Secondary prevention of ischemic stroke: prospects and reality

What is a stroke?

Dysfunction of the blood circulation in the brain is called stroke. With sudden surges in pressure, the vessels burst due to a sharp increase in their walls. This happens in stressful situations and prolonged stress.

Less commonly, with constantly elevated pressure, blood is gradually squeezed into the brain tissue. After a significant amount of fluid accumulates, neurological symptoms develop.

The disease is seasonal, occurring most often in the spring. If previously it was considered an age-related disease, recently it has become younger and is increasingly occurring in young people. Patients who have suffered a stroke experience headaches and speech impairment.

Stroke in men and women

The development of the disease differs in men and women. If in the former it most often develops from the age of 40, then in the latter it develops after 60 years. But at the same time, the age category of women from 18 to 40 years old occupies a leading position in the development of stroke. The risk of developing pathology in pregnant women increases.

Ladies endure the disease more difficult, they are less likely to recover and return to their previous lifestyle. The male body tolerates the disease more easily because their body responds better to treatment. They often manage to fully recover.

In the female half of the population, the disease occurs with complications. They are more likely to show early signs of the disease. After 30 years, women with bad habits are at risk of developing a stroke.

Cases of pathology appearing in patients taking birth control pills have become more frequent. Menopause can also trigger the disease. During this period, all processes in the female body slow down, blood flow worsens, and problems with blood vessels and heart appear.

In this regard, the prevention of stroke in women has acquired particular importance.

Secondary prevention

The goal of secondary prevention is to prevent recurrent ischemic stroke or recurrent TIA.

Antithrombotic therapy

Every patient who has had a stroke/TIA should receive antithrombotic therapy. The choice of antithrombotic therapy depends on the cause of the ischemic stroke or TIA. In this regard, determining the pathogenetic subtype of ischemic stroke or TIA is a fundamental issue.

Early secondary prevention

The goal of early secondary prevention is to prevent recurrent stroke within 24–48 hours of an acute cerebral ischemic event. The risk of developing a recurrent stroke in the first week is: for the cardioembolic pathogenetic subtype, approximately 2.8%; with atherothrombotic – 8.1%; with lacunar – 3.0%.

In the first 24–48 hours after a stroke, the patient should be prescribed Aspirin at an initial dose of 160 mg per day, followed by a transition (from the second day) to low doses of Aspirin (75–100 mg).

If a stroke occurs while taking Aspirin, it is recommended to prescribe a loading dose of Ticagrelor 180 mg in the first 24 hours, and from the second day switch to a regimen of 90 mg twice a day for at least 90 days. It is advisable to discontinue Ticagrelor after 90 days and switch to Clopidogrel 75 mg per day.

If a stroke occurs while taking Aspirin, increasing the dosage of the latter is not advisable.

If a decompressive craniotomy is planned, the administration of antithrombotic therapy is postponed.

Immediate administration of anticoagulants in therapeutic doses to all patients in order to prevent recurrent strokes is not recommended.

Continuous infusion of Heparin while maintaining aPTT of 1.5–2.0 normal may be useful in patients with IS who have:

• cardiac sources of embolism with a high risk of recurrence (artificial heart valves, myocardial infarction with intracardiac thrombus, atrial fibrillation with verified thrombus in the left atrium, intracardiac thrombi or myocardial infarction within the last 4 weeks);
• symptomatic extracranial or intracranial stenosis with recurrent TIA or IS of the “crescendo” type;
• occlusion of the basilar artery before or after intra-arterial thrombolysis or thromboextraction;
• verified coagulopathies.
• dissection of cerebral arteries.
• thrombosis of the venous sinuses, with recurrent TIA/IS.

During treatment with Heparin, it is necessary to examine a clinical blood test with platelet count at least 2 times a week (due to the risk of developing heparin-induced thrombocytopenia).

Due to the high risk of bleeding (including the development of symptomatic hemorrhagic transformation of cerebral infarction), long-term anticoagulation with UFH should not be used if the patient has verified:

• uncontrolled hypertension;
• severe neurological deficit (NIHSS > 20);
• large volume of cerebral infarction (more than 1/3 of the middle cerebral artery, extensive cerebellar infarction);
• aortic dissection;
• infective endocarditis;
• alcohol addiction;
• liver disease with the development of liver failure;
• damage with bleeding;
• malignant tumor;
• retinopathy with a high risk of bleeding;
• pronounced microvascular changes in the brain;
• cerebral artery aneurysm;
• previous spontaneous cerebral hemorrhage;
• hemorrhagic diathesis (for example, with coagulopathy, thrombocytopenia).

