Atherosclerosis of the abdominal aorta and its branches

Atherosclerosis is a well-known and widespread disease that affects the arteries and is accompanied by the formation of cholesterol deposits on the internal vascular walls. If the abdominal part of the aortic vessel, which passes through the lower part of the abdominal cavity, is involved in the process, the doctor makes a diagnosis of "atherosclerosis of the abdominal aorta". The disease can cause serious complications, including disability and death. However, it is not so easy to suspect the pathology, which is due to the vagueness of the symptoms and the frequent latent course.

Epidemiology

In every second patient with aortic circulation disorder, the abdominal part of the vessel is affected. This part is responsible for supplying blood to the abdominal organs, lower limbs and pelvis.

Over the past few years, the incidence of atherosclerosis has increased significantly, and mortality from this disease has exceeded the rates caused by injuries, infectious pathologies and oncology. Most often, atherosclerosis of the abdominal aorta is found in men aged 45-55 years. Women get sick approximately 3-4 times less often, and the risk of getting sick increases significantly with the onset of menopause. [ 1 ]

The disease is quite common: it is diagnosed in approximately every twentieth person over 65 years of age.

In European countries and the United States of America, atherosclerosis of the abdominal aorta is much more common than in African countries. The greatest prevalence of the disease is noted in the United States, Canada, Great Britain, Finland, and Australia. The lowest incidence is recorded in Japan. [ 2 ]

Atherosclerosis and its complications currently remain the main cause of morbidity and mortality in many countries of the world, including the post-Soviet space. Abdominal aortic lesions are detected in more than 75% of autopsies of patients who died from coronary heart disease. [ 3 ] In more than half of cases, the pathology is determined only against the background of the development of acute mesenteric circulatory disorder.

Causes atherosclerosis of the abdominal aorta.

Atherosclerosis of the abdominal aorta is a chronic pathology. The disease is characterized by specific vessel damage, connective tissue proliferation against the background of fatty infiltration of the inner wall, which generally leads to organ and general circulatory disorders.

There are several theories of the pathology occurrence – in particular, the theory of lipoprotein infiltration, and the most common one – caused by the occurrence of pathological changes due to damage to the vessel wall. Such damage is not the result of mechanical trauma to the endothelium, but a violation of its function. We are talking about an increase in permeability, adhesiveness, and an increase in the synthesis of procoagulant and vasoconstrictor factors. [ 4 ]

Disruption of endothelial function can be caused by infection (for example, herpes virus), intoxication (smoking, etc.), [ 5 ] hormonal imbalance (hyperinsulinemia), hemodynamic disturbance (hypertension), etc. But scientists unanimously consider hypercholesterolemia to be the main link.

The basic cause of abdominal aortic atherosclerosis is impaired lipid-protein metabolism, which provokes the appearance of typical atherosclerotic plaques. Nutritional disorders lead to metabolic disorders, damage to the vascular walls, and changes in their structure. [ 6 ] Regular hypothermia, weakened immunity, frequent stress and psychoemotional tension, infectious and inflammatory processes, hormonal changes, and injuries all lead to damage to the inner vascular wall. The situation can be aggravated by: an unhealthy lifestyle with a lot of bad habits, excess weight, endocrine pathologies, and taking certain medications. Concomitant diseases also play a significant negative role: hypertension, obesity, diabetes, [ 7 ] coronary pathologies.

Experts identify the following main causes of the disease:

• alimentary (nutritional) disorders;
• neurogenic factors (stress, emotional instability, neuroses);
• endocrinopathies;
• prolonged increase in blood pressure, hypoxic conditions;
• autoimmune pathologies;
• hereditary predisposition; (the influence of maternal hypercholesterolemia during pregnancy on the progression of early atherosclerotic lesions in childhood has been proven) [ 8 ];
• excess weight, various degrees of obesity; [ 9 ]
• insufficient physical activity;
• alcohol, nicotine, drug addiction.

Risk factors

Factors that can lead to the development of atherosclerosis of the abdominal aorta can be divided into several groups: permanent factors, transient and potentially transient.

Eternal factors are permanent and cannot be eliminated:

• age over 40-45 years;
• male gender (men suffer from atherosclerosis more often than women);
• hereditary predisposition (the disease is often found in people whose relatives also suffer from atherosclerosis of the abdominal aorta). The formation of fatty streaks occurs in the aorta of the human fetus and is significantly enhanced by maternal hypercholesterolemia. [ 10 ]
• ethnic risk factors. [ 11 ], [ 12 ]

Experts point out that hereditary predisposition contributes to the earlier onset of the development of pathology.

