2 mg 3-5 minutes before the decrease in heart rate to 60-70 per minute or to reach the total dose of 0.15 mg / kg, while the administration time should be more than 30-60 minutes. This drug in such doses reduces ventricular contractility and resists the reflex chronotropic effects of sodium nitroprusside. The introduction of propranolol in this mode can be repeated every 2-4 hours to support the blockade. Patients with COPD or asthma can be assigned more cardioselective b-adrenoblockers. As another option, metoprolol can be administered 5 mg intravenously up to 4 doses with the administration after 15 minutes or esmolol at 50-200 μg / kg per minute by a continuous intravenous infusion, or labetalol (a- and b-adrenoblocker) 1-2 mg / min continuous intravenous infusion or 5-20 mg intravenously first bolus with the addition of 20-40 mg every 10-20 minutes until the control of blood pressure or a total dose of 300 mg, then it is prescribed in a dose of 20-40 mg every 4-8 hours for days. An alternative to non-blockers includes calcium channel blockers [eg, verapamil at 0.05-0.1 mg / kg intravenously bolus or diltiazem 0.25 mg / kg (up to 25 mg) intravenously bolus or 5-10 mg / hour continuous maintenance].

If the systolic blood pressure remains> 1 10 mm Hg. Despite the use of b-adrenoblockers, it is possible to use sodium nitroprusside with a continuous intravenous injection at an initial dose of 0.2-0.3 μg / kg per minute with an increase (often up to 200-300 μg / min), as necessary up to control of blood pressure. Sodium nitroprusside can not be administered without b-blockers or calcium channel blockers, because reflex parallel sympathetic activation in response to vasodilation can increase the ventricular inotropic effect and, accordingly, the arterial wall tension exacerbating the stratification.

Use only drug therapy can be tried only with uncomplicated stable stratification limited to the descending part of the aorta (type B), and with a stable isolated stratification of the aortic arch. Surgical treatment is practically always shown if the bundle involves the proximal part of the aorta. Theoretically, it is necessary to use surgical intervention in ischemia of organs or limbs, uncontrolled hypertension, prolonged aortic dilatation, increase of stratification and signs of aortic rupture irrespective of the type of stratification. Surgery may also be the best method of treatment for patients with distal division in Marfan syndrome.

The purpose of the operation is to eliminate the entrance to the false canal and prosthetics of the aorta with a synthetic prosthesis. If severe aortic regurgitation is found, plasty or aortic valve replacement should be performed. Surgical results are best with early active intervention; mortality is 7-36%. Predictors of an unfavorable outcome include arterial hypotension, renal failure, age over 70 years, a sharp debut with chest pain, a pulse deficit and a ST segment rise on an electrocardiogram.

Stenting with the stent that closes the entrance to the false lumen and improves the uniformity and integrity of the flow in the main vessel, balloon plastic (in which the balloon is inflated at the entrance of the false canal, pressing the resulting valve and dividing the true and false lumen), or both methods can be non-invasive an alternative for patients with type A separation and continuing permanent postoperative ischemia of peripheral organs for patients with type B stratification.

All patients, including those who have been treated surgically, receive long-term antihypertensive therapy with drugs. Usually ß-adrenoblockers , calcium channel blockers and inhibitors ACE inhibitors are usually used. Almost any combination of antihypertensive agents is acceptable. The only exception is preparations with a predominantly vasodilating effect (eg, hydralazine, minoxidil) and ß-adrenoblockers with intrinsic sympathomimetic activity (eg, acebutolol, pindolol). It is usually recommended to avoid excessive physical activity. MRI is performed before discharge from the hospital and again at 6 months, 1 year, then every 1-2 years.

The most important late complications include re-stratification, the formation of limited aneurysms in the weakened aorta, and the progression of aortic regurgitation. These complications can become an indication for surgical treatment.

Prognosis of aortic dissection

Approximately 20% of patients with aortic dissection die before coming to the hospital. Without treatment, the mortality rate is 1 -3% per hour for the first 24 hours, 30% for 1 week, 80% for 2 weeks, and 90% for 1 year.

Hospital mortality in the background of treatment is approximately 30% for proximal dissection and 10% for distal. For the treated patients who survived the acute episode, the survival rate is approximately 60% for 5 years and 40% for 10 years. About a third of late deaths are due to complications of stratification, others - for other reasons.