Other antithrombotic drugs are usually not prescribed as a means of secondary prevention of stroke in the first 48 hours (with the exception of early stenting).

Cardioembolic stroke

Atrial fibrillation

About 30% of cryptogenic strokes occur against the background of an unverified paroxysmal form of atrial fibrillation. In order to diagnose a hidden rhythm disturbance such as atrial fibrillation, it is desirable to conduct at least 72-hour Holter ECG monitoring; for a more accurate diagnosis, prolonged ECG monitoring (patch-monitors, external loop recorders) is optimal. .

For patients with newly diagnosed non-valvular atrial fibrillation, it is preferable to prescribe one of the NOACs (dabigatran, apixaban or rivaroxaban) rather than vitamin K antagonists.

In patients with valvular (moderate or severe mitral stenosis of rheumatic etiology, mechanical prosthetic heart valves or biological prostheses in the first 6 months after installation) atrial fibrillation, Warfarin is indicated, with the need for dose titration while maintaining a target INR value of 2.5 (2.0 interval – 3.0) – for an artificial valve in the aortic position, INR 3.0 (2.5 - 3.5) – for an artificial valve in the mitral position. The use of NOACs in such patients is contraindicated.

Before starting NOAC therapy, it is necessary to assess the risk of recurrent stroke/systemic thromboembolism (CHA2DS2-VASC scale, the risk of bleeding (identification of modifiable risk factors and their correction is advisable, a high risk on the HAS-BLED scale is not a contraindication for the use of NOACs), and renal function ( calculating creatinine clearance according to Cockcroft-Gault or glomerular filtration rate according to MDRD or CKD-EPI).

For patients who require oral anticoagulants, but Warfarin at a selected dose (INR from 2 to 3) cannot be used due to the difficulties of maintaining a therapeutic level of hypocoagulation (TTR<70%), the inability to closely monitor the INR, side effects, drug-drug interactions, it is recommended to take one of the following non-vitamin K antagonists: dabigatran, apixaban or rivaroxaban. The start of taking NOACs is carried out after discontinuation of Warfarin and achievement of INR<2.

In patients taking dabigatran, apixaban or rivaroxaban, there is no need for routine monitoring of blood coagulation parameters.

Dabigatran etexilate at a dose of 150 mg 2 times a day, compared with warfarin, effectively reduces the risk of stroke/systemic embolism, as well as stroke of unspecified etiology, has comparable safety in terms of major bleeding, its use is associated with lower risks of hemorrhagic stroke, intracranial hemorrhage , the overall incidence of bleeding and life-threatening bleeding.

Dabigatran etexilate at a dose of 110 mg 2 times a day compared with warfarin is no less effective in reducing the risk of stroke/systemic embolism and is significantly safer, causing fewer major bleedings, life-threatening bleedings, hemorrhagic strokes, and intracranial hemorrhages.

Apixaban is more effective than warfarin in reducing the risk of stroke/systemic embolism, lower risk of major bleeding, hemorrhagic stroke, intracranial hemorrhage, and reduces all-cause mortality.

Apixaban is prescribed to patients with atrial fibrillation at a dose of 5 mg twice daily.

The dose of Apixaban should be reduced to 2.5 mg twice daily in patients with two or more of the following characteristics: age over 80 years; body weight less than 60 kg or plasma creatinine concentration ≥133 µmol/l. Another indication for reducing the dose of Apixaban to 2.5 mg twice daily is a creatinine clearance of 15 to 30 mL/min.

Rivaroxaban is noninferior to warfarin in reducing the risk of stroke/systemic embolism, a comparable risk of major bleeding, and a lower risk of hemorrhagic stroke and intracranial hemorrhage.

Rivaroxaban for patients with atrial fibrillation is prescribed at a dose of 20 mg once a day.

The dose of rivaroxaban should be reduced to 15 mg once daily in patients with a creatinine clearance between 15 and 50 mL/min.

The use of apixaban or rivaroxaban is contraindicated in patients with creatinine clearance <15 ml/min or in those patients undergoing hemodialysis.