Transient risk factors include those that can be eliminated:

• smoking, its negative impact on the elasticity of blood vessels;
• poor nutrition, consumption of large amounts of animal fats;
• physical inactivity, passive lifestyle, excess weight.

Potentially transient factors include diseases that can be corrected, controlled and prevented from developing further:

• hypertension, which promotes the deposition of lipids in the vascular wall and the formation of atherosclerotic plaques; [ 13 ]
• dyslipidemia, a disorder of fat metabolism, which is accompanied by an increase in the level of cholesterol, lipoproteins and triglycerides;
• diabetes mellitus and obesity increase the risk of developing atherosclerosis of the abdominal aorta several times, which is due to the simultaneous disruption of lipid metabolism; [ 14 ]
• Infectious and intoxicative processes contribute to damage to the vascular walls.

If you know and take into account the main provoking factors, then you can determine the basic rules for preventing the disease. [ 15 ]

Pathogenesis

The development of atherosclerosis of the abdominal aorta is caused by a combination of factors, in particular, endothelial dysfunction, inflammatory response, immunological process, dyslipidemia, plaque rupture, external negative influences (for example, smoking).

The endothelium produces substances necessary to control the blood coagulation function and metabolic processes in the brain, regulate vascular tone and blood pressure, filtering renal function and contractile cardiac activity. The first stage of atherosclerosis development is provoked by a violation of the endothelial vasodilator function, which, in turn, is a consequence of the loss of nitric oxide by the endothelium. Dysfunction of the endothelium is also caused by increased cholesterol levels in the blood, diabetes mellitus, long-term hypertension, and nicotine addiction. The disorder occurs under the influence of oxidation of low-density lipoproteins. [ 16 ]

• Inflammatory processes in atherosclerosis were observed in almost all cases. They involved macrophages, cytokines, monocyte chemotactic protein, growth factors, interleukin-1, -3, -6, -8, -18, tumor necrosis factor α, CD40 ligand. Atherosclerotic development is also associated with serum C-reactive protein. Elevated levels of lipoprotein-associated phospholipase increase the likelihood of complications; the involvement of cytokines, which induce cell proliferation and stimulate the production of active oxygen forms, activate matrix metalloproteinases and expression of tissue factor, is also possible.
• Lipid disorders are an important factor in the development of abdominal aortic atherosclerosis. The risk is particularly increased with serum cholesterol levels greater than 3.9 mmol/liter.
• Increased pressure in the cerebral and coronary arterial vessels increases the tension of the vascular wall, which negatively affects regenerative processes and contributes to the formation of pathological protrusions. [ 17 ]
• Nicotine dependence has a negative impact during all stages of atherosclerosis development, and this impact is quite intense: endothelium-dependent vasodilation worsens, proinflammatory factors (including C-reactive protein, interleukin-6 and tumor necrosis factors α) increase, platelet NO availability decreases, oxidative modification of LDL increases and plasma paraoxonase activity decreases.
• Elevated insulin levels lead to an increase in the content of cytokines (-6 and MCP-1), which contribute to the growth of atherosclerotic processes.

Particularly important underlying factors are considered to be an increase in LDL and a decrease in HDL. The former accumulate in atherosclerotic plaques (foam cells), which entails mitochondrial dysfunction, apoptosis and necrosis, with the release of cellular proteases, proinflammatory cytokines and thrombotic molecules. Oxidation of LDL provokes inflammatory and immune changes, platelet aggregation increases, and plaques become unstable. [ 18 ]

High-density lipoproteins promote the activation of cholesterol reversal, support endothelial function, and protect against increased thrombus formation.

The main pathogenetic links in the development of atherosclerosis are considered to be:

• Disorder of fat metabolism.
• Non-fatty changes (hemodynamic disorders, deterioration of blood rheological properties, primary pathologies and damage to the vascular wall, genetic predisposition).

There is evidence that myostatin (a skeletal muscle growth inhibitor involved in metabolic disorders and cardiac fibrosis) is a new player in the progression of atherosclerosis. According to the study, myostatin mediates the progression of abdominal aortic atherosclerosis by causing vascular smooth muscle cell dysfunction. [ 19 ]

Symptoms atherosclerosis of the abdominal aorta.

Atherosclerosis of the abdominal aorta in most cases occurs without specific symptoms, but the pathology can be detected during diagnostic measures. Non-specific signs appear as the disease progresses:

• discomfort in the abdomen and lower back;
• regular abdominal pain that intensifies after eating (especially after a large meal);
• digestive disorders without an obvious cause (diarrhea, constipation, bloating);
• unpleasant belching, regular heartburn after eating;
• progressive emaciation.

