Non-stenotic atherosclerosis

Cholesterol deposits and plaque on the inner walls of vessels may not completely block the arterial lumen, but only narrow it, which leads to vascular insufficiency of a certain degree. In this situation, a diagnosis of "non-stenotic atherosclerosis" is made. This is an early stage of well-known atherosclerotic changes, in which the complete closure of the artery is far away, but the process has already started. The danger of this condition is that the clinical picture of pathology is mostly hidden, the symptoms are non-intense. As a result, patients do not hurry to seek medical help, and the disease in the meantime continues to worsen. [1]

Epidemiology

Non-stenotic atherosclerosis is a common chronic pathology, which is characterized by the lesion of large arterial vessels. Such arteries actively transport oxygen, nutrients, hormones to organs and tissues. The largest vessel that affects atherosclerosis is the aorta.

In non-stenosing atherosclerosis, the internal arterial walls are gradually covered with plaque or nodules composed mainly of lipids and calcium. Simultaneously with the plaque, the vessels lose elasticity and the arterial lumen narrows to less than half. If this narrowing continues to progress, we are talking about the stenotic (obliterating) form of the pathology - a dangerous condition in which blood circulation deteriorates sharply and the risk of complications increases.

According to statistical data, there is a clear predominance of the disease among the male population. Thus, men suffer from atherosclerosis 3.5 times more often than women. In most cases, the pathology affects middle-aged and elderly people (from 40-45 years old and above).

The prevalence of non-stenotic atherosclerosis in the world has its own peculiarities. For example, the disease is extremely widespread among the American population. It is often the cause of death, and even overtakes cancer in this respect. But in the southern regions, the problem is much less common. For comparison, in Americans, coronary atherosclerosis accounts for more than 42% of all cardiovascular disorders, and in Italians this figure rarely exceeds 6%. In African countries, the incidence is even rarer.

The highest percentage of people with atherosclerosis is found in the United States, Australia, Canada, Great Britain and Finland. The lowest percentage is expected to be found in Japan, which is due to dietary and lifestyle habits.

The main reason for the development of pathology scientists call the failure of fat and protein metabolism, which leads to the formation of the well-known plaques. The impetus for such a failure is given by improper nutrition, and aggravate the situation with stress, weak immunity, hormonal and genetic disorders in the body, as well as trauma to the vessels. Additional negative contribution is made by bad habits, poor physical activity, diabetes mellitus and other endocrine and cardiovascular diseases. [2]

Causes of the nonstenotic atherosclerosis.

Elevated cholesterol is the underlying cause of non-stenotic atherosclerosis. The buildup of lipids and calcium on the inner wall of the arteries provokes a persistent disorder of blood flow. Additional causes include the following:

• Alcohol abuse - disrupts the course of metabolic processes, impairs the nervous system, contributes to the circulation of large amounts of cholesterol in the blood.
• Overweight, obesity of any degree - causes a pronounced metabolic disorder and diseases of the digestive system, impairs digestion, impedes the work of all organs and systems.
• Prolonged or systematic increase in blood pressure can be both a consequence and a precursor of non-stenotic atherosclerosis. In many patients, lipid deposits are formed as a result of hypertension, contributing to blood clotting and circulatory disorders.
• Stresses - disrupt the nervous system, upset the processes of supply and assimilation of nutrients and oxygen in the tissues, impede the removal of toxins and cholesterol from the bloodstream.
• Smoking - causes vasospasm, their deformation, which generally leads to impaired blood circulation and promotes the deposition of cholesterol plaques.
• Improper nutrition - implies over saturation of the body with animal fats, trans fats, sugars, which worsens the condition of vascular walls and creates favorable conditions for layering of fat and calcium deposits.
• Hypodynamia - causes slow blood flow, as a result of which tissues and organs begin to lack oxygen and nutrients, and metabolic processes slow down.