The use of dabigatran is contraindicated in patients with creatinine clearance <30 ml/min or in those patients undergoing hemodialysis.

The effectiveness and safety of the combination of NOACs (dabigatran, apixaban or rivaroxaban) with antiplatelet drugs has not been studied and cannot be routinely used in practice outside of clinical trials.

The choice of an oral anticoagulant in a patient with atrial fibrillation should be individualized and based on risk factors, cost of the drug, tolerability, potential interaction with other drugs, and comorbid condition.

If you do not take any oral anticoagulants (warfarin, dabigatran, apixaban or rivaroxaban), antiplatelet monotherapy is not effective in preventing recurrent stroke or TIA.

Timing for initiation of therapy with oral anticoagulants in patients who have suffered an ischemic stroke or TIA (H. Diener):

• TIA - on the first day, as soon as a CT scan of the brain is performed and a hemorrhagic type of stroke is excluded;
• minor stroke (NIHSS<8 points) – on the 3rd day, if hemorrhage was excluded during the initial CT scan of the brain;
• moderate stroke (NIHSS-8–15 points) – on day 6, with mandatory repeated CT or MRI of the brain and exclusion of hemorrhagic transformation of ischemic stroke;
• severe stroke (NIHSS>16 points) - on the 12th day, with mandatory repeated CT or MRI of the brain and exclusion of hemorrhagic transformation of ischemic stroke.

Acute myocardial infarction and thrombus in the left ventricle

For patients with ischemic stroke or TIA due to myocardial infarction or left ventricular thrombus, it is advisable to prescribe a vitamin K antagonist with an INR level of 2.0–3.0 for a period of 3 months to 1 year.

Dilated cardiomyopathy

In patients with ischemic stroke or TIA and dilated cardiomyopathy, both Warfarin (target INR 2.5; range 2.0–3.0) and antiplatelet therapy may be recommended to prevent relapse.

For patients with stroke or TIA who have cardiomyopathy with systolic dysfunction (left ventricular ejection fraction <35%) in sinus rhythm, the benefit of Warfarin and NOACs has not been established.

Damage to native heart valves

In patients with ischemic stroke or TIA and rheumatic mitral valve disease, regardless of the presence of atrial fibrillation, long-term therapy with Warfarin is justified (target INR value 2.5; range 2.0 - 3.0).

Antiplatelet drugs should not be routinely added to Warfarin as this combination increases the risk of bleeding.

Antiplatelet therapy is warranted in patients with mitral valve prolapse and ischemic stroke or TIA.

Patients with mitral regurgitation and mitral valve orifice calcification without atrial fibrillation may be treated with antiplatelet therapy or Warfarin (target INR 2.5; range 2.0 to 3.0).

In patients with ischemic stroke or TIA and aortic valve disease without atrial fibrillation, antiplatelet therapy is warranted.

Warfarin is indicated for patients with moderate or severe mitral stenosis of rheumatic etiology (target INR values ​​of 2–3 for unoperated valvular disease). The use of NOACs is contraindicated.

Artificial heart valves

Patients with atrial fibrillation and mechanical prosthetic heart valves are advised to take Warfarin (target INR values ​​of 2–3 for an artificial valve in the aortic position; 2.5–3.5 for an artificial valve in the mitral position). The use of NOACs is contraindicated.

For patients with ischemic stroke or TIA with biologic prosthetic heart valves who have no other sources of cardiogenic embolism, Warfarin (target INR 2.5; range 2.0 to 3.0) is recommended for 3 to 6 months.

In patients with a prosthetic heart valve, ischemic stroke and systemic embolism, despite adequate therapy with oral anticoagulants, it is advisable to search for and correct another possible cause of stroke.

Currently, there are 2 tactics for managing such patients: increasing the dose of Warfarin while maintaining the INR at 3.0 (within 2.5–3.5) or prescribing a combination of Aspirin at a dose of 75–150 mg/day and Warfarin with maintaining the INR at level 2.5 (within 2.0–3.0).

Non-cardioembolic stroke

In patients who have had noncardioembolic ischemic stroke (atherothrombotic, lacunar, or stroke of unknown etiology), antiplatelet therapy is indicated to prevent recurrent stroke and recurrent acute vascular events.