As other organs become involved in the process, other symptoms appear:

• pain in the kidney and/or groin area;
• swelling of the extremities;
• swelling of the face in the morning;
• urinary disorders;
• increased blood pressure.

Since the symptoms are non-specific, the patient may be misdiagnosed and given the wrong treatment. Moreover, abdominal aortic atherosclerosis often coexists with other pathologies, including chronic ones, which also complicates the correct diagnosis.

First signs

In most patients, atherosclerosis of the abdominal aorta begins to develop at a young age, progressing over the years. Moreover, for a long time, the patient does not complain about anything at all, and the first signs begin to appear only when a large artery narrows significantly or becomes blocked.

Among the most typical pathological signs are the following:

• pain in the epigastrium, not associated with stomach diseases, radiating to the lower back, groin;
• digestive disorders, heartburn, not associated with pathologies of the gastrointestinal tract;
• cold feet;
• a feeling of tingling, numbness in the legs;
• male impotence;
• decreased muscle tone in the lower limbs;
• weakness or absence of arterial pulsation in the area of the feet, knees, and groin;
• the appearance of intermittent claudication (when the lesion spreads to the vessels of the lower extremities).

If atherosclerosis affects not only the abdominal but also the thoracic part of the aorta, then chest pain appears after physical exertion or stress, radiating to the back or neck, as well as heartburn, a feeling of discomfort in the chest, without connection with cardiac pathology. [ 20 ]

If the pathology spreads to the renal arteries, arterial hypertension develops. [ 21 ] Urine examination reveals proteinuria, erythrocyturia, and cylindruria. Damage to the cerebral arteries manifests itself in memory loss and intellectual impairment, dizziness, sleep disturbance, and in severe cases, the risk of stroke and thrombosis increases.

With atherosclerotic changes in the mesenteric arteries, the blood supply to the intestines worsens, severe pain appears several hours after eating - localized in the umbilical area or epigastrium. The pain can last for several hours (usually 1-3 hours), in many cases it goes away after taking Nitroglycerin.

Stages

In its development, atherosclerosis of the abdominal aorta goes through the following stages:

1. Vascular microdamages and focal slowing of blood flow favor the deposition of lipids in the aortic wall. The duration of the lipid stage may vary: fat deposits and diffuse thickening of the intima and proteoglycans of the extracellular matrix [ 22 ] can only be seen microscopically.
2. The stage of liposclerosis is accompanied by an increase in areas of connective tissue in the areas of fat deposition. An atherosclerotic plaque gradually forms, the composition of which is represented by fats and connective tissue fibers. At this stage, plaques can still be eliminated, since they can be dissolved with medication. However, fragments of these deposits can clog blood vessels, and the aortic wall in the area of the attached plaque loses elasticity and is damaged: the risk of thrombus formation increases at this point.
3. The atherocalcinosis stage is characterized by plaque compaction and deposition of calcium salts in it. Plaques increase in size, narrowing the lumen of the vessel, worsening the blood supply to the organs. The risk of occlusion or aneurysm increases.

The clinical stages of development of atherosclerosis of the abdominal aorta are as follows:

1. The person leads a normal life, has no associated symptoms, and the pathology can only be detected using a Doppler study.
2. The patient begins to complain of abdominal pain after eating a large meal.
3. Abdominal pain appears even after a normal, light meal.
4. The pain becomes constant and intensifies after eating.

Forms

There are several variants of classification of abdominal aortic atherosclerosis. Thus, according to the course of the inflammatory process, the disease is divided into complicated and uncomplicated. The type and location of the pathological process are also distinguished: atherosclerosis can affect the proximal segment of the abdominal aorta, the infrarenal section, or the entire abdominal part of the vessel.

• Atherosclerosis of the abdominal aorta and its branches is most often accompanied by a clinical picture of abdominal ischemic disease, which is otherwise called chronic abdominal ischemia syndrome, or abdominal toad. The patient may complain of a feeling of heaviness and fullness in the abdomen, epigastric pain without obvious irradiation, dysfunction of the stomach and intestines, and stable weight loss. Functional systolic murmur in the epigastric zone is noted. [ 23 ]
• Atherosclerosis of the abdominal aorta and iliac arteries is called Larisch syndrome. This is a clinical symptom complex that develops against the background of severe narrowing or complete blockage of the abdominal aorta. Characteristic symptoms include intermittent claudication, no pulse on the dorsum of the foot, as well as in the popliteal and femoral artery, the formation of trophic ulcers on the fingers and feet, decreased systolic blood pressure in the legs, a constant feeling of cold feet, and impaired libido. Externally, there is muscular hypotrophy of the lower extremities, signs of trophic disorders on the skin and nails, and systolic noise in the abdominal aorta and femoral artery.
• Obliterating atherosclerosis of the abdominal aorta is caused by blockage of the vessel lumen by an atherosclerotic plaque and can be observed in the area of branching of the main trunk, or in the area of its division into branches of the first and second order. The pathology is predominantly unilateral, although bilateral lesions also occur.
• Stenosing atherosclerosis of the abdominal aorta is caused by stenosis of the vessel and is characterized by the appearance of abdominal attacks, which have an unfavorable prognosis and can end in ischemic disorders, reversible intestinal dystrophy or thrombosis and intestinal infarction.