Risk factors

The main reason for the development of non-stenosing atherosclerosis is the improper metabolism of cholesterol in the body. Factors contributing to the development of the pathological process are:

• Age. The risks of developing nonstenotic atherosclerosis increase significantly in virtually all people over the age of 40.
• Male gender. In men, pathology develops earlier and more often than in women. Scientists attribute this to the peculiarities of nutrition, lifestyle and hormonal background.
• Hereditary predisposition. Many people are genetically predisposed to disorders of lipid metabolism, cardiovascular pathologies, disorders of hormonal balance. A certain role is also played by the activity of immunity.
• Harmful habits. Smoking and alcohol abuse contribute to the activation of the development of non-stenosing atherosclerosis.
• Obesity. Superfluous even a few kilograms much complicate the work of the body, which leads to a violation of metabolic processes and increased load on the vascular system.
• Diabetes Mellitus. People suffering from diabetes get complications such as heart attack, stroke, hypertension and vascular atherosclerosis in most cases.
• Improper nutrition. Irrational, chaotic, poor-quality nutrition with harmful products, predominance of meat fatty foods in the diet is the main factor in the development of both non-stenosing and stenosing (obliterating) atherosclerosis.

Pathogenesis

The development of non-stenotic atherosclerosis includes all stages and factors that contribute to the onset of the pathological process. However, a special role is played by the processes of atherogenic lipoproteinemia and increased permeability of arterial wall membranes. It is these factors that lead to subsequent damage to the vascular endothelium, accumulation of plasma modified lipoproteins in the intimal membrane, proliferation in the intima of smooth muscle cells and macrophages with further transformation into "foam cells", which are directly related to the formation of all atherosclerotic transformations.

The pathogenetic essence of the atherosclerotic process is as follows. Mushy lipid-protein detritus appears in the arterial intima, connective tissue grows focally, which becomes the basis for the formation of atherosclerotic layering, narrowing (stenosing, obliterating) the vascular lumen. The lesion primarily affects muscular-elastic and elastic vessels, medium and large-caliber vessels. The processes of formation of non-stenosing atherosclerosis go through successive morphogenetic stages:

• The appearance of lipid spots and streaks;
• the formation of fibrous plaques;
• the appearance of ulceration of plaques, hemorrhages and accumulation of thrombotic masses;
• atherocalcinosis.

Lipid spots and streaks are areas of yellowish-grayish color, sometimes merging but not rising above the surface of the intimate membrane. Fatty inclusions are present in these spots.

Fibrous plaques also contain fat, but they rise above the surface of the intima. Sometimes merge with each other. More often affect those vascular areas that undergo hemodynamic impact. In particular, the bifurcation areas of arteries are more often affected - that is, places with unevenly distributed blood flow.

Atheromatous changes occur against the background of predominant breakdown of lipid-protein complexes and the formation of detritus resembling the contents of atheroma. The aggravation of such changes leads to destruction of the plaque cover, ulceration, intraplaque hemorrhage and formation of thrombotic layers.

Atherocalcinosis is the final stage of atherosclerotic changes. Calcium salts are deposited in fibrous plaques, calcium calcification, petrification, deformation of the vascular wall occurs. [3]

Symptoms of the nonstenotic atherosclerosis.

The clinical picture is most often latent and does not correspond to the morphologic stage of the disease. Only with increasing obliteration of the vascular lumen, symptoms of ischemia of the corresponding organ may occur. The predominant lesion of one or another arterial basin is typical, which determines the symptomatology of non-stenotic atherosclerosis.

Coronary lesions usually cause a picture of coronary insufficiency and, in particular, signs of coronary heart disease. Atherosclerotic changes in cerebral arteries are manifested by signs of transient cerebral ischemia or strokes. When the vessels of the extremities are affected, there is intermittent claudication, dry gangrene. Involvement in the process of mesenteric arteries entails ischemia and infarction of the intestine (so-called mesenteric thrombosis). If the renal arteries are affected, Goldblatt syndrome may develop. [4]

First signs of non-stenotic atherosclerosis

The initial manifestations are nonspecific and depend on the specificity of the affected vessel.

When the brachycephalic arteries are affected, various structures of the brain suffer from nutritional deficiency. Patients complain of weakness, dizziness when turning the head sharply or changing the position of the body, and "goosebumps" in front of the eyes.

In some patients, the first signs of non-stenotic atherosclerosis are tinnitus in the ears or head, transient numbness of the extremities. Often among the first complaints there is a headache, which is difficult to control with conventional painkillers. In addition, patients become distracted, concentration suffers, insomnia, increased fatigue.