The following antiplatelet therapy regimens are possible:

• Clopidogrel (75 mg) per day;
• Aspirin 25 mg + Dipiridamol slow release 200 mg, 2 times a day;
• Aspirin (50–325 mg) per day;
• Ticagrelor (90 mg) 2 times a day.

The choice of antiplatelet therapy regimen should be individualized and based on the patient's risk factor profile, drug tolerability, and other clinical characteristics. In order to reduce the incidence of headaches when prescribing the combination of Aspirin 25 mg + Dipiridamol with slow release 200 mg, it is necessary: ​​in the first 3 days, recommend the combination of Aspirin 25 mg + Dipiridamol with slow release 200 mg once and additionally prescribe Aspirin 50 mg; from the 4th day, increase the combination of Aspirin 25 mg + Dipiridamol with slow release 200 mg to a regular dose 2 times a day, and discontinue Aspirin 50 mg; If headache or other symptoms of intolerance occur, the dose increase is postponed until 14 days.

In patients with contraindications to Aspirin therapy, Clopidogrel is recommended.

Adding Aspirin to Clopidogrel increases the risk of bleeding and is not recommended for general use in patients. Exceptions are patients with IS and unstable angina, or non-Q-forming myocardial infarction, or recent stenting of the coronary arteries, who need to be prescribed a combination of Aspirin 75 mg/day and Clopidogrel 75 mg/day (the duration of dual antiplatelet therapy depends on the type of implanted stent).

For those patients who have an ischemic stroke while taking Aspirin, there is no evidence that increasing the dose of Aspirin provides additional benefit. It is generally accepted in this situation to re-evaluate the pathogenetic mechanisms of stroke development and prescribe other antithrombotic drugs, although neither the use of one of these drugs nor their combination has been studied in such patients.

For those patients whose stroke developed while taking Aspirin, Ticagrelor (90 mg 2 times a day) is recommended.

Correction of risk factors

Risk factors (RFs) for stroke are various clinical, biochemical, behavioral and other characteristics characteristic of an individual (and individual populations), as well as external influences, the presence of which indicates an increased likelihood of developing a stroke. Identification and timely correction of risk factors is the most important direction in the fight against recurrent strokes.

FRs are divided into correctable and non-correctable.

Correctable risk factors include:

• hypertension;
• hyperlipidemia;
• diabetes;
• smoking;
• alcohol abuse;
• obesity;
• obstructive sleep apnea syndrome;
• low physical activity;
• metabolic syndrome.

Non-correctable risk factors include:

• floor;
• age;
• ethnicity;
• heredity.

Hypertonic disease

Hypertension is usually understood as a chronic disease, the main manifestation of which is hypertension, not associated with the presence of pathological processes in which the increase in blood pressure is caused by known causes that are often eliminated in modern conditions (symptomatic hypertension).

Taking antihypertensive drugs is indicated for patients in the acute period of ischemic stroke no earlier than the second day. The maximum increase in systolic blood pressure on the first day, which does not require antihypertensive correction, is up to 220 mmHg. The exception is the following situations: the need for systemic and/or intra-arterial thrombolysis, the presence of hemorrhagic transformation.

Additional indications for lowering blood pressure levels in the acute phase of ischemic stroke are: ACS, heart failure, aortic dissection, intracranial hemorrhage after thrombolytic therapy, preeclampsia/eclampsia. In these patients, a reduction in blood pressure of at least 15% is shown.

The absolute values ​​of target BP and the level of BP reduction are unknown and must be determined individually, but benefit is associated with an average reduction in BP of 10/5 mmHg. Art.

The patient should be recommended the following non-drug methods of lowering blood pressure: quitting smoking; normalization of body weight; reducing the consumption of alcoholic beverages to less than 24 g (in terms of pure alcohol) of alcohol per day in men and less than 12 g per day in women; increasing aerobic physical activity; reducing the consumption of table salt to 5 g/day; changing the diet with increasing consumption of vegetables, fruits, grains, low-fat dairy products, reducing consumption of animal fats.

For patients who have suffered a stroke or TIA, it is recommended to prescribe antihypertensive therapy in any rational combination depending on the individual characteristics of the patient with achieving a target blood pressure level below 140/90 mm Hg.

Hyperlipidemia

Changes in the concentrations of lipid fractions alone, as well as in combination with other risk factors, lead to the development of atherosclerosis and an increased risk of cardiovascular and cerebrovascular diseases.