Complications and consequences

The most common adverse effects of abdominal aortic atherosclerosis are considered to be the development of an aortic aneurysm or a dissecting hematoma of the aorta. This is a local expansion of a vascular section associated with increasing weakness of its walls, or an intramural hematoma leading to vessel dissection. A pulsating tumor-like formation appears in the abdominal cavity, located at the level of the navel or slightly below it, on the left. Rupture is dangerous for an aneurysm, when the vessel breaks through into the abdominal cavity or retroperitoneal space. With a dissecting hematoma, death may occur due to progressive blood loss. The patient experiences severe pain, collapse may develop, symptoms of acute blood loss appear; typically, there are no signs of myocardial infarction on the electrocardiogram. The aneurysm may manifest itself as a rough systolic murmur. [ 24 ]

Additional signs of an aneurysm may include:

• pressing, pulling, aching pain in the abdomen and lower back without an obvious cause;
• a feeling of pulsation, a sensation of the presence of a pulsating formation inside the abdomen.

Signs of developing complications in the form of a rupture of the abdominal aorta:

• sudden onset or increase of pain;
• severe lumbar pain radiating to the groin area, inner thighs, genitals;
• symptoms resembling myocardial infarction
• reduction of blood pressure;
• signs of increasing anemia;
• vomiting blood, etc.

Due to the lack of specificity of the clinical picture, complications are often mistaken for other diseases. Therefore, a qualified and comprehensive approach to each patient is very important: according to statistics, in 70% of cases, when an aneurysm becomes complicated, an incorrect diagnosis is made, which leads to extremely unfavorable consequences. If medical assistance is not provided in time, the patient with a rupture dies within a few hours. [ 25 ]

However, aneurysm and dissection of the abdominal aorta are not the only possible complications. Atherosclerosis eventually leads to cellular hypoxia and necrotic processes in tissues. The vascular walls lose elasticity, become dense and fragile, prone to damage. Intravascular plaques increase in size, can break off and block smaller vessels. The main complications of this kind include:

• spread of the atherosclerotic process to vascular branches, including capillaries;
• insufficient oxygen supply to the myocardium and brain, to the abdominal organs;
• vascular stenosis, the beginning of the development of necrotic processes;
• atherosclerotic plaque rupture, vascular occlusion;
• development of necrosis, gangrene (for example, of the intestines);
• myocardial infarction, cardiac ischemia, stroke, renal failure;
• Cases of penetrating atherosclerotic ulcers of the abdominal aorta have been described. [ 26 ]

Early competent diagnostics allows to identify existing disorders and conduct appropriate treatment in a timely manner. Atherosclerosis of the abdominal aorta in the early stages can be stopped if all medical recommendations are followed.

Left ventricular hypertrophy and aortic wall thickness may predict lifetime cardiovascular disease risk.[ 27 ]

Diagnostics atherosclerosis of the abdominal aorta.

Physical examination should include mandatory palpation of the abdominal area, followed by percussion and auscultation of the abdominal cavity using a phonendoscope. Pulse and blood pressure measurements are taken separately.

Tests often include measurements of total cholesterol, LDL, HDL, and triglycerides.

Blood analysis helps to determine the general condition of the aortic bed and assess the likelihood of atherosclerosis. The most indicative assessment criteria are:

• total cholesterol level with a norm of 3.1-5.2 mmol/liter;
• HDL (good cholesterol) level with a norm of 1.42 (women) and 1.58 (men);
• LDL (bad cholesterol) level with a norm of up to 3.9 mmol/liter;
• triglyceride level with a norm of 0.14-1.82 mol/liter;
• atherogenic index (good cholesterol in relation to bad) with a norm of up to 3.

