I. What causes carotid artery stenosis?
It is generally believed that carotid plaque causes cerebral ischemia mainly through the following two pathways: one pathway is the alteration of hemodynamics caused by severely stenosed carotid artery, resulting in hypoperfusion in the corresponding part of the brain; the other pathway is the dislodgement of microemboli in the plaque or microthrombi on the surface of the plaque, causing cerebral embolism. There is no consensus on which of the above two mechanisms is more dominant, but most believe that plaque stenosis, plaque morphological characteristics are closely related to cerebral ischemic symptoms, and the two together induce neurological symptoms, while the relationship between stenosis and symptoms may be closer.
What are the early symptoms of carotid artery stenosis?
Clinically, carotid stenosis is divided into two categories: symptomatic and asymptomatic, depending on whether it produces cerebral ischemic symptoms.
1.Symptomatic carotid artery stenosis
(1) Cerebral ischemic symptoms: tinnitus, vertigo, blackness, blurred vision, dizziness, headache, insomnia, memory loss, drowsiness, dreaminess, etc. Eye ischemia manifests as vision loss, hemianopia, diplopia, etc.
(2) Localized transient loss of neurological function in TIA: clinical manifestations include transient impairment of sensory or motor function of one limb, transient monocular blindness or aphasia, etc., usually lasting only a few minutes, with complete recovery within 24h after onset. There is no focal lesion on imaging.
(3) Ischemic stroke: common clinical symptoms include sensory impairment of one limb, hemiparesis, aphasia, cerebral nerve damage, and in severe cases, coma, etc., with corresponding neurological signs and imaging features.
2.Asymptomatic carotid artery stenosis
Many patients with carotid stenosis do not have any clinical signs and symptoms of the nervous system. Sometimes, only a weakened or absent carotid pulsation is detected during physical examination, and a vascular murmur is heard at the root of the neck or at the carotid meridian. Asymptomatic carotid artery stenosis, especially severe stenosis or plaque ulceration, is recognized as a “high-risk lesion” and is receiving increasing attention.
(1) Men older than 60 years old with a history of long-term smoking, obesity, hypertension, diabetes and hyperlipidemia, and other risk factors for cardiovascular disease.
(2) Carotid murmur found during physical examination.
(3) The diagnosis can be made by the comprehensive analysis of the results of non-invasive auxiliary tests.
How to prevent carotid artery stenosis?
Because the main cause of this disease is atherosclerosis, aortitis, trauma and radiation injury, active treatment and prevention of the primary disease is the key to prevent this disease.
2. Carotid percutaneous transluminal angioplasty or carotid stenting implantation can be done to eliminate the potential source of emboli and prevent the occurrence of stroke if significant carotid stenosis is found.
D. How should carotid stenosis be treated?
The treatment of carotid stenosis aims to improve cerebral blood supply, correct or relieve the symptoms of cerebral ischemia; prevent TIA and ischemic stroke. Treatment depends on the degree of carotid stenosis and the patient’s symptoms, including medical treatment, surgical treatment and interventional treatment.
1.Medical treatment
The purpose of conservative medical treatment is to reduce the symptoms of cerebral ischemia, reduce the risk of stroke, and control the existing diseases such as hypertension, diabetes, hyperlipidemia and coronary heart disease. Internal conservative treatment includes the following.
(1) Reducing body weight.
(2) Smoking cessation.
(3) Limiting alcohol consumption.
(4) Anti-platelet aggregation therapy: Many large randomized, prospective multicenter clinical trials have confirmed that anti-platelet aggregation drugs can significantly reduce the incidence of cerebral ischemic disease, the drugs commonly used in clinical practice are aspirin, ticlopidine (ticlopidine, the trade name of resistance to kleenex) and so on.
(5) Improve the symptoms of cerebral ischemia.
(6) Regular ultrasound examination, dynamic monitoring of changes in the condition.
2.Surgical treatment
The aim of surgical treatment of carotid stenosis is to prevent the occurrence of stroke, and secondly, to prevent and slow down the onset of TIA. The standard surgical procedure is carotid endarterectomy.
Carotid endarterectomy was introduced in 1954, and some initial attempts showed poor results. The three most influential trials were the ECST, NASCET, and the Asymptomatic Carotid Atherosclerosis Study.
The ECST and NASCET were both conducted in patients with symptomatic severe carotid stenosis, and the findings of both trials were consistent.
(1) CE treatment was more effective than medical drug therapy for symptomatic carotid stenosis, and patients with carotid stenosis of 70% to 99% benefited significantly from CE;
(2) Patients with 0% to 29% stenosis have a low probability of stroke within 3 years, and the risk of CE far outweighs the benefit, so it is not recommended;
(3) Patients with stenosis of 30% to 69% are initially considered not suitable for CE, but further verification is needed.