Early detection of pathological symptoms and contacting doctors is an important step in preventing the development of stenosing atherosclerosis, which causes arterial blockages and other related complications.

Non-stenotic atherosclerosis of brachiocephalic arteries

Nutrients are delivered to the brain via the main vessels, particularly the carotid artery and the brachiocephalic trunk, which form the closed circle of Willis. In non-stenotic atherosclerosis, the supplying vessels are not completely blocked, but all brachiocephalic arteries are narrowed, resulting in an incorrect distribution of blood and a decrease in its overall flow.

Among the most likely symptoms:

• tinnitus in the ears and head;
• seizure-like dizziness;
• transient darkening of the eyes, appearance of flies in front of the eyes;
• intermittent sensations of numbness in the upper extremities.

Nonstenotic atherosclerosis of extracranial sections of brachiocephalic arteries is more pronounced:

• there are frequent and quite severe head pains;
• concentration of attention is disturbed, speech and memory are affected, and sometimes personality changes are noted.

If you pay attention to your own health, non-stenotic atherosclerosis of the main arteries of the head can be suspected in the early stages of development and thus prevent the development of formidable complications. The main vessels of the head are important blood arteries that provide blood flow to the structures of the brain. Non-stenotic atherosclerosis of cerebral arteries poses a risk of possible neuronal death, development of strokes, deterioration of brain functions.

Non-sclerosing atherosclerosis of lower limb arteries

Lesions of the arteries of the lower extremities are somewhat less common than brachiocephalic arteries. This pathology also has its own clinical picture. In particular, patients in many cases voice the following complaints:

• contracture-like pain with a limp;
• sharp cramps in the lower extremities;
• pain while walking;
• cold feet;
• weakness of the pulse on the back of the foot.

Symptoms appear and disappear depending on the physical activity of the patient. With increasing physical activity, the picture worsens, and the symptoms that disappeared earlier return.

Non-stenotic atherosclerosis of the carotid arteries

Atherosclerotic lesions of the carotid arteries narrow the large blood supply vessels in the neck, called carotid arteries. These vessels branch off the aorta and then run along the neck and into the cranial cavity, transporting blood to the brain.

Signs of this disorder may include:

• transient sensations of numbness or weakness in the face or upper extremities, more often unilateral;
• impaired speech capabilities;
• visual impairment;
• frequent dizziness, balance problems;
• head pain (sudden, severe, unreasonable).

Blood pressure fluctuations are possible.

Non-stenotic aortic atherosclerosis

In non-stenotic atherosclerosis, the aorta is affected along its entire length or partially, for example, in the thoracic or abdominal section. Symptomatology is characterized by corresponding manifestations:

• painful and other unpleasant sensations in the abdominal or breast area;
• with an increase in systolic blood pressure;
• Auscultatory - a murmur in one or another aortic section.

Other possible manifestations include coughing, hoarseness of voice, headache, dyspepsia, etc., depending on the affected aortic segment.

For example, nonstenotic atherosclerosis of the abdominal aorta is most commonly manifested:

• acute abdominal pain, increasing after eating or exercise;
• digestive disorders, gastrointestinal malfunctions;
• nausea, heartburn;
• a pulsating sensation in the belly button area;
• swelling of the face and/or extremities.

In thoracic lesions, non-coronary chest pain, dizziness and fainting, and paresthesias of the upper extremities are noticed.

Diffuse non-stenotic atherosclerosis

The term "diffuse" means "mixed, scattered". It means that in this form of the disease, different arteries leading to the heart, brain, limbs, etc. Are affected simultaneously. Diffuse non-stenotic atherosclerosis can cause the development of threatening complications, such as heart failure, heart attack and stroke, liver, kidney and lung pathologies.

Patients have sclerosis of multifocal peripheral vessels, trophic ulcers occur. Among the main symptoms:

• headaches;
• tinnitus;
• balance problems;
• a feeling of weakness and fatigue;
• memory impairment, strokes and paralysis;
• heart or abdominal pain;
• difficulty breathing;
• nausea, digestive distress;
• tachycardia, shortness of breath;
• blood pressure fluctuations;
• decreased performance.

Diffuse non-stenosing atherosclerosis is a chronic disease leading to a deficit in blood supply to internal organs: it requires urgent medical consultation.