Instrumental diagnostics includes the following studies:

• Aortic radiography – helps to detect changes in vessel size, the presence of calcium deposits or aneurysm. The dilated aorta is manifested by an increase in the transverse size of the shadow, an increase in the protrusion of the aortic arches into the lung fields. From the anterior-left oblique projection, the shadow becomes expanded, the aortic window increases in size. The elongated vessel changes size upward and to the right and forms the right upper contour of the vascular shadow, strongly protruding into the area of the shadow of the superior vena cava. Increased pulsation is noted during fluoroscopy of the aneurysm.
• Contrast-enhanced X-ray aortography helps determine the location and size of existing aneurysms or areas of vessel narrowing. A doubled contour of the abdominal aorta is a sign of wall dissection.
• Two-dimensional ultrasound allows detecting such pathological changes as thickening, compaction, parietal calcification, roughness of the inner vascular wall, curvature or elongation of the artery, the presence of atherosclerotic plaques. An aneurysm is indicated if there is a limited protrusion of the wall or a diametrical increase in the abdominal aorta by two times, compared to the normal value.
• X-ray computed tomography and MRI clearly reveal morphological abnormalities in the aorta and major branches. [ 28 ] Allows the evaluation of indices for classifying the location, severity and progression of calcified lesions of the abdominal aorta. [ 29 ]
• The selective angiography method is prescribed if surgical intervention is planned.

Pathological examination of the atherosclerotic plaque demonstrates the following changes:

• protein-fat detritus in the center;
• around the circle - connective tissue.

Macro specimen for examination: aorta and large or small arteries of muscular and muscular-elastic type. Lipid spots and stripes, fibrous structures, calcification, less often ulcerations, thrombotic masses are detected.

Differential diagnosis

Differentiation should be carried out with the following pathologies:

• appendicitis;
• inflammation of the gallbladder;
• inflammation of the pancreas;
• nephrolithiasis, cholelithiasis;
• gastric ulcer and duodenal ulcer;
• pseudoabdominal ischemia.

It is important to promptly differentiate the pathology from glomerulonephritis, pyelonephritis, renal amyloidosis, renovascular (vasorenal) arterial hypertension, atherosclerosis of the renal vessels, polycystic kidney disease, fibromuscular aplasia, nonspecific aortoarteritis, primary aldosteronism, pheochromocytoma, Itsenko-Cushing syndrome, coarctation of the aorta, aortic valve insufficiency, congestive heart failure.

As a rule, an ECG, echocardiogram, and ultrasound of the abdominal organs are performed to clarify the diagnosis. Less often, angioscopy, digital subtraction angiography, and optical coherence tomography are used.

Treatment atherosclerosis of the abdominal aorta.

If the patient does not notice any pathological symptoms, has a low risk level (less than 5% according to SCORE), and the total cholesterol level exceeds 5 mmol/liter, then treatment involves only lifestyle correction:

• elimination of smoking and other bad habits;
• change in diet;
• maintaining physical activity.

After normalizing the level of total cholesterol to 5 mmol/liter, and LDL to 3 mmol/liter, regular preventive examination is prescribed every 3-5 years.

Patients with a high risk according to SCORE and a total cholesterol level of more than 5 mmol/liter should also change their lifestyle with control laboratory diagnostics after 3 months. If the situation stabilizes after this period, then preventive diagnostics are prescribed annually. If the indicators are unstable or if typical symptoms of atherosclerosis are present, conservative treatment is prescribed.

Drugs that eliminate hyperlipidemia are represented by several classes of medications: statins (drugs that inhibit HMG-CoA reductase), Ezetimibe, sequestrants (drugs that bind bile acids), fibrates, nicotinic acid preparations, polyunsaturated fatty acids, lipase inhibitors. [ 30 ]

• Statins are drugs that inhibit HMG-CoA reductase: Lovastatin, Simvastatin, Atorvastatin, Pravastatin, Fluvastatin, Rosuvastatin.
• Drugs that inhibit cholesterol absorption in the intestine: Ezetemibe is an active hypocholesterolemic agent.
• Bile acid sequestrants are drugs that enhance the elimination of bile acids from the body, the basic product of cholesterol metabolism (Cholestyramine, Colestipol).
• Fibric acid derivatives – fibrates – are represented by Gemfibrozil, Bezafibrate, Ciprofibrate, Fenofibrate, Clofibrate.
• Nicotinic acid preparations – niacin – have a hypocholesterolemic property and reduce lipoprotein levels.
• Omega-3 polyunsaturated fatty acids in sufficiently large doses (up to 4 g per day) eliminate hypertriglyceridemia.

In case of atherosclerosis of the abdominal aorta, combination therapy is appropriate, which allows stopping the development of the pathological process and preventing the occurrence of complications.