Patients with stroke due to hyperlipidemia or cerebral artery atherosclerosis should be advised to change lifestyle, diet limited in animal fats, and drug therapy with statins.

The following groups of drugs are used to correct hyperlipidemia:

• 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors (statins);
• fibrates;
• bile acid sequestrants;
• niacin (nicotinic acid);
• selective cholesterol absorption inhibitors (ezetimibe);
• inhibitors of proprotein convertase subtilisin-kexin type 9 (PCSK9 inhibitors) – regulators of LDL receptor expression.

Treatment is carried out under dynamic monitoring of LDL levels.

Patients who have suffered an IS or TIA are at very high risk. The target LDL level in patients with very high total cardiovascular risk is <1.8 mmol/L (<70 mg/dL); or involves a decrease in LDL cholesterol levels of at least 50% from baseline (if baseline value is 1.8–3.5 mmol/L (70–135 mg/dL)).

Old age should not be an obstacle to prescribing statins: the indications for taking this class of drugs in elderly patients are the same as in young people.

It is advisable to start treatment of elderly patients with lower doses of drugs, given the higher risk of adverse reactions.

If the patient was taking statins during the development of IS, it is necessary to continue this lipid-lowering therapy in the acute period.

The preferred therapy is Atorvastatin at a dose of 40 (80) mg/day.

Statins are a relatively safe group of drugs. The risk of adverse events requiring drug discontinuation is comparable to placebo. The most common pathological increase in the activity of liver enzymes develops (0.3–5%, often at the beginning of treatment, is dose-dependent; in a number of studies, similar figures are observed when taking placebo).

Currently, assessment of liver function in patients taking statins is only required before starting therapy, with further repeat liver enzyme tests after 8 weeks.

An increase in AST or ALT by 3 times is an indication for discontinuation of the drug.

Patients after ischemic stroke or TIA with low HDL levels (less than 1 mmol/l) can be recommended to take Ac. Nicotinici or Gemfibrozilis.

In patients with ischemic stroke, it is reasonable to consider prescribing PCSK9 drugs in addition to optimal statin therapy to reduce the risk of cardiovascular death, myocardial infarction, or stroke.

Diabetes

In patients with ischemic stroke due to diabetes mellitus, tighter control of blood pressure and lipid levels is recommended. The drugs of choice for antihypertensive therapy in these patients are ACE inhibitors and calcium channel blockers.

It is necessary to achieve normoglycemia in this category of patients through diet and drug therapy in order to reduce micro- and macroangiopathy.

The target for glycosylated hemoglobin (HbA1c) in stroke patients is <7%.

The choice in favor of taking oral hypoglycemic agents and/or insulin replacement in a specially selected mode close to physiological secretion, in each individual case, is made taking into account the individual characteristics of the patient.

Obesity and physical inactivity

Obesity is diagnosed in patients with a body mass index >30 kg/m2.

Obese individuals are advised to follow a weight loss diet.

For post-ischemic stroke or TIA patients who are capable of physical activity, a minimum of 30 minutes of moderate-intensity exercise 7 times per week (eg, brisk walking, exercise machine, bicycle) can be recommended.

For patients with disability after an ischemic stroke, at the beginning of the selection of a regimen of neurorehabilitation exercises, it is necessary to conduct classes under the guidance of rehabilitation specialists.

Obstructive sleep apnea syndrome

Obstructive sleep apnea syndrome is a condition characterized by the presence of snoring, periodic collapse of the upper airway at the level of the pharynx and cessation of pulmonary ventilation with continued respiratory effort, decreased oxygen levels in the blood, severe sleep fragmentation and excessive daytime sleepiness.

Factors contributing to the development of OSA are obesity, male gender, age, family history, hypothyroidism, nasal obstruction, and smoking.

During sleep, people with OSA experience characteristic transient occlusions of the upper airway, which lead to episodes of partial (hypopnea) or complete (apnea) cessation (interruption) of air flow. In severe forms of OSA, up to 400–500 breathing stops per night with a total duration of up to 3–4 hours can be observed, which leads to acute and chronic lack of oxygen during sleep. Which, in turn, significantly increases the risk of developing arterial hypertension, diabetes, heart rhythm disturbances, myocardial infarction, stroke and sudden death during sleep. Each cessation of breathing is accompanied by a partial or complete awakening of the brain, which leads to a sharp deterioration in the quality of sleep.

