Aortic dissection

Aortic dissection is the penetration of blood through cracks in the inner lining of the aorta with dissection of the inner and middle linings and the creation of a false lumen.

Intimal tears may be primary or secondary, resulting from hemorrhage within the media. Dissection may occur anywhere in the aorta and extend proximally and distally to other arteries. Hypertension is an important etiologic factor. Symptoms of aortic dissection include severe, sudden chest or back pain. Dissection may lead to aortic regurgitation and vascular compromise in the arterial branches. Diagnosis of aortic dissection is made with imaging studies (eg, transesophageal echocardiography, computed tomography with angiography, magnetic resonance imaging, contrast aortography). Treatment of aortic dissection always involves strict blood pressure control and periodic studies to monitor the dynamics of dissection. Surgical treatment of aortic aneurysm and replacement with a synthetic graft is necessary for ascending aortic dissection and certain descending aortic dissections. One fifth of patients die before reaching the hospital, and about a third die from surgical and perioperative complications.

Signs of dissection are found in approximately 1-3% of all autopsies. Representatives of the Negroid race, men, the elderly, and people with hypertension are at particular risk. The peak incidence is at 50-65 years of age, and in patients with congenital anomalies of connective tissue (e.g., Marfan syndrome) - at 20-40 years.

Aortic dissection is classified anatomically. The most widely used classification system, DeBakey, distinguishes the following types:

• dissections beginning in the ascending aorta and extending at least to the aortic arch, sometimes below (type I, 50%);
• dissections beginning and limited to the ascending aorta (type II, 35%);
• dissections beginning in the descending thoracic aorta below the origin of the left subclavian artery and extending distally or (less commonly) proximally (type III, 15%).

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

Although dissection can occur anywhere in the aorta, it most commonly occurs in the distal ascending aorta (within 5 cm of the aortic valve) or descending thoracic aorta (just beyond the origin of the left subclavian artery). Occasionally, dissection is limited to specific single arteries (eg, coronary or carotid), usually occurring in pregnant or postpartum women.

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What causes aortic dissection?

Aortic dissection always occurs in the setting of preexisting degeneration of the aortic media. Causes include connective tissue diseases and injury. Atherosclerotic risk factors, especially hypertension, contribute in more than two-thirds of patients. Following rupture of the intima, which is the primary event in some patients and secondary to hemorrhage into the media in others, blood leaks into the media, creating a false channel that dilates the distal or (less commonly) proximal portion of the artery.

Dissections may re-communicate with the lumen through a distal intimal rupture, maintaining systemic blood flow. However, severe sequelae usually occur in such cases: disruption of the blood supply to dependent arteries (including the coronary arteries), aortic valve dilation and regurgitation, heart failure, and fatal rupture of the aorta through the adventitia into the pericardium or left pleural cavity. Acute dissections and those less than 2 weeks old are most likely to cause these complications; the risk decreases after 2 weeks or more if there is compelling evidence of thrombosis of the false lumen and loss of communication between the true and false vessels.

Variants of aortic dissection include separation of the intima and media by an internal hematoma without obvious intimal tear, tear of the intima and bulging without hematoma or false lumen, and dissection or hematoma caused by ulceration of an atherosclerotic plaque. These variants are thought to be precursors to classic aortic dissection.

Symptoms of aortic dissection

Typically, there is sudden, excruciating pain in the precordial or interscapular region, often described as "tearing" or "rending." The pain often migrates from the initial location as the dissection spreads through the aorta. Up to 20% of patients faint due to intense pain, aortic baroreceptor irritation, extracranial cerebral artery obstruction, or cardiac tamponade.

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

Approximately 20% of patients have a partial or complete deficit of the central arterial pulse, which may wax and wane. Blood pressure in the extremities may vary, sometimes by more than 30 mm Hg, reflecting a poor prognosis. A murmur of aortic regurgitation is heard in approximately 50% of patients with proximal dissection. Peripheral signs of aortic regurgitation may be present. Heart failure occasionally develops as a result of severe aortic regurgitation. Penetration of blood or inflammatory serous fluid into the left pleural space may cause symptoms of pleural effusion. Occlusion of an artery in a limb may cause signs of peripheral ischemia or neuropathy. Occlusion of a renal artery may cause oliguria or anuria. Pulsus paradoxus and jugular venous tension may occur with cardiac tamponade.

Diagnosis of aortic dissection

Aortic dissection should be suspected in any patient with chest pain, pain radiating across the posterior chest, unexplained syncope or abdominal pain, stroke, or acute heart failure, especially when pulses or blood pressures are different in the extremities. Such patients require chest radiography: in 60-90%, the mediastinal shadow is widened, usually with a circumscribed convexity showing the site of the aneurysm. Left-sided pleural effusion is often found.

If the chest radiograph is suspicious for dissection, transesophageal echocardiography (TEE), computed tomography angiography (CTA), or magnetic resonance angiography (MRA) is performed immediately after the patient has stabilized. The findings of a ruptured intima and double lumen confirm dissection.

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

MRA has almost 100% sensitivity and specificity for aortic dissection, but it is time-consuming and not suitable for critical care. It is probably best used in stable patients with subacute or chronic chest pain when dissection is suspected.

Contrast angiography is the method of choice in preparation for surgical treatment. In addition to identifying the presence and extent of dissection, the severity of aortic regurgitation and the extent of involvement of the main branches of the aorta are assessed. Aortography helps determine whether simultaneous coronary artery bypass grafting is necessary. Echocardiography is also necessary to identify aortic regurgitation and determine the need for simultaneous aortic valve repair or replacement.