Medicines

Conservative treatment most often involves the use of the following medications:

• Anticoagulants - for example, Heparin at an initial dosage of 5 thousand U by injection under the control of blood clotting, or Enoxaparin sodium at 20-40 mg per day in the form of subcutaneous injections, or Nadroparin calcium at 0.2-0.6 ml in the form of subcutaneous injections 1-2 times a day (depending on the patient's weight).
• Antiplatelet agents – for example, acetylsalicylic acid in the amount of 75-325 mg daily orally, or Clopidogrel 75-300 mg daily orally, or Dipyridamole 50-600 mg per day orally. Patients should take such drugs for a long time (sometimes for life), under regular laboratory monitoring. Chaotic intake of drugs in large doses can lead to hemorrhagic complications, the appearance of signs of heart failure.
• To relieve pain, the following is prescribed:
  • non-steroidal anti-inflammatory drugs, if there are no contraindications (Ketorol, Ibuprofen), paravertebral blocks;
  • opioids (Morphine, Fentanyl) – in severe cases, if non-steroidal anti-inflammatory drugs do not help.
• Drugs that normalize microcirculation and improve the condition of blood vessels (angioprotectors):
  • Pentoxifylline 100-300 mg by injection;
  • Alprostadil 20-60 mcg injection daily.

Possible side effects when taking angioprotectors may include allergic reactions, abdominal pain, and digestive disorders. [ 31 ]

• Anticholesterolemic drugs are taken for several months (usually up to a year, depending on the cholesterol levels in the blood). Simvastatin and Atorvastatin are usually prescribed orally. Side effects such as allergies, myopathy, and dyspeptic symptoms rarely develop.
• Pathogenetic treatment drugs are often represented by β-blockers - Propranolol, Bisoprolol, Metaprolol. The dosage is standard, the therapy is carried out under regular monitoring of heart rate and blood pressure. These drugs are discontinued gradually.

Diet for atherosclerosis of the abdominal aorta

Diet correction is an effective way to stop the development of atherosclerosis. And this method is in no way inferior to drug therapy, and often even surpasses it. Many doctors point out that one should not rely only on drugs: without changes in nutrition, one cannot count on a stable and long-term effect from treatment.

As a rule, patients with abdominal aortic atherosclerosis are prescribed diet table No. 10 - the corresponding dietary nutrition normalizes the cholesterol level in the blood and slows down the progression of the disease. In addition, the diet includes a large amount of plant products rich in dietary fiber and polyunsaturated fatty acids, which help increase the amount of "good" cholesterol.

In addition to following a diet, it is important to monitor food calorie intake. With little physical activity, you should not consume more than 2,500 kilocalories per day. And for overweight patients, a doctor can help you choose the daily calorie intake.

In case of atherosclerosis, animal and hydrogenated fats are prohibited, as they contribute to an increase in cholesterol levels and its deposition on the vascular walls. It is important to exclude the following products from the diet:

• fatty meat, lard;
• butter, margarine, vegetable fat mixtures, lard;
• offal (including liver);
• broths made from meat or bones;
• sausages, hot dogs, frankfurters;
• any parts of poultry except skinless fillets;
• milk, hard cheese, fatty cottage cheese, cream, condensed milk, sour cream, ice cream;
• fast food;
• potato;
• sauces;
• sugar, baked goods, confectionery.

You should also limit your alcohol consumption, or better yet, eliminate it altogether.

The diet should include the following products:

• peeled chicken and turkey fillet;
• milk-fed veal;
• fish, seafood;
• fermented milk products (low-fat cottage cheese, kefir, yogurts without additives);
• eggs (no more than 2 per week);
• any vegetables, fruits, greens, berries;
• durum wheat pasta;
• cereals (buckwheat, rice, barley, wheat, oatmeal, bulgur, couscous);
• legumes (beans, chickpeas, mung beans, lentils, peas);
• dark bread, bran;
• herbal teas, green tea, dried fruit compotes, fruit drinks;
• dried fruits.

You should never neglect dietary correction. Diet plays a fundamental role in the treatment of atherosclerosis, and also serves as a preventative measure against complications, in particular, myocardial infarction and other cardiovascular pathologies. [ 32 ]

Physiotherapy treatment

Physiotherapy is an effective treatment using natural and physical factors. These are thermal effects, ultrasound effects, magnetic fields, laser, water, therapeutic mud, massage, etc. The methods are usually simple and at the same time extremely effective: with a minimum of side effects, an intensive positive effect is noted, allowing to reduce the dosage of the medications used. A particularly pronounced effect is noted if physiotherapy is used in the early stages of the development of pathology.

