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EAA - exogenous allergic alveolitis ECG - electrocardiography ECS - pacemaker, pacing

ERCP - endoscopic retrograde cholangiopancreatography EF

- electrophysiological EchoCG - echocardiography PUD - peptic ulcer UC - ulcerative colitis

ADA - adenosine deaminase deficiency AH - vascular damage

CDC (The Centers - Center for Disease Control, USA for Disease Control) ECM - extracellular matrix eNOS -

endothelial NO synthesis

ERK - signal-related kinase

FISH - fluorescent in situ hybridization

GRACE – Global Registry of Acute Coronary Events HCV - hepatitis C virus

HP - Helicobacter pylori

IFTA - interstitial fibrosis and tubular atrophy Ig - immunoglobulin

IL - interleukin

IM - mononuclear infiltration oLPS - lipopolysaccharide

LVPP - regimen including leukeran, vinblastine, natulan, prednisolone MALT lymphoma - Mucosal Associated Lymphoid Tumor

MCP - regimen including mitoxantrone, leukeran, prednisolone MDRD – Modification of Diet in Renal Disease

m-TOR is an animal target of rapamycin NDRD - non-diabetic kidney disease

NFAT - nuclear factor that activates T cells

NPM - nucleophosmin

PDGF - platelet growth factor

PG - peptidoglycan

PKC - protein kinase C

RAAS - renin-angiotensin-aldosterone system

SAP - SLAM-associated protein

SD - slit diaphragm

TCR - T cell receptor

TGF - transforming growth factor

TNFRI – tumor necrosis factor receptor I

UAE - urinary albumin excretion

WPW - Wolff-Parkinson-White syndrome

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FOREWORD

New data are constantly appearing in medical science and practice, which makes it necessary to regularly update the educational literature. This tutorial was written by the staff departments of therapeutic profile, having many years of teaching experience.

This allows us to hope that the textbook is presented in an accessible language for students and contains up-to-date information on the issues covered. This is a textbook for students, not a manual for physicians, so we have only touched on the basic data on all issues.

A good knowledge of the issues of propaedeutics of internal diseases will contribute to their better development.

A significant place in the textbook is given to questions of treatment, but given that the questions pharmacokinetics are discussed in detail in the relevant department, we present only

the main, main directions in the treatment of individual nosological forms. There are also possible options for the formulation of diagnoses, information is given on the differential dia

gnostics.

When writing the textbook, the authors adhered to the program approved by the Minister health care of the Russian Federation for medical higher educational institutions.

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Chapter 1

DISEASES OF THE

CARDIOVASCULAR SYSTEM

1.1. RISK FACTORS FOR CARDIOVASCULAR DISEASES

Definition. Risk factors are signs, the presence and / or severity of which correlated with the likelihood of developing cardiovascular disease or the onset of

death caused by them. The concept of cardiovascular risk factors is relevant to diseases whose morphological basis is atherosclerosis.

Classification. Risk factors for cardiovascular disease are usually divided into non-modifiable and modifiable. Non-modifiable risk factors include age, male sex, and a poor family history. Modifiable risk factors

There are more than 200 cardiovascular diseases. The main modifiable risk factors are smoking, dyslipidemia, arterial hypertension (AH),

diabetes mellitus (DM), obesity, low physical activity.

pathogenic significance. Each of the modifiable risk factors increases the likelihood of developing coronary heart disease (CHD). For example, smokers

the risk of developing coronary artery disease is 1.6 times greater than in non-smokers, in patients with hypertension - 3 times more,

than in persons with normal blood pressure (BP), in patients with hypercholesterolemia

- 4 times more than in persons without lipid metabolism disorders. Combination of the above

factors is accompanied by a significant increase in the individual risk of developing coronary artery disease.

So, with a combination of hypertension and smoking, the risk of coronary artery disease increases by 4.5 times, with a combination of smoking

and hypercholesterolemia - 6 times, with a combination of hypertension and hypercholesterolemia - 9 times, and with

combination of all three factors - 16 times.