Complications and consequences

The main complication of non-stenosing atherosclerosis is its transition to the stenosing form, in which the latent course becomes clinically apparent. Subsequent possible deterioration is conditionally divided into ischemic, thrombotic and sclerotic.

• Ischemic complications are manifested by symptoms of ischemic heart disease, including the appearance of angina attacks, the development of cerebral ischemia, impaired blood circulation in the area of renal, femoral and mesenteric arteries. Heart failure gradually increases, irreversible changes in the myocardium appear.
• Thrombotic complications include acute circulatory failure, development of thrombosis, thromboembolism, sudden strokes or heart attacks.
• Sclerotic complications are due to the replacement of parenchyma by scar tissue, they are associated with the development of hepatic, renal failure and brain dysfunction.

Diagnostics of the nonstenotic atherosclerosis.

In order to establish an accurate diagnosis of non-stenosing atherosclerosis and to determine the localization of the affected vessels, it is necessary to consult several specialists at once: cardiologist, pulmonologist, gastroenterologist, angiosurgeon. Based on the collected history of life and disease, the specialist can suspect one or another problem in the patient's body.

It is obligatory to conduct an external examination of the patient, perform some functional tests. Then the patient is referred to additional laboratory and instrumental diagnostic procedures.

Most significant laboratory tests:

• The HC indicator (total cholesterol, with a normal range of 3.1 to 5.2 mmol/liter).
• HDL (high-density lipoproteins, with a normal of 1.42 in women and 1.58 in men).
• LDL (low-density lipoproteins, with a norm of 3.9 mmol/liter or less).
• Triglyceride reading (TG, with a normal range of 0.14 to 1.82 mol/liter).
• Atherogenicity index (demonstrates the ratio of high-density lipoproteins to low-density lipoproteins, the norm is up to 3).

To confirm the diagnosis of non-stenosing atherosclerosis, instrumental diagnostics is prescribed:

• electrocardiography with load and at rest;
• Vascular Doppler;
• Daily monitoring of blood pressure readings;
• angiography, coronary angiography;
• rheoencephalography, rheovasography;
• Ultrasound of the heart, carotid arteries, etc.

Immediately after conducting and evaluating the diagnostic results, the doctor makes a final diagnosis and prescribes the appropriate treatment. [5]

Echographic signs of non-stenotic atherosclerosis

One of the most frequent findings detected during ultrasound of the vessels of the heart, neck, extremities is non-stenotic or stenotic (obliterating) atherosclerosis. In most people over 40 years of age, the initial signs of atherosclerotic changes are already present, but with the right approach, further aggravation of the pathological process can be prevented or significantly slowed down. In contrast to severe forms of the disease, in non-stenosing atherosclerosis, the lumen is blocked by less than 50%, which slightly worsens blood flow, but does not block it completely.

The classification of stenoses on ultrasound is usually as follows:

• Echogenicity, ultrasound structure: echonegative, hypoechogenic, mesoechogenic, echogenic-mixed.
• Homogeneity of the ultrasound structure: homogeneous or heterogeneous.
• Shape: local, prolonged, eccentric, circular, undermined, shielding.
• Surface type: smooth, irregular, with ulceration, with elements of decay, mixed type, with intrabasal hemorrhage, with or without destructive changes of atheroma cover.

Additionally, the degree and localization of plaque accumulation, its size, changes in the angle of the artery bend, features of ulceration (if any), the presence of calcifications and other lesions are studied.

Differential diagnosis

Nonstenotic atherosclerosis of the carotid and cerebral arteries is distinguished from such pathologies:

• structural intracranial disorders (tumor processes, subdural hematoma, arteriovenous malformations);
• metabolic encephalopathy (sodium or calcium deficiency in the blood, hypoglycemia, non-ketogenic hyperglycemia, alcohol or drug intoxication, hepatic encephalopathy, etc.);
• traumatic brain injury;
• brain abscesses or encephalitis;
• MS;
• peripheral nerve disease;
• hypertensive encephalopathy, etc.

Thoracic aortic atherosclerosis is differentiated:

• from nonspecific aortoarteritis, aortitis (syphilitic, infectious, tuberculous, rheumatic, etc.);
• from coarctation of the aorta, aortic lesions in Marfan's syndrome;
• from a carotid stricture.