For atherosclerosis of the abdominal aorta, the most common types of physiotherapy procedures are the following:

• Electrophoresis with novocaine, as well as vasodilators, antiplatelet, anti-inflammatory drugs, anti-inflammatory agents. Potassium iodide, sodium salicylate, heparin, lithium, zinc, multivitamin preparations, magnesium sulfate, nicotinic acid, mesaton, etc. are often used.
• Darsonvalization has a pronounced antispasmodic effect on the vascular wall, as a result of which it relieves spasms and improves blood flow. The effect is explained by the irritation of nerve receptors by impulse currents.
• Hyperbaric oxygenation is a method of oxygen saturation under high pressure. Special hyperbaric chambers are used for the procedure.

Sanatorium and resort treatment includes balneotherapy and mud therapy. A pronounced positive effect is found after taking hydrogen sulphide, carbon dioxide, iodine-bromine, pearl, turpentine baths.

Application of natural mud is indicated for patients with stage 1-2 atherosclerosis.

Herbal treatment

Atherosclerosis of the abdominal aorta in the early stages of development responds well to treatment with folk remedies, provided that lifestyle is corrected and bad habits are eliminated. [ 33 ] The most common and effective herbal medicine recipes are considered to be the following:

• 1 tbsp. of buckwheat flowers is brewed in a thermos in 1 liter of boiling water, infused for an hour, filtered. Take 100 ml three times a day between meals.
• Peel 300 g of garlic, pour into a container and add 0.5 l of vodka. Keep in a dark place for a month, then filter and take 20 drops daily with 100 ml of milk, between meals.
• Take 1 tbsp. of birch leaves, brew 300 ml of boiling water, leave to cool, filter. Take 100 ml three times a day half an hour before meals.
• Pour 1 tbsp. of hawthorn flowers with 300 ml of boiling water, leave to cool, filter. Take 100 ml three times a day half an hour before meals.
• Take 2 tbsp. rose hips, pour into a thermos, add 300 ml of boiling water. Infuse for 15 minutes, filter. Take 100 ml three times a day 20-30 minutes before meals.
• Drink the juice of one lemon daily, during or after meals.
• Squeeze 200 ml of onion juice, mix with 200 ml of honey. Store this remedy in the refrigerator and take 1 tbsp. three times a day between meals for 8-10 weeks.
• Prepare a mixture of 10 g lemon balm, 10 g betony, 40 g hawthorn flowers, 30 g strawberry leaves. Brew 1 tbsp of the mixture with 300 ml of boiling water and drink instead of tea throughout the day (you can add honey for taste).
• Take 100 g of fresh sage herb, pour 500 ml of vodka and leave for one and a half months in a dark place. Then filter the tincture and take 1 tbsp. with water in the morning and before meals, 3 times a day in total.
• Squeeze the juice from fresh horseradish root. Mix half and half with honey and take 1 tbsp. in the morning, an hour before the first meal. Duration of treatment is 1 month.

Surgical treatment

If conservative therapy is ineffective or inappropriate, the patient is prescribed invasive treatment – therapeutic apheresis – plasmapheresis and LDL apheresis. Surgical treatment may be required in case of high risk or established development of arterial occlusion – thrombus or plaque. If atherosclerosis affects the heart vessels and the risk of myocardial infarction increases, coronary artery bypass grafting is performed.

Cardiac surgery involves open interventions or minimally invasive endovascular surgeries. For example, to eliminate ischemic processes in the lower half of the body and to stabilize hemodynamics, vascular stenting is prescribed. And in the case of aortic aneurysm, prosthetics and endoprosthetics of the abdominal aorta are indicated. [ 34 ]

If the diametrical size of the pathological protrusion in an aneurysm is less than 50 mm, then the patient undergoes drug therapy aimed at normalizing cardiovascular activity with regular monitoring. If the diameter of the aneurysm is equal to or exceeds 50 mm, then surgical treatment is prescribed to prevent aortic rupture. Also, an indication for surgery may be a protrusion with a diameter of 30 mm, with an annual rapid increase in size by 6 mm.

Surgical treatment can be performed at any age, if the patient does not have the following contraindications:

• acute cerebrovascular or coronary circulatory disorders with obvious neurological insufficiency;
• circulatory failure stage II-b or III.