An ECG is almost always ordered. However, the range of data obtained varies from normal to markedly abnormal (in acute coronary artery occlusion or aortic regurgitation), so the study has no diagnostic value. The study of soluble elastin fragments and myosin heavy chains of smooth muscle cells is under study; it looks promising, but is not usually available. Serum CPK-MB and troponin can help distinguish aortic dissection from myocardial infarction, except in cases where dissection causes myocardial infarction.

Routine laboratory studies may reveal mild leukocytosis and anemia if blood is leaking from the aorta. Increased LDH activity may be a nonspecific sign of mesenteric or iliac artery involvement.

At the stage of early diagnostic search, consultation with a cardiothoracic surgeon is necessary.

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Treatment of aortic dissection

If the patient does not die immediately after aortic dissection, he or she should be hospitalized in the intensive care unit with intra-arterial pressure monitoring. A permanent urinary catheter is used to monitor the amount of urine excreted. Blood typing is necessary: 4 to 6 packs of packed red blood cells are likely to be required during surgery. Hemodynamically unstable patients should be intubated.

Administration of drugs to reduce blood pressure, arterial wall tension, ventricular contractility, and pain is started immediately. Systolic blood pressure should be maintained at <110 mm Hg or at a lower level capable of maintaining the required cerebral, coronary, and renal blood flow. A beta-blocker is usually used initially. Propranolol 0.5 mg is administered intravenously at 1-2 mg every 3-5 minutes until the heart rate decreases to 60-70 beats per minute or the full dose of 0.15 mg/kg is reached, while the administration time should be more than 30-60 minutes. This drug in such doses reduces ventricular contractility and counteracts the reflex chronotropic effects of sodium nitroprusside. Administration of propranolol in this regimen can be repeated every 2-4 hours to maintain the blockade. Patients with COPD or asthma can be prescribed more cardioselective beta-blockers. Another option is to administer metoprolol 5 mg intravenously up to 4 doses given every 15 minutes, or esmolol 50-200 mcg/kg per minute by continuous intravenous infusion, or labetalol (an alpha- and beta-blocker) 1-2 mg/min by continuous intravenous infusion or 5-20 mg intravenously initially as a bolus with the addition of 20-40 mg every 10-20 minutes until blood pressure is controlled or a total dose of 300 mg is administered, then it is administered at a dose of 20-40 mg every 4-8 hours during the day. Alternatives to no-blockers include calcium channel blockers [eg, verapamil 0.05-0.1 mg/kg IV bolus or diltiazem 0.25 mg/kg (up to 25 mg) IV bolus or 5-10 mg/h continuously].

If systolic BP remains > 1 10 mm Hg despite the use of beta-blockers, sodium nitroprusside may be given by continuous intravenous infusion at an initial dose of 0.2-0.3 mcg/kg per minute and titrated up (often to 200-300 mcg/min) as needed until BP is controlled. Sodium nitroprusside should not be given without beta-blockers or calcium channel blockers because reflex parallel sympathetic activation in response to vasodilation may increase the ventricular inotropic effect and, accordingly, arterial wall tension, worsening dissection.

Medical therapy alone should be tried only in uncomplicated stable dissections limited to the descending aorta (type B) and in stable isolated aortic arch dissections. Surgery is virtually always indicated if the dissection involves the proximal aorta. Theoretically, surgery should be used for organ or limb ischemia, uncontrolled hypertension, prolonged aortic dilation, enlarging dissection, and signs of aortic rupture regardless of the type of dissection. Surgery may also be the best treatment for patients with distal dissection in Marfan syndrome.

The goal of the operation is to eliminate the entrance to the false canal and replace the aorta with a synthetic prosthesis. If significant aortic regurgitation is detected, aortic valve repair or replacement should be performed. Surgical results are best with early active intervention; mortality is 7-36%. Predictors of poor outcome include arterial hypotension, renal failure, age over 70 years, abrupt onset with chest pain, pulse deficit, and ST-segment elevation on the electrocardiogram.

Stenting with placement of a stent to close the entrance to the false lumen and improve the uniformity and integrity of flow in the parent vessel, balloon angioplasty (in which a balloon is inflated at the entrance to the false lumen, compressing the resulting valve and separating the true and false lumens), or both may serve as a noninvasive alternative for patients with type A dissection and ongoing persistent postoperative peripheral organ ischemia for patients with type B dissection.

All patients, including those treated surgically, receive long-term antihypertensive drug therapy. Beta-blockers, calcium channel blockers, and ACE inhibitors are commonly used. Almost any combination of antihypertensive agents is acceptable. Exceptions include drugs with predominantly vasodilatory action (eg, hydralazine, minoxidil) and beta-blockers with intrinsic sympathomimetic activity (eg, acebutolol, pindolol). Avoidance of excessive physical activity is usually recommended. MRI is performed before discharge from the hospital and again after 6 months, 1 year, and then every 1-2 years.

The most important late complications include re-dissection, formation of localized aneurysms in the weakened aorta, and progression of aortic regurgitation. These complications may be indications for surgical treatment.

Prognosis of aortic dissection

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

In-hospital mortality with treatment is approximately 30% for proximal dissection and 10% for distal dissection. For treated patients who survive the acute episode, the survival rate is approximately 60% at 5 years and 40% at 10 years. About one-third of late deaths are due to complications of dissection, the remainder to other causes.