Arterial entrapment is the gradual peeling and expansion of the intima due to a localized tear in the intima, which is subjected to a strong blood shock, creating two lumens, true and false, within the artery. This leads to a number of manifestations including tear-like pain. The aorta is the main blood vessel of the body, bearing the pressure directly from the beating heart, with a huge blood flow. The occurrence of a tear in the intimal layer has a very high chance of rupture and a very high mortality rate if proper and timely treatment is not provided.
Disease Overview.
The normal human arterial vasculature is composed of 3 layers of structures, the intima, the mesentery and the epima, and the 3 layers fit closely together to carry the blood flow through. Arterial entrapment, on the other hand, is a localized tear in the endothelium that is subjected to a strong blood shock, and the endothelium gradually peels off and expands, forming two lumens, a true and a false, within the artery. This leads to a number of manifestations including tear-like pain. Depending on the site of the rupture and the location of the artery, the entrapment can involve various parts of the body. The most common and most dangerous is aortic entrapment, while others include superior mesenteric artery entrapment, carotid artery entrapment, etc. The manifestations vary depending on the site of blood supply. This article focuses on aortic coarctation.
Causes.
Aortic coarctation is one of the most common aortic diseases in which blood passes through a fissure in the intima of the aorta, enters the aortic wall and causes a separation of the normal arterial wall. So what kind of people are prone to aortic coarctation? That is, what is the cause or causes of aortic coarctation?
Aortic coarctation is the result of the interaction of abnormal mid-membrane structure and abnormal hemodynamics of the aorta. When the aortic structure is abnormal is naturally prone to aortic dissection, common factors include: Marfan syndrome, congenital cardiovascular malformations, idiopathic aortic mesenteric degenerative changes, aortic atherosclerosis, aortic inflammatory disease, etc. We know the American female volleyball player Hyman and the male volleyball player Zhu Gang as these reasons, and collapsed on the sports field. Arterial wall damage is also easily caused when hemodynamics are altered. The most common cause is hypertension, and almost all patients with aortic coarctation have poorly controlled hypertension. In other words, the control of hypertension has a comprehensive impact on the prevention, treatment, and prognosis of aortic coarctation, and is the most basic and least negligible means of treatment and prevention. Pregnancy is another high incidence factor, associated with altered hemodynamics during pregnancy. Among women who develop the disease before the age of 40, 50% occur during pregnancy. The ratio of male to female incidence of aortic coarctation is 2 to 5:1; the common age of onset is 45 to 70 years, with the youngest patient reported so far being only 13 years old.
There are two major medical classifications of aortic coarctation based on the location of the intimal fissure and the extent of coarctation involvement. The most widely used is the 3-type classification proposed by Professor DeBakey et al, in 1965. Type I: aortic coarctation involving the ascending aorta to the descending aorta and even to the abdominal aorta. Type II: Aortic coarctation involving only the ascending aorta. Type III: Aortic coarctation involving the descending aorta, such as downward involvement of the abdominal aorta is type IIIA; downward involvement of the abdominal aorta is type IIIB. In 1970, Professor Daily of Stanford University and others proposed another classification method based mainly on the location of the proximal endothelial fissure: Stanford type A: equivalent to DeBakey type I and II, Stanford type B: equivalent to DeBakey type III. Type A: equivalent to DeBakey type I and II, and Stanford B: equivalent to DeBakey type III.
Clinical manifestations.
Disease symptoms.
In actual cases it can be manifested in different situations, also called clinical symptoms, which mainly include some of the following.
1. Typical patients with acute aortic coarctation often present with sudden, severe, chest and back, tearing-like pain. Severe cases can present with heart failure, syncope, or even sudden death; most patients are accompanied by uncontrollable hypertension.
2.Aortic branch artery occlusion can lead to corresponding ischemic symptoms in brain, limbs, kidneys, and abdominal organs: such as cerebral infarction, oliguria, abdominal pain, pale legs, weakness, florid spots, and even paraplegia.
3.In addition to the above main symptoms and signs, because of the wide area of aortic blood supply, the performance varies according to the accumulation range of the entrapment. Other conditions include: disappearance of peripheral arterial pulsation, vocal cord paralysis when the left recurrent laryngeal nerve is compressed, hemoptysis and vomiting of blood when the entrapment penetrates the trachea and esophagus, superior vena cava syndrome when the entrapment compresses the superior vena cava, dyspnea when the trachea is compressed, and Compression of the cervicothoracic ganglion results in Horner syndrome, compression of the pulmonary artery results in pulmonary embolism, and involvement of the mesenteric and renal arteries by the entrapment may cause intestinal paralysis or even necrosis and renal infarction. Pleural effusion is also a common sign of aortic coarctation, mostly on the left side.
Disease risk.
The greatest danger of aortic coarctation is death. The aorta is the main blood vessel of the body, subjected to pressure directly from the beating heart, with tremendous blood flow. A tear in the intimal layer occurs, and without proper and timely treatment, the chances of rupture are very high and the mortality rate is very high. Previous literature reported mortality rates of up to 50% within 1 week and between 60-70% within a month.