Clinically, OSA is manifested by loud snoring, noticeable by strangers, pauses in breathing during sleep; patients complain of waking up at night with a feeling of lack of air, lack of feeling of a full night's rest, and daytime sleepiness.

To diagnose OSA, cardiorespiratory monitoring (CRM) or polysomnography (PSG) is performed.

A generally accepted criterion for the severity of OSA is the frequency of apnea and hypopnea per hour - the apnea/hypopnea index (AHI).

The severity classification of OSA is presented in Table 1.

Table 1. Classification of severity of OSA in adults.

The following main areas of treatment for OSA are distinguished:

• general preventive measures;
• ensuring free nasal breathing;
• the use of electromechanical stimulating (stimulating awakening) devices;
• use of intraoral devices;
• the use of pharmacological agents to relieve snoring;
• surgical treatment (surgical, laser);
• treatment with non-invasive assisted ventilation using continuous positive airway pressure.

The method of choice for the treatment of OSA of any etiology is currently Continuous Positive Airway Pressure Therapy (CPAP) - non-invasive auxiliary ventilation with constant positive pressure in the airways during sleep through a mask. This technique is the main one in the treatment of moderate and severe OSA.

The essence of this method is to maintain positive pressure in the respiratory tract throughout the entire respiratory cycle, as a result of which an obstacle is created to their collapse and, accordingly, the substrate of OSA is eliminated.

Smoking

Patients who have had a stroke should be advised to quit smoking.

It is advisable to avoid passive smoking.

Psychological support, nicotine-containing products and smoking cessation medications are effective in helping people quit smoking.

Counseling and the use of nicotine substitutes in conjunction with smoking cessation are recommended

Behavioral therapy is necessary during inpatient treatment, aimed at stopping the patient from smoking

It is recommended to use medicinal correction of nicotine addiction using varenicline during hospitalization

Patients after ischemic stroke should avoid “passive” smoking.

Alcohol abuse

Patients who have suffered a stroke should be advised to stop drinking alcohol.

Daily intake of low doses of alcohol (24 mg based on 100% ethyl alcohol for men and 12 mg for women) is associated with a reduction in the risk of stroke.

Patients who did not drink alcohol before the stroke should not start taking it.

Metabolic syndrome

Metabolic syndrome is characterized by a combination of three or more disorders: high fasting blood glucose, arterial hypertension, low high-density lipoprotein levels, high triglyceride levels and abdominal obesity.

In patients with metabolic syndrome, therapy should include lifestyle changes (diet, exercise, weight loss) to reduce the risk of recurrent strokes.

Wall-occlusive lesions of cerebral arteries

Extracranial stenosis of the carotid arteries

If symptomatic stenosis of the carotid arteries is detected more than 70% according to Doppler ultrasound scanning of the brachiocephalic arteries and more than 50% according to CT angiography or cerebral angiography, surgical treatment (CE or TBAS) is indicated.

In patients with symptomatic stenosis less than 50%, CE or transluminal balloon angioplasty with stenting (TBAS) of the internal carotid arteries (ICA) is not indicated.

Since in the atherothrombotic pathogenetic subtype of IS the risk of recurrent stroke is extremely high, CE must be performed early.

In patients with mild nondisabling stroke (modified Rankin score 0–2), it is reasonable to undergo carotid artery surgery between 48 hours and 7 days after the acute event, unless there are contraindications to early revascularization.

For other patients, it is advisable to perform surgery on the carotid arteries within the first two weeks from the onset of stroke.

Antiplatelet medications must be taken before and after surgery.

TBAS is an alternative to CE for symptomatic patients at intermediate or low risk of endovascular complications.

Carotid artery stenting is preferable to CE in the following cases: there is an increased risk of intraoperative complications with CE, there are contraindications to CE, the stenosis is located in a surgically inaccessible location, restenosis after CE, stenosis after radiation therapy. Patients undergoing stenting should receive a combination of Clopidogrel 75 mg and Aspirin 75 mg immediately before, during, and for at least 1 month after the procedure.

Both CE and TBAS can be performed in patients of different age groups, but in young patients TBAS is preferable, in older patients - CE.

Carotid artery surgery should be performed only in centers where the perioperative complication rate (any stroke, myocardial infarction, or death) does not exceed 6%.

Patients with stroke who have undergone CE (TBA) are prescribed therapy with antiplatelet drugs and statins, as well as correction of risk factors.