ACAS randomized groups of patients with asymptomatic carotid atherosclerosis to CE and drug therapy, and the results showed that the cumulative stroke and mortality rates in the two groups were 5.1% and 11.0%, respectively, for patients with carotid stenosis ≥ 60%, and the effect of CE was much better than that of drug therapy. CE is generally considered feasible in asymptomatic carotid stenosis ≥ 60%, and some scholars believe that surgery can be performed when the stenosis is ≥ 80% due to the low incidence of cerebrovascular events in asymptomatic patients. complications of CE include perioperative stroke and death; and cerebral nerve injury, wound hematoma infection, postoperative hypertension, and postoperative hyperperfusion syndrome; the incidence of myocardial infarction and hypotension is low.
3.Interventional treatment
(1) Carotid artery percutaneous transluminal angioplasty
Percutaneous transluminal angioplasty is a relatively mature technique for revascularization, which is mainly used to dilate the stenosed blood vessels by squeezing them from inside to outside with a filling balloon, causing fracture and damage to the vessel wall. This technique has been widely used in various vascular diseases throughout the body, such as renal artery, iliac artery, coronary artery, etc. Compared with other vascular diseases, the application of PTA in carotid artery stenosis has progressed slowly because of technical reasons such as the complexity of the PTA operation route, and the fear of complications such as vessel rupture and embolus dislodgement causing cerebral infarction. Since the late 1980s, when carotid PTA was introduced into clinical practice, PTA is gradually becoming an alternative therapy to CE.
The main complication of PTA is postoperative restenosis, which has not been reported in the literature, but the incidence of restenosis is 5.0%-16.0%. (2) Carotid artery stenting
(2) Carotid artery stenting
Although PTA has achieved certain results in the treatment of stenosis, there are still problems such as intraoperative intimal tears, postoperative vascular elastic retraction and restenosis, which are caused by.
(i) For eccentric plaques, the balloon support is only in the arterial wall opposite to the eccentric plaque, so the filling balloon cannot tear the eccentric plaque, and as a result, the dilated segment of the vessel will undergo elastic retraction after removal of the filling balloon;
(ii) The high restenosis rate of simple balloon dilatation is due to elastic retraction in the early stage and further development of atherosclerosis in the later stage;
(iii) For severe circumferential calcified plaques, dilation requires higher pressure and is prone to the formation of arterial entrapment. In contrast, the implantation of carotid stents can cover and tightly adhere to the vessel wall of the treated segment, close the entrapment caused by balloon dilation, and limit the contact between the artery and the material causing intimal hyperplasia within the circulating blood, thus improving the efficacy and reducing the incidence of restenosis.
Currently, the technical success rate of carotid artery stenting is greater than 98%, the complication rate is 2% to 6%, and the mortality rate is <1%, indicating that carotid artery stenting may be safe and effective in the treatment of carotid stenosis. However, the clinical efficacy of internal carotid artery stenting depends not only on the immediate efficacy and complication rate, but also on the long-term efficacy to determine the value of stenting in the treatment of carotid artery disease. Several multicenter, randomized, prospective, controlled clinical trials of carotid stenting versus CE for carotid artery stenosis are currently underway, and more definitive conclusions are expected soon.
Complications of carotid artery stenting.
(i) Postoperative restenosis rate;
②Low incidence of stent deformation, collapse, and displacement;
(iii) other complications such as vasospasm, stroke, and hematoma formation are similar to those of PTA.
In addition, in recent years, in order to reduce the incidence of TIA and cerebral embolism caused by embolus dislodgement during carotid artery stenting and to improve the safety of the operation, intraoperative cerebral protection devices have been used in clinical practice. The device can prevent the debris dislodged from the vessel wall during the operation from entering the skull with the blood flow and reduce the incidence of intraoperative cerebral embolism, and its long-term efficacy needs to be further confirmed.
(3) Comparison of PTA, carotid artery stenting and CE The effectiveness of CE has been proved by several large clinical trials, but it also has certain limitations.
(1) Some patients require general anesthesia, and many patients cannot tolerate the procedure;
②The procedure is only applicable to lesions limited to the extracranial segment of the carotid artery;
(3) The procedure has certain complications.
PTA and carotid artery stenting have the following advantages over CE.
(1) General anesthesia is not required and can be tolerated by some patients with severe co-morbidities;
②The lesion may not be limited to the extracranial carotid artery;
③Small trauma and short operation time;
④The carotid artery, vertebral artery and coronary artery can be treated simultaneously.
PTA and carotid artery stenting also have some problems.
(i) Although the stenosis is improved, the potential source of emboli is not eliminated;
(ii) Most reports of carotid PTA and stenting implantation are small in size, with short follow-up periods, and long-term outcomes await further validation in randomized, large-scale clinical trials.
In conclusion, each of the three treatment approaches has its own advantages and disadvantages and should be further investigated to enrich the treatment of carotid artery stenosis disease.