In addition to this, even if the patient survives, the enlargement of the false lumen and the increase in pressure, which decreases the blood flow to the true luminal vessels, leads to ischemia of the organs in the region supplied by the aorta.
Diagnostic differential.
Auxiliary tests: The main auxiliary tests to confirm the diagnosis of aortic coarctation are: CT angiography (CTA), magnetic resonance imaging (MRA) or direct digital silhouette angiography (DSA).
I. Chest radiographs.
An ordinary chest X-ray can provide a clue for diagnosis. For patients with acute chest and back tear-like pain with hypertension, if a widened upper mediastinal shadow or a widened aortic shadow is found in the chest X-ray, further CTA and other examinations must be performed to clarify the diagnosis.
II. Aortic CTA.
It is the most commonly used preoperative imaging assessment method with a sensitivity of more than 90% and its specificity close to 100%. CTA tomography can observe that the intercalated septum divides the aorta into true and false chambers, and the reconstructed image can provide two-dimensional and three-dimensional images of the whole aorta. its main disadvantage is that contrast agent has to be injected and corresponding complications may occur, and the artifacts produced by aortic pulsation can also interfere with the image and diagnosis.
III. Aortic MRA.
The diagnostic sensitivity and specificity for patients with aortic coarctation are close to those of CTA, and the enhancer used in MRI is not nephrotoxic; its disadvantage is that it takes longer to scan and is not suitable for emergency patients with unstable circulatory status, and it is also not suitable for patients with magnetic metal implants in the body.
IV. Digital silhouette angiography (DSA).
At present, although aortic angiography still retains its status as the “gold standard” for the diagnosis of aortic coarctation, it has largely been replaced by CTA and, because it is an invasive test and requires the use of iodine-containing contrast agents, it is currently used only in endoluminal repair procedures and not as a preoperative diagnostic tool.
V. Ultrasonography.
Its advantages are that it is noninvasive, does not require contrast agent, can locate the endocardial fissure, shows the status of the true and false chambers and blood flow, and can also show the complications of aortic valve closure insufficiency, pericardial effusion and obstruction of the branch arteries of the aortic arch. However, it is also limited by the patient’s obesity and other conditions. Transthoracic ultrasound is easier to perform with simplicity, and its sensitivity and specificity are not as good as transesophageal ultrasound, but transesophageal ultrasound may cause nausea, vomiting, tachycardia and hypertension, which may instead aggravate the condition, and therefore often needs to be performed under anesthesia. Intravascular ultrasound is a diagnostic program developed in recent years, which can clearly display the three-dimensional structure of the aortic lumen and is undoubtedly more diagnostically accurate than conventional ultrasound. However, because it is an intravascular operation, it is mainly used in the determination of entrapment rupture and residual endoleaks during minimally invasive interventions.
Disease treatment.
Treatment of aortic coarctation mainly includes conservative treatment, interventional treatment and surgical treatment. Interventional endoluminal repair techniques have enriched the treatment of aortic coarctation and have made the procedure less invasive and safer.
Conservative treatment.
However, in patients with acute entrapment, whatever further treatment we want to take, the first step should be the appropriate conservative treatment: blood pressure control and pain control. This usually requires the application of powerful drugs such as sodium nitroprusside for hypotension and morphine for analgesia. For patients in critical condition, emergency tracheal intubation, ventilator-assisted breathing and emergency resuscitation surgery are often required, but they also imply a very high risk and mortality rate.
Surgical and interventional treatment.
After the patient is appropriately stabilized, the choice of treatment modality depends mainly on the type of entrapment. For the current state of treatment, for Stanford type B aortic coarctation, minimally invasive endoluminal therapy is the mainstay. The basis for treatment includes the following conditions, or indications for surgery: persistent enlargement of the entrapment, as evidenced by a rapidly increasing diameter and extent of the aortic entrapment, thoracic hemorrhage, and uncontrollable pain; or ischemia of major branches of the aorta, such as the superior mesenteric artery and renal artery.
Traditional minimally invasive endoluminal repair of aortic coarctation technically requires at least a 1.5 cm anchorage zone on the aorta to prevent incomplete proximal occlusion and endoleaks. However, with improvements in endoluminal repair devices and advances in endoluminal repair techniques, this indication has been expanded to allow treatment of Stanford type B aortic coarctation with a main cleft within 1.5 cm of the left subclavian artery opening by hybridization or various endoluminal repair coarctures (chimney, open window, modular branch stent).
Intraluminal repair of Stanford type A aortic coarctation with a cleft in the ascending aorta has been described with placement of a clad stent in the ascending aorta to isolate the proximal coarctation cleft, but this procedure requires specific anatomic constraints. In the acute phase, ascending aortic replacement is performed, and Sun’s procedure remains the current mainstay of treatment for type A aortic coarctation.
Disease follow-up.
Once again, it is important to note that regular follow-up and blood pressure and heart rate control are essential for both surgical treatment and endoluminal interventional repair. The occurrence of aortic coarctation, rupture, and other complications can be effectively prevented by lowering blood pressure and reducing the rate of left ventricular systole to reduce the impact of fluctuating waves of blood flow on the aortic wall.