Extracranial stenoses of the arteries of the vertebrobasilar region

For all patients with stroke or TIA and vertebral artery stenosis, optimal drug therapy is recommended, which should include antiplatelet drugs, statins, and risk factor modification.

Endovascular and open surgical treatment may be recommended for patients with symptomatic extracranial vertebral artery stenosis who develop stroke or TIA despite optimal medical therapy (including antiplatelet agents, statins, and satisfactory control of risk factors).

Intracranial stenoses

In patients with stroke or TIA due to 50–99% stenosis of a major intracranial artery, Aspirin is preferred over warfarin. The optimal dose of Aspirin in this population has not been established, but based on overall safety and efficacy data, a daily dose of 75 mg to 150 mg of Aspirin is recommended.

In patients with stroke or TIA due to 50–99% stenosis of a large intracranial artery, long-term maintenance of blood pressure <140/90 mmHg makes sense. Art. and LDL level <1.8 mmol/L.

For patients with recent stroke or TIA (within 30 days) associated with severe intracranial stenosis (70% to 99%) of the main cerebral artery, the addition of clopidogrel 75 mg/day to aspirin for 90 days may be warranted.

Percutaneous transluminal angioplasty and/or stenting may be used in patients with symptomatic intracranial stenoses ≥50%. Currently, there is insufficient evidence to support the routine use of this intervention, so decisions about treatment tactics in patients with intracranial stenoses must be made individually.

In patients with stroke or TIA due to 50–99% stenosis of a large intracranial artery, extra-intracranial bypass surgery (creating an anastomosis between the branches of the superficial temporal and middle cerebral arteries) is not recommended.

Cerebral artery occlusions

Patients with cerebral artery occlusions are advised to undergo conservative therapy aimed at correcting vascular risk factors. Extra-intracranial bypass surgery has a high risk of intraoperative complications and has no advantages over conservative treatment.

Symptoms that predict a stroke

The pathology does not develop gradually, but lasts from several hours to a day. The appearance of causeless nausea and deterioration of vision should alert a person. Such symptoms indicate negative changes in the blood vessels of the brain.

A stroke has many other symptoms:

sudden jumps in blood pressure;

uncharacteristic apathy and drowsiness;

migraine, dizziness;

rapid change in temperature readings of the patient’s body;

sudden fatigue for no reason.

All symptoms may disappear as suddenly as they appear. Then they appear again, but in a more pronounced form. Vivid signs of the disease: numbness of the limbs, disturbance of smell, impaired speech and sound perception, memory loss, inability to recognize familiar people.

Patients with such symptoms require urgent medical attention.

Types of stroke

Help for the patient will be effective only if the correct diagnosis is established. It is important to establish the type of pathology, because depending on this, a treatment regimen is selected.

According to the nature of development, stroke is of two types:

Hemorrhagic. It develops when blood leaves a vessel, leading to compression of tissues and their death.

Ischemic. It occurs under the influence of negative factors that interfere with the free flow of blood through the vessels and the supply of oxygen to brain cells. It is provoked by spasms, narrowing of the lumen, and blockage. It accounts for 85% of cases of the disease.

The disease is also classified according to the type of course and severity of manifestation:

Initial stage. It manifests itself in the form of neurological disorders and is mild. Symptoms disappear on their own within 10-14 days.

Average degree. Signs disappear after using medications. There is no symptom of cerebral edema.

Severe degree. Characterized by dysfunction of the central nervous system. In most cases, patients are unconscious and there is swelling and brain damage.

If disturbances are observed for several hours and then disappear, then the patients have experienced a transient ischemic attack. This condition is considered a harbinger of complications and serious illness. When it appears, it is necessary to engage in prevention and treatment.

Basic measures to prevent violations

As mentioned above, the prevention of strokes should be carried out taking into account the factors that can cause them.

It is necessary to take into account that such cerebral circulation disorders do not arise, as they say, “out of nowhere.” The development of a stroke is preceded by certain diseases and conditions, which serve as the impetus for this kind of vascular catastrophe.

Preventive measures to prevent the disease should be aimed primarily at eliminating the factors that may cause it.

Prevention of strokes can be primary and secondary. Primary measures include measures to eliminate the factors that cause such violations. Secondary prevention refers to methods to prevent recurrent strokes.

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