Smoking contributes to the development of cardiovascular diseases mainly due to

due to endothelial damage, increased blood viscosity and platelet activation. The adverse effects of tobacco smoking include a decrease in the oxygen capacity of the blood,

a decrease in the content of high density lipoproteins (HDL) and an increase in the content of low density lipoproteins (LDL) in the blood, an increase in the level of fibrinogen. These

pathological effects contribute to the development of atherosclerosis and the formation of intravascular thrombi. The risk of cardiovascular disease increases in proportion to the number of cigarettes smoked. Smoking linked to myocardial infarction

(MI) and sudden death. Patients who continue to smoke after the development of myocardial infarction have more

higher risk of recurrent MI and death than patients who quit smoking. Smoking cessation leads to a rapid reduction in the risk of death in general and from cardiovascular diseases.

reasons in particular.

Dyslipidemias are a heterogeneous group of conditions characterized by a pathological increase (or decrease) in the blood plasma content of one or more lipoproteins. Between levels of total cholesterol (Cholesterol), LDL cholesterol and the risk of developing coronary artery disease there is a direct relationship. At the same time, between the level of HDL-C and the incidence

IHD is inversely correlated. A low level of HDL-C is often combined with an increased content of triglycerides (TG) in the blood, which also correlates with the risk of progression of atherosclerosis

and the development of coronary artery disease. Mortality from coronary artery disease increases progressively as

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increase in the level of total cholesterol and LDL cholesterol in the blood. A decrease in the severity of

dyslipidemia, on the contrary, makes it possible to slow down the progression of atherosclerosis and coronary artery disease.

High blood pressure has been linked to the risk of cardiovascular disease numerous epidemiological studies. It is currently considered that

AH is a leading risk factor for coronary artery disease, stroke, heart and kidney failure. Regular treatment of hypertension provides a significant improvement in the prognosis of patients cardiovascular diseases. So, with a stable decrease in blood pressure to the target level

the risk of stroke is reduced by 40%, the risk of MI by 8%. In a population, BP control allows reduce mortality from stroke by 40-50%, and mortality from coronary artery disease by 15-20%.

The presence of diabetes mellitus increases the risk of cardiovascular diseases in men by 2 times, in women by 3 times. The risk of death from cardiovascular diseases in patients

with diabetes mellitus is 3 times higher than in persons without diabetes mellitus. 75% of patients with diabetes people with diabetes die from cardiovascular causes, most often from MI and stroke. In the vast

majority of cases, adults develop type 2 diabetes mellitus,

which is not a lack of insulin, but the resistance of tissues to its action. In patients, suffering from type 2 diabetes mellitus, macroand microvascular lesions develop,

which are the morphological basis of IHD, chronic cerebrovascular insufficiency, diabetic nephropathy (DN), retinopathy and cardiomyopathy. Raise

risk of cardiovascular disease in patients with diabetes mellitus is mainly due to

in the form of an increase in the content of LDL and TG in the blood plasma and a decrease in the level of HDL, an increase in the oxidation of LDL (and, consequently, an increase in proatherogenic activity), an increase in the aggregation ability of platelets, an increase in the levels of fibrinogen and a plasminogen activator inhibitor in the blood, and progression of endothelial dysfunction. The control glycemia and a decrease in insulin resistance of tissues are considered the main condition for success primary and secondary prevention of cardiovascular diseases in patients with diabetes

type 2 diabetes and people with impaired glucose tolerance.

Obese individuals are 50% more likely to develop hypertension, and the risk of developing diabetes diabetes - 3-10 times (depending on the degree of obesity) higher than in people with normal

body weight. Of particular danger is the central type of obesity with a predominant deposition of fat in the abdominal region. The criterion for abdominal obesity is an increase in waist circumference of 8 102 cm in men and 8 88 cm in women.

metabolic syndrome, more stringent criteria for abdominal obesity apply: waist circumference for men 8-94 cm, for women 8-80 cm.

Visceral obesity is usually associated with carbohydrate and lipid disorders.

exchanges, hypertension and respiratory distress during sleep, which increases the likelihood of developing and

progression of coronary artery disease, as well as the risk of sudden death.