Abdominal aortic surgery for atherosclerosis

Abdominal aortic replacement is performed using an open approach (15-20 cm incision) or a mini-approach in the form of an incision on the abdominal wall of about 5-7 cm. The surgeon treats the surgical field, makes the necessary incisions, and clamps the abdominal aorta above and below the affected area. The aneurysm is excised and a pre-prepared vascular implant is sewn in place of the removed segment. After making sure the sutures are tight, the doctor installs drains and sutures the wound. The most common vascular implants are those impregnated with silver: they are more resistant to infectious effects. The intervention lasts about 3.5 hours, then the patient is transferred to the intensive care unit, where his condition is monitored for 24 hours. The general term of hospital stay is about a week (provided there are no complications). [ 35 ]

A more modern surgical method is considered to be aortic endoprosthetics. The damaged segment of the abdominal aorta is replaced with a special vascular prosthesis, which is placed directly in the aneurysm cavity under X-ray observation. Such a technique allows to prevent a large number of complications, reduce the patient's stay in the hospital, and speed up rehabilitation. Perhaps the only drawback of such an intervention is its high cost. [ 36 ]

Possible contraindications to surgical treatment:

• sepsis;
• severe disorders of vital organs, such as acute liver or kidney failure, cerebrovascular accidents, myocardial infarction, etc.

Prevention

To determine the most effective prevention of the development of atherosclerosis of the abdominal aorta, it is necessary to remember the main risk factors and try to influence them:

• get rid of bad habits – in particular, smoking and drinking alcohol;
• maintain adequate blood cholesterol levels, have regular blood tests;
• monitor blood pressure readings;
• normalize body weight, lead an active lifestyle;
• avoid emotional tension and stress;
• eat properly and with high quality.

If the main predisposing factors are eliminated, it is possible to prevent and slow down the development of the disease and prevent the occurrence of adverse complications.

It is important to plan your diet wisely and reduce the consumption of foods that contain a lot of cholesterol. These include animal fats and butter, eggs, fatty dairy products, and offal. You should also avoid easily digestible carbohydrates, sweets, and sugar. Preference should be given to vegetable oils, fish, white meat, seafood, and plant foods. Fiber and complex carbohydrates should have a special place in the menu. The proportion of raw vegetables, fruits, and greens should make up ¾ of the diet, due to the high content of pectin in plant foods, which inhibits the absorption of cholesterol in the intestines. [ 37 ]

Proteins are also a very important component of the diet. The body can get them from white meat of poultry, fish, legumes, and greens.

It is important to monitor your body weight, prevent the development of obesity, quit smoking and not abuse alcohol.

Sufficient physical activity is the key to normal heart function and sufficient oxygen supply to the myocardium. In addition, regular physical exercise prevents excess weight gain and maintains normal vascular tone. The degree of physical activity is proportionate to age and general health. It is optimal to practice walking for 30-40 minutes daily.

In addition, prevention should be supplemented by eliminating stressful situations, preventing overwork of the body. It is important to train stress resistance, establish a high-quality work and rest regime, and normalize night sleep.

Forecast

Today, one of the main areas of activity of cardiologists is the search for solutions for the optimal treatment of atherosclerosis of the abdominal aorta. It should be taken into account that this pathology is a prerequisite for the development of irreversible pathological processes - in particular, coronary heart disease, renal artery stenosis, aortic aneurysm, ischemic stroke, etc. [ 38 ]

Prognosis for patients varies, they cannot be unambiguous, as they depend on the patient's age and the presence of concomitant diseases, the stage of the pathological process, etc. If you follow all the doctor's recommendations (changes in nutrition, elimination of bad habits, high-quality and timely drug treatment), then the prognosis can be relatively favorable, since further development of the disease can often be slowed down. If you ignore the recommendations, break the diet, smoke, etc., then the risk of complications increases significantly: aortic aneurysm, myocardial infarction, stroke, etc. [ 39 ]

Unfortunately, it is impossible to completely get rid of the disease: atherosclerosis of the abdominal aorta is a chronic disease with gradual progression of pathological changes.

Disability

Obtaining a disability group for atherosclerosis of the abdominal aorta is possible if severe functional disorders of organs have developed as a result of pathological processes, and loss of working capacity has occurred. Despite the fact that the disease is very common, and its complication is often fatal, disability is assigned not because of the atherosclerotic lesion itself, but as a result of the development of adverse consequences.

A patient may be declared incapacitated if he or she has the following complications:

• microstroke, stroke;
• acute coronary circulatory disorder;
• aortic stenosis and aneurysm.

Any of the above conditions, as well as paralysis of the limbs, cerebrovascular accidents may be grounds for registration of disability based on the results of medical and social examination. Atherosclerosis of the abdominal aorta without clinical manifestations or with signs that can be corrected with medication is not an indication for disability.