Nonstenotic atherosclerosis of the abdominal aorta and mesenteric arteries is differentiated with such diseases:

• cholecystitis, pancreatitis;
• kidney stone disease;
• gallstone disease;
• stomach ulcer.

Atherosclerotic lesions of the renal arteries should be distinguished from obliterative thrombangiitis (Buerger's disease). [6]

What is the difference between stenosing atherosclerosis and non-stenosing atherosclerosis?

Non-stenotic atherosclerosis is accompanied by the deposition of lipid plaques mainly along the vessels, which does not cause a sharp and significant reduction in the blood channel (less than ½ of the lumen is blocked). Blood supply is impaired, but not critically, complete occlusion does not occur.

In stenotic pathology, plaques increase across the vascular lumen, covering more than half of the available space. The risks of complete blockage of blood flow in this case significantly increase. This process leads much faster to severe complications - in particular, to thrombosis, ischemia and necrosis of the tissues of the supplied organ.

It can be understood that the non-stenotic type of pathology is less dangerous than the stenotic type. However, the insidiousness of the disease lies in the fact that without timely and competent medical care, the first type gradually progresses to the second type, which again becomes potentially life-threatening for the patient.

Treatment of the nonstenotic atherosclerosis.

In the absence of clinical manifestations, patients with nonstenotic atherosclerosis, moderate risk (less than 5% on the SCORE scale), with total cholesterol values greater than 5 mmol per liter are recommended lifestyle intervention, including:

• Quitting smoking and drinking alcoholic beverages;
• switching to a diet;
• optimizing physical activity.

As total cholesterol levels stabilize to 5 mmol per liter and LDL less than 3 mmol per liter, regular follow-up examinations are scheduled every 2 years.

If the patient's risks exceed 5% on the SCORE scale, and total cholesterol exceeds 5 mmol per liter, then treatment begins with changes in lifestyle and diet, with a follow-up examination after three months. Further control examinations are carried out annually. If the situation does not normalize, then additionally prescribe drug therapy.

If patients already have some symptoms and complaints associated with non-stenotic atherosclerosis, it is mandatory to prescribe, and lifestyle changes and drug treatment.

Four categories of hypolipidemic agents can be used. These are bile acid sequestrants (Cholestyramine, Colestipol), statins (Simvastatin, Rosuvastatin), fibrates (Clofibrate, Fenofibrate) and nicotinic acid. These drugs stabilize the atherosclerotic plaque, improve the condition of the inner surface of blood vessels, block the development of the pathological process and affect the quality of lipid metabolism. The choice of the drug is always made by the doctor individually. Most often prescribe statins - medications that successfully prevent most cardiovascular complications. The dose is selected specifically for each patient, the drug is taken daily at night. In addition, it is possible to use other drugs - for example, essential phospholipids, anticoagulants (Warfarin), angioprotectors (Detralex, Troxevasin), neuroprotectors (Piracetam).

Surgical treatment in non-stenosing atherosclerosis is practically not used, since the threat of complete disruption of blood flow through the affected artery is minimal. Surgery to restore the patency of vessels is more appropriate in stenotic (obliterative) pathology.

Statins

Statin drugs are able to significantly lower LDL-C by suppressing the production of cholesterol, increasing the activity of LDL-receptors, and removing low-density lipoproteins from the circulation. Thanks to statins, the condition of atherosclerotic plaque is stabilized:

• the lipid core shrinks in volume;
• the plaque is getting stronger;
• proliferation of smooth muscle cells decreases, the number of formed foam cells decreases;
• inhibits the inflammatory response;
• reduces platelet aggregation and the risks of thrombosis (both wall and intraplaque);
• endothelial function improves, reducing the likelihood of spasm.

It is possible to prescribe first and second generation statins. The first generation includes natural drugs: Lovastatin, Mevastatin, Simvastatin, Pravastatin. The second generation is represented by synthetic agents: Fluvastatin, Rosuvastatin, Atorvastatin.

Lovastatin and Pravastatin are considered the most effective for primary prevention, and Simvastatin and Pravastatin for secondary prevention. In case of signs of ischemia, Atorvastatin is recommended.