The association of a sedentary lifestyle with the development of cardiovascular diseases and overall mortality is confirmed by the results of numerous population studies. Physically active people are less likely to develop hypertension, coronary artery disease, stroke, diabetes mellitus, obesity, and the risk of death from all causes decreases. Regular exercise contributes to the utilization of oxygen by skeletal muscles, the normalization of blood pressure, and the reduction of TG levels.

and increase blood HDL levels, improve carbohydrate metabolism and reduce weight

body.

Calculation of individual risk. To assess the individual risk of death from cardiovascular diseases in the next 10 years, a table developed by

within the research project SCORE (Systemic Coronary Risk Evaluation). Scale SCORE is based on the results of studies conducted in European countries, including

Russia. Individual risk assessment is carried out taking into account gender, age, smoking status,

Blood pressure and total cholesterol levels in blood plasma. The risk is considered very high if it exceeds

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10%, high if it is in the range of 5 - 9%, moderate if the value is 1 - 4% and low,

if it is less than 1% (see color incl., fig. 1.1). The SCORE scale allows you to determine the risk

not only deaths from cardiovascular diseases, but also the overall risk of developing coronary artery disease and other non-fatal cardiovascular events in the next 10 years. For this you need

multiply the individual risk score by 3 for men and 4 for women. A more accurate calculation of risk is possible using modified SCORE scales developed taking into account the level

HDL cholesterol.

Since the factors used to estimate the risk of death from cardiovascular diseases, can be partially corrected by lifestyle changes and the use of drugs, the table allows you to clearly demonstrate to the patient

positive consequences of giving up bad habits, following dietary recommendations and medical treatment. In this regard, the SCORE table can be used to ensure patient adherence to the doctor'srecommendations.

The SCORE table is designed to assess the risk of death in individuals without clinical manifestations of cardiovascular disease. Assessment of the probability of death of patients with existing cardiovascular diseases and / or risk factors for their occurrence may be

carried out according to the methodology proposed by the experts of the Russian Society of Cardiology and the National Society for the Study of Atherosclerosis, taking into account the following features:

Categories of 10-year risk of death from cardiovascular diseases

Very high risk category:

-patients with ischemic heart disease and/or symptomatic atherosclerosis of peripheral arteries, ischemic stroke, confirmed by diagnostic methods (coronary angiography, radionuclide research methods, stress echocardiography, duplex scanning of arteries);

-Patients with type 2 diabetes mellitus or patients with type 1 diabetes mellitus and damage to target organs (microalbuminuria);

-patients with chronic kidney disease and symptoms of renal failure from the mind

– 10-year SCORE risk 8 10%. High risk category:

- at least one pronounced risk factor, for example, the level of total cholesterol > 8.0 mmol /

l or severe hypertension;

–10-year SCORE 8 risk of death 5% and < 10%. Moderate risk category:

–10-year risk of death on a SCORE 8 scale of 1% and <5%; further risk assessment is made taking into account the presence of a family history of early cardiovascular diseases (men < 55 years and women < 65 years), the presence of abdominal obesity, the degree physical activity, level of HDL cholesterol, TG, highly sensitive C-reactive protein lipoprotein

(a), fibrinogen, homocysteine, apolipoprotein B and social status. Low risk category:

–10-year SCORE risk < 1%.

It should be emphasized that risk assessment is now considered a mandatory component of the analysis of data obtained from the examination of a patient with a suspected or proven disease of the cardiovascular system.

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1.2. ATHEROSCLEROSIS

Definition. Atherosclerosis is a systemic disease characterized by

damage to all layers of the vascular wall of large and medium-sized arteries of the muscular type in the form local inflammation, endothelial dysfunction, lipid deposition, smooth muscle cell proliferation,

fibrous tissue development, and calcification leading to decreased

elasticity of the vascular wall, the formation of stenosis or occlusion, and impaired blood flow in the affected area of the vessel. The term "atherosclerosis" comes from the Greek words

"atere" - gruel and "sclerosis" - thickening, thereby reflecting the main morphological changes in the arteries in this disease - the formation of atherosclerotic plaques

with lipid core and fibrous capsule.

