A dissection of the vessel wall is defined as dissection or aortic dissection,
which originates from a laceration of the intima and propagates distally and
proximally. The blood penetrates into the myintimal flap and forms a hematoma
that propagates in the muscular tunic both distal and proximal.
The dissection may stop near a large collateral, but may also continue within or
beyond it. Or the hematoma may re-enter through a distal myocardial breach, thus
creating a double lumen of sliding a true and a false. By convention,
dissections are defined as "acute" when observed within the first 14 days and "chronic"
after this period. The real incidence is not known, because many dissections
lead to sudden death and are interpreted as cardiac infarcts. However, it is
estimated that in the Western world there are about 10 cases per year per
100,000 inhabitants, with a ratio between men and women 3: 1 and an average age
of around 60.
Aortic dissections can be classified in relation to the site of the laceration and the extension of the dissecting process. In most cases it begins in the vicinity of the aortic valve or in the ascending aorta and in less than a third of cases in the descending aortic arch, typically shortly after the origin of the left subclavian. They then propagate with variable extension along the average aorta tapestry, occupying about half the circumference and assuming a thick spiral course.
This author first distinguished 3 types, regardless of the entrance door:
- type I, affects the ascending aorta and extends in various degrees to the arch,
to the descending aorta and possibly also to the abdominal area;
- type II, is limited to the ascending aorta and stops at the first supraortic
trunk, the anonymous;
- type III, affects only the descending aorta (a) and possibly also the
abdominal (b).
Taking into account that the most at-risk segment of acute complications with an
ominous outcome is the ascending aorta.
Stanford classification
The first two types were later combined more simply into one type A, while type
B includes all the dissections that save the ascending aorta.
Two factors predominate in the pathogenesis of aortic dissections: parietal degeneration and arterial hypertension. Some pathological conditions are so frequently associated with aortic dissections to be considered causal or strongly predisposing. Especially in type A congenital connective diseases are often present, often in hereditary components (there are also cases in pediatric age) such as Marfan syndrome, Turner of Ehler-Danlos. Giant cell alterations, systemic lupus erythematosus, recurrent polychondritis, cystinuria, polycystic kidney, Cushing are also found, which are likely to act through arterial hypertension. A third trimester pregnancy is present in at least half of aortic dissections in women under the age of 40. Sometimes the dissection results from recent interventions on the aorta for clamping trauma or aisutura. In type B dissections patients are generally older, often severe atherosclerotic and chronic bronchitic. In many cases the aortic wall is not different from that of the subjects of the same age, in others predominate degenerative aspects specific to connective diseases, in others still frankly atherosclerotic aspects. In the medium tunic are in fact found, in extremely variable proportions, degenerative phenomena with reduction of elastic fibers, muscle necrosis with loss of myocellulas, atherosclerosis, inflammatory infiltrates.
In type A dissections degenerative and necrotic lesions prevail, which can take on the appearance of true cystic shortcomings (cystic medionecrosis), classically in Marfan's and Ehler-Danlos's syndrome. Both hypertension and cystic medionecrosis were observed during pregnancy, probably in relation to hormonal changes. Above all Type B dissections are atherosclerotic phenomena and only in a minority of cases abnormal degenerative aspects, in the form of mucoid and mixoid gaps. Globally, from two thirds to three quarters of patients are hypertensive. It is not clear whether hypertension causes an intimal tear by pure mechanical effect or induces a qualitative degeneration of the wall. The intimal tear occurs where there is a mechanical constraint of pericardium reflection, isthmus, origin of large collateral) or where the wall tension is maximum in relation to diameter (bulb and ascend) or the diameter changes as slightly above the aortic bulb. A particular mechanical constraint is also represented by atherosclerotic and calcific plaques, which have been found sometimes involved in the intimal laceration of the descending aorta.
The modalities of presentation of the resections vary considerably, above all in
relation to type A or B and to the rapidity of the evolution. In principle, type
A dissections present with hypotensive status until shock due to hypovolaemia
due to rupture in the pleural cavity or to heart failure due to tamponade,
infarction or valvular insufficiency.
Type B dissections occur more often with hypertension and followed by shock,
when present, is hemorrhagic for hemothorax or haemorroperitoneum. The outward
appearance of patients with Marfan syndrome or the signs of a recent cardiac
surgery can in themselves give rise to a type A aortic dissection. The patient
is usually able to report the initial pain that is always present. , violent and
maximum at the beginning (different from the growing pain of myocardial
infarction). It is perceived as a "tear" in the precordial or subclavic region
in the A-type tears. Propagation of the proximal dissection is evidenced by the
appearance of a breath of aortic valvular insufficiency and congestive
decompensation; or an acute atrio-ventricular block due to penetration of the
hematoma into the interatrial septum; or myocardial infarction for stenosing or
occlusive hematoma with coronary thrombosis.
Dissection pain is generally resistant to the most common analgesic and does not recur with the administration of trinitrine.
The rapid migration of pain indicates distal propagation. It may refer to the neck or chin or jaw when the dissection affects the aortic arch and its branches. In the dissections of the descending aorta (type B or propagation of type A) pain is felt posteriorly, interscapular, and then migrated to become lumbar or abdominal. The obstructive complications of the aortic branches, particularly cerebro-afferent with loss of consciousness, TIA and stroke may predominate. Paraplegia may appear by medullary ischemia due to progressive intercostal occlusion. Renal involvement causes acute renal failure and hypertension. The progressive occlusion of the tripod and mesenteric causes intestinal infarction. The femoral wrists may vary due to the presence of myintimal flap, stenosis from the hematoma, reopening in the true lumen, but the persistent disappearance of a peripheral pulse is indicative of extension to the iliac.
The prognosis of aortic dissection left to itself is highly unfortunate, but
with differences between the two types. Type A leads to a significantly worse
prognosis due to the high risk of acute and early complications in the proximal
tract. If not urgently operated, these patients die in 60% of cases within 24
hours and 90% within a month. Most of the deaths occur due to rupture, usually
with cardiac tamponade due to breakage in the initial dilation; or for coronary
involvement infarction with the creation of stenosis, flap and thrombosis; o due
to aortic valvular insufficiency due to flattening of the annulus or flaps.
Other times the involvement of the supraortic trunks causes severe cerebral
ischemia.
Type B dissection has a relatively better prognosis. Even if 30% of patients die
in the acute phase, about 60% of patients are alive at one year with only
medical therapy aimed at controlling hypertension. In one third of the cases the
false lumen undergoes thrombosis and in another third aneurysmal dilatation with
a tendency to break in the left pleural cavity. Often a re-entry door of the
false light is created within the real one. Predominate to the aneurysmal
evolution a bad pressure control, the existence of a cystic connective
degeneration and an initial dilatation of more than 4 cm. Other times the
evolution leads to district ischemias, both in the acute phase and in that of
chronicity due to progression of the dissection: renal failure, intestinal
infarction, acute ischemia of the lower limbs, paraplegia for medullary ischemia
(occlusion of the intercostal arteries T8-L2, from which the medullary branches
start).