Possible side effects of statins include:

• Abdominal bloating, diarrhea, constipation, nausea, abdominal pain;
• head pain, dizziness;
• muscle twitching, muscle pain;
• deterioration of the liver;
• fatigue, sleep disturbances, itchy skin.

Such signs occur rarely (about 1.5% of cases) and disappear after dosage adjustment or drug withdrawal.

Contraindications to prescribing statins:

• pronounced liver dysfunction, initially high liver enzymes;
• periods of pregnancy and lactation;
• allergies to the drugs.

The use of HMG-CoA reductase inhibitors is discontinued if the patient develops a severe condition, including acute infectious disease, an attack of arterial hypotension, trauma, marked metabolic, electrolyte or endocrine disorders, as well as in case of the need for surgical intervention.

Diet

The principles of the diet involve the following changes:

• Reducing the proportion of foods containing cholesterol (total daily intake of cholesterol with food should not exceed 300 mg).
• Correction of the total caloric value of the diet (the optimal energy value per day is about 1.8-2 thousand calories).
• Minimize the share of fats to 25-30% of the total energy value (complete avoidance of fats is not recommended, it is desirable to replace animal fats with vegetable fats).
• Increased intake of polyunsaturated and monounsaturated fatty acids against a background of decreased intake of saturated fatty acids up to 8% of the total dietary energy value.
• Sharp restriction or complete refusal of simple easily digestible carbohydrates (sugar, jams, candies, etc.). In general, the proportion of carbohydrates in the diet should be about 55%, but it should be represented not by easily digestible sugars, but by fruits, berries, cereals, vegetables.

Few people know, but alcoholic beverages (in particular, beer and wine) significantly affect the increase in the level of high-density lipoproteins. Therefore, it is better to give up alcohol completely.

Severely restricted or completely eliminated from the diet:

• fatty meats, red meat;
• lard;
• offal (lungs, kidneys, liver, etc.);
• butter, margarine;
• cream, sour cream, full-fat milk;
• sugar.

If the patient is overweight, they are advised to take measures to reduce this weight and then maintain a normal weight for a longer period of time. It is optimal to reduce weight by approximately 10% over a six-month period.

Prevention

In addition to dietary correction and exclusion or minimization of cholesterol-containing products (see above) to prevent the development of non-stenosing atherosclerosis, it is important to eliminate adverse psycho-emotional influences, avoid depressive and stressful states, solve problematic household and work issues in a timely manner.

It is important to maintain normal physical activity:

• walk for at least half an hour every day or every other day;
• if possible, do gymnastics, swimming, cycling or brisk walking for 45 minutes 5-7 days a week;
• Get in the habit of walking instead of taking transit, taking the stairs instead of riding the elevator or escalator.

It is necessary to control your habits, stop smoking, do not overeat, give preference to high-quality and healthy food, avoid alcohol, control blood pressure readings.

For people at high risk of developing non-stenotic atherosclerosis, hypolipidemic drugs are prescribed simultaneously with lifestyle and dietary changes, regardless of low-density lipoprotein values. In addition, such patients are mandatorily prescribed antiaggregant therapy:

• acetylsalicylic acid in the amount of 75-325 mg per day;
• if the above drug is contraindicated, then Clopidogrel in the amount of 75 mg per day or Warfarin is used.

Diabetes patients should keep their blood sugar levels under control, get regular check-ups and follow their doctor's recommendations.

Forecast

The prognosis for a person with nonstenotic atherosclerosis can not be called unambiguous. If the patient carefully follows all medical recommendations (adheres to the diet, refuses bad habits, carefully takes prescribed drugs), then we can talk about a relatively favorable prognosis: the process of increasing atherosclerotic plaques can be significantly slowed down. In patients who do not follow the recommendations of doctors, the picture is not so optimistic, because they still have a high risk of stroke or myocardial infarction.

What should be done to prevent non-stenotic atherosclerosis from transforming into obliterative atherosclerosis with the development of life-threatening complications? At the appearance of the first suspicious symptoms, it is necessary to consult a cardiologist, and in the presence of risk factors, it is important to visit a doctor for preventive examination annually. Do not waste time on the use of unproven methods, supposedly able to "dissolve" cholesterol plaques. It is proven that to date, no means can do this: meanwhile, medications and diet can slow the growth of layers and prevent further aggravation of the pathological process.