Prevalence. Atherosclerosis is an extremely common disease. Its first manifestations in the form of local accumulations of lipids - lipid strips

inside the intima of the arteries are found in children and adolescents. With age, the prevalence of atherosclerosis increases. Signs of atherosclerosis expressed to varying degrees

available in all people over 60 years of age. However, the rate of progression of atherosclerosis can vary significantly depending on the genetic and other individual characteristics, as well as the living conditions of the patient. In men, atherosclerosis develops earlier and is more common than in women. These differences are associated with the protective effect of estrogen, since

after the onset of menopause, they gradually smooth out.

Etiology. The concept of risk factors underlies modern ideas about

etiology of atherosclerosis. In addition to dividing into non-modifiable and modifiable, risk factors for atherosclerosis are divided into causal, predisposing and conditional. Causative factors include smoking, hypertension, hypercholesterolemia, and/or elevated cholesterol levels.

LDL in the blood, low HDL cholesterol, hyperglycemia. For predisposing factors

include male gender, obesity, physical inactivity, early manifestation of coronary artery disease in

immediate relatives (MI or sudden death in men before 55 years of age, in women - before 65 years of age), and also socio-economic, behavioral and ethnic factors. To conditional factors

include elevated blood triglyceride levels, high lipoprotein (a) levels, hyperhomocysteinemia, hyperfibrinogenemia, elevated blood levels of an activator inhibitor

plasminogen.

Pathogenesis. The current understanding of the pathogenesis of atherosclerosis is based on two main hypotheses: the lipid hypothesis and the hypothesis of chronic endothelial damage. These

hypotheses are not mutually exclusive. The mechanisms of atherogenesis described in each of them are closely

are interconnected.

The atherosclerotic process begins with damage to the endothelium, which is characterized by a violation of the cytoskeleton, a weakening of intercellular connections, and a change in the distance between cells. The causes of primary damage to the endothelium are diverse. Among them refers to the increase in the mechanical effect of blood on the vascular wall in hypertension. Exactly therefore, atherosclerotic plaques most often form at the sites of branching and bifurcation of the arteries, which are subjected to the most severe hemodynamic shock. Except

In addition, various exogenous and endogenous chemical factors have a damaging effect on the endothelium: tobacco smoke metabolites, catecholamines, angiotensin II, products of peroxidation and glycosylation. An important factor in the primary damage to the endothelium is bacterial and viral infection with concomitant immune responses.

(autoimmune) reactions.

In parallel with morphological disorders, endothelial dysfunction develops, which is expressed in the weakening of its antithrombogenic and antiadhesive properties. To the plots

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monocytes attach to damaged endothelium. Penetrating into the subendothelial space, monocytes are transformed into macrophages, which capture LDL modified as a result of peroxidation and turn into foam cells, clusters

which form lipid streaks. Oxidized LDL initiates a local inflammatory reaction, which results in the death of endothelial cells and progression of endothelial dysfunction. Stimulation of macrophages and endothelial cells by oxidized LDL promotes the release of cytokines. acting on smooth muscle

media cells, cytokines cause their proliferation and migration to the intima, which is accompanied by the transformation of smooth muscle cells into fibroblasts with complete or partial loss of contractile properties. In addition, cytokines stimulate the

secretion of collagen and other connective tissue proteins. As a result, inside the vascular wall is form fibrous capsule separating the lipid core of an atherosclerotic plaque from others

fabrics. The composition of the lipid core of an atherosclerotic plaque includes foam cells, extracellular lipids - mainly cholesterol and its esters, shells of destroyed cells. As maturation in atherosclerotic plaques calcium accumulates.

Lipids are a variety of substances vital for the human body.

However, lipid metabolism disorders are associated with an increased risk of

atherosclerosis. The important role of dyslipidemia in the genesis of atherosclerosis was first demonst in classical experimental studies by N. N. Anichkov and S. S. Khalatov (1912).

Subsequently, the significance of dyslipidemia as a risk factor for atherosclerosis has been repeatedly confirmed in clinical studies and has been studied in detail.

The main lipids in human blood plasma are TG, phospholipids and cholesterol. TG are esters of the trihydric alcohol glycerol and higher fatty acids. TG serve

the main source of energy for working muscles. The half-life of TG in plasma is relatively short, they are rapidly hydrolyzed and taken up by various tissues (the main

way, adipose tissue). After ingestion of a fatty meal, the plasma TG level rises markedly and remains high for several hours. CS belongs to the group of steroids. Non-esterified (free) cholesterol is a structural component of cell membranes and is involved in ensuring their selective permeability. In the human body, cholesterol

necessary for the synthesis of bile acids, steroid and sex hormones. cholesterol is synthesized in the liver from acyl coenzyme A. The key enzyme in the synthesis of cholesterol is 3-

hydroxy-3-methy lglutaryl-coenzyme A reductase (HMG-CoA reductase). The main source of exogenou CS are food products of animal origin, however, its intake into the body from the outside

is not mandatory, since the amount of endogenous synthesized in

liver cholesterol is enough to fully meet the needs of the body. With an excess

free cholesterol in liver cells, the enzyme acylcholesterol acetyltransferase is activated, which catalyzes the formation of cholesterol esters, i.e. its metabolically inert form, in the form of which the depot of cholesterol is created. Phospholipids are esters of glycerol or sphingosine containing fatty acids and phosphoric acid. Phospholipids,

together with cholesterol, are part of cell membranes, forming their structural basis, the phospholipid bilayer.

Due to the fact that plasma lipids are hydrophobic compounds and not

dissolve in aqueous media, they are transported in the form of special spherical particles - lipoproteins. The core of such a particle consists of esters of CS and TH, the shell - of free cholesterol, phospholipids and proteins - apolipoproteins. Apolipoproteins have an affinity for various receptors and enzymatic activity. Blood plasma lipoproteins differ in size,

density, protein composition, and electrophoretic activity. There are five classes of lipoproteins: chylomicrons (XM), very low density lipoproteins

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(VLDL), intermediate density lipoproteins (LDL), low density lipoproteins (LDL), high density lipoproteins (HDL) (Table 1.1).

Table 1.1

Main characteristics of blood plasma lipoproteins

XM are the largest particles, containing predominantly TG. The main function of HM

– transfer of TG from the intestine, where they are absorbed, into the blood and then to the place of use as an energy source. In peripheral capillaries, most of the triglyceride contained in HM is cleaved under the influence of lipoprotein lipase to fatty acids and

glycerin. Fatty acids are utilized by myocytes or, having undergone reesterification, deposited in adipose tissue in the form of TG. Residual, or remnant, CM particles containing

CS enter the liver, where they are completely destroyed. The atherogenicity of HM has not been proven, however, HM remnants are atherogenic. VLDL compared to HM have less

sizes, contain less TG, but more cholesterol, phospholipids and protein. VLDL are formed mainly in the liver and serve to transfer endogenous TG from the liver to the muscles. After hydrolysis of TG contained in VLDL, they, like HM, are converted into remnant particles

(or DILI), which are then transferred to the liver. DILI are atherogenic and can

taken up by macrophages. Unlike HM remnants, LPPP are not utilized in the liver, but under the influence of hepatic lipoprotein lipase are transformed into LDL, which contain

the maximum amount of cholesterol and are characterized by the greatest atherogenicity.

Each LDL particle contains one apolipoprotein B-100 macromolecule, which binding of LDL to a specific receptor is mediated. After binding to the receptor, the LDL

particle is captured by the liver cell, where it is lysosomally destroyed. The number of LDL receptors located on one cell varies from 15 to

70 thousand. The formation of LDL receptors is regulated by a mechanism that is sensitive

to the content of intracellular cholesterol, according to the feedback principle. Therefore, with excess intake of dietary cholesterol, which is captured by liver cells from the remnants of cholesterol

and is included in the intracellular pool of free cholesterol, the number of LDL receptors decreases. As a result, there is an accumulation of LDL cholesterol in the blood plasma. An insufficient number of LDL receptors may also be due to a genetic defect, which

is the cause of familial (hereditary) hypercholesterolemia.

HDL is synthesized in the liver and intestines. These particles capture cholesterol in cells organism and transfer it to the liver, providing the so-called "reverse transport of cholesterol

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sterol." With its own antioxidant effect, HDL prevents oxidation

LDL. In addition, HDL can stimulate endothelial production of prostacyclin, a compound with vasodilating and antiaggregatory effects. So

Thus, HDL prevent the development of atherosclerosis.

In addition to the five main classes of lipoproteins, lipoprotein (a) is also isolated. Particles lipoprotein (a) are identical in lipid composition to LDL, but additionally contain apo lipoprotein (a), a polymorphic protein, structurally similar to plasminogen. Isolated particles of lipoprotein

(a) are capable of spontaneous aggregation, an increase in their content in plasma is associated with an increased risk of coronary thrombosis.

The concentration of total cholesterol, HDL cholesterol and TG in plasma (serum) is determined chemical or enzymatic methods. To determine the concentration of VLDL cholesterol

and LDL, the calculation method is applied. The most important parameter for the choice of treatment tactics is the level of LDL cholesterol, which is calculated according to the formula of WT Friedwald [et al.]:

LDL-C = Total-C - HDL-C - TG: 5 (in mg/dL)

or

LDL cholesterol \u003d Total cholesterol - HDL cholesterol - TG: 2.2 (in mmol / l)

The formula is applicable at TG levels not exceeding 4.5 mmol/L.

Optimal values of lipid parameters of blood plasma depending on the category risk are given in table. 1.2.

Table 1.2

Optimal values of lipid parameters of blood plasma depending on risk category (mmol/l)

When determining the risk of developing atherosclerosis, it is advisable to evaluate the ratio lipoproteins with atherogenic and anti-atherogenic properties. For this, a special indicator proposed by A. N. Klimov is used - the atherogenic coefficient, which is calculated by the following formula:

CA \u003d (Total Cholesterol - HDL Cholesterol): HDL Cholesterol

It is considered normal to consider the values of the coefficient of atherogenicity, not exceeding 4.0.

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In 1965, Fredrickson proposed a classification of hyperlipidemias, which in

1970 was approved by the WHO as an international one. This classification provides for the allocation of 6 types of hyperlipidemia (Table 1.3). In daily practice there are

predominantly hyperlipidemia IIa, IIb and IV types.

Table 1.3

Classification of hyperlipidemias

*Type IV is atherogenic if it is accompanied by a low concentration of HDL cholesterol, as well as other metabolic disorders: hyperglycemia, insulin resistance, impaired glucose tolerance.

With an excess of lipoproteins in the blood plasma, they are captured by macrophages. This the process is also regulated by the feedback principle: when a certain concentration of lipoproteins in the macrophage cytoplasm is reached, their entry into the cell stops.

The mechanism that regulates the uptake of lipoproteins by macrophages is disrupted upon admission to cells of modified (predominantly oxidized) lipoproteins. Thereby

there is an overload of macrophages with lipoproteins and their transformation into foam cells, accumulations of which form lipid bands in the subendothelial space. After the destruction of the foam cells, their content, mainly cholesterol and its esters, enters

extracellular space and form the lipid core of an atherosclerotic plaque.

The slow growth of atherosclerotic plaques that occurs over a number of years can lead to severe stenosis of the affected vessel and the development of chronic ischemia

area of tissue in the pool of its blood supply. Distinguish between stable and unstable state of atherosclerotic plaque. A stable atherosclerotic plaque has a dense lipid core and a relatively strong cap. An unstable condition of atherosclerotic plaque develops as a result of thinning, cracking or ulceration

tires due to an increase in its tension due to the rapid growth of the lipid core and the progression of the inflammatory process. An important role in reducing the mechanical strength of the atherosclerotic plaque cap is played by T-lymphocytes, which produce

gamma-interferon, which inhibits collagen synthesis, as well as macrophages and mast cells, which produce proteases that destroy the connective tissue matrix of the capsule. Under the influence of external physical factors (amplification of the pulse wave due to an increase in BP or tachycardia, sudden vasodilation or vasospasm), tire integrity may

break down. Upon contact of the blood flowing through the vessel with the contents of atherosclerotic plaques, a cascade of coagulation reactions is triggered, as a result of which on the surface

or a thrombus forms inside the damaged plaque, completely or partially blocking the lumen of the vessel. Occlusion or sudden narrowing of the vessel lumen causes acute ischemia

organ (tissue) in the pool of its blood supply with the corresponding clinical symptoms.

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