Materials for preparing for a practical lesson on the topic: “Coronary heart disease. Cerebrovascular diseases"

1. Graphological structures

2. Lecture

3. Microspecimens

4. Illustrative material

5. Situational tasks

6. Test tasks

7. Standards of answers to test tasks

1. GRAPHYLOGICAL STRUCTURES Coronary heart disease

The essence of the disease: relative or absolute ischemia of a limited area of ​​the myocardium.

Background diseases: atherosclerosis, hypertension.

Risk factors: hyperlipidemia, hypertension, physical inactivity, psycho-emotional stress, smoking, family history, obesity.

Course: acute, chronic.

Forms of IHD

acute: ischemic myocardial dystrophy, myocardial infarction;

chronic: atherosclerotic small-focal cardiosclerosis, post-infarction large-focal cardiosclerosis, chronic cardiac aneurysm.

Localization: infarction of the anterior, posterior, lateral wall of the left ventricle, interventricular septum, papillary muscles, subendocardial, intramural, transmural.

Stages of development of a heart attack:

pre-necrotic;

necrotic;

organizations;

post-infarction changes.

Complications: cardiogenic shock, myocardial rupture, thromboembolism, pericarditis, acute or chronic heart failure, pulmonary edema.

Cerebrovascular disease

Essence of the disease: acute cerebrovascular accidents and their consequences.

Background diseases: atherosclerosis, hypertension, less often - symptomatic hypertension, etc.

Pathogenesis: psycho-emotional stress; spasm, paresis of blood vessels, plasma impregnation of their walls; thrombosis, thromboembolism of the cerebral, carotid, vertebral arteries.

Clinical and anatomical manifestations: transient cerebral ischemia; hemorrhages in the brain substance, subarachnoid space (hemorrhagic stroke); ischemic cerebral infarction (ischemic stroke).

Localization: subcortical nodes, cerebellum, pons (hemorrhagic stroke); cerebral cortex, less often - subcortical nodes (hemorrhagic infarction).

Outcome: transient disorders are reversible; hemorrhagic and ischemic strokes - formation of cysts.

Meaning: dysfunction of the brain depending on the location and volume of the process.

Consequences: paralysis, paresis, death.

2. LECTURE Coronary heart disease

Relevance of the problem

Coronary heart disease (CHD) is a group of diseases caused by absolute or relative insufficiency of coronary circulation. Therefore, coronary disease is coronary heart disease. It is identified as an “independent disease”. World Health Organization in 1965 due to its great social significance. Coronary disease is now widespread throughout the world, especially in economically developed countries. The danger of coronary heart disease is sudden death. It accounts for approximately 2/3 of deaths from cardiovascular diseases. Men aged 40-65 years are most often affected.

Coronary heart disease is a cardiac form of atherosclerosis and hypertension, manifested by ischemic myocardial dystrophy, myocardial infarction, and cardiosclerosis.

Coronary heart disease occurs in waves, accompanied by coronary crises, i.e. episodes of acute (absolute) coronary insufficiency occurring against the background of chronic (relative coronary insufficiency). In this regard, acute and chronic forms of coronary heart disease are distinguished.

Acute coronary heart disease is morphologically manifested by ischemic myocardial dystrophy and myocardial infarction, chronic ischemic heart disease (CHD) - by cardiosclerosis (diffuse small-focal and post-infarction large-focal), sometimes complicated by chronic cardiac aneurysm.

Ischemic myocardial dystrophy, or acute focal myocardial dystrophy, develops during relatively short-term episodes of coronary crisis, when characteristic changes in the electrocardiogram occur in the absence of myocardial necrosis (there is no increase in the activity of transaminases, lactate dehydrogenase, etc.). The myocardium is flabby and pale, in areas of ischemia it is sometimes mottled and edematous. Often a fresh thrombus is found in the coronary artery.

Macroscopically, when treating the cut surface of the myocardium with a solution of tetrazolium salts, potassium tellurite, ischemic areas look light against the dark background of unchanged myocardium, because in ischemic areas the activity of redox enzymes is sharply weakened and therefore formazan grains, as well as reduced tellurium, do not fall out.

Microscopically, dilatation of capillaries, stasis and sludge phenomenon of erythrocytes, edema of interstitial tissue, perivascular hemorrhages, and accumulations of leukocytes along the periphery of the ischemic zone are found. Muscle fibers lose their cross-striations, are deprived of glycogen, they are intensely stained with eosin, fuchsin, pyronin and Schiff's reagent, which indicates necrobiotic changes. Stained with acridine orange, they give a green, rather than orange, glow in a fluorescent microscope, which makes it possible to distinguish the ischemic zone from the intact myocardium. Polarization optical detection reveals an abundance of contractures. Early electron microscopic and histochemical changes are reduced to a decrease in the number of glycogen granules, a decrease in the activity of redox enzymes (especially dehydrogenases and diaphorases), swelling and destruction of mitochondria and the sarcoplasmic reticulum. These changes, associated with impaired tissue respiration, increased anaerobic glycolysis and uncoupling of respiration and oxidative phosphorylation, appear within a few minutes from the onset of ischemia.

A complication of ischemic myocardial dystrophy is most often acute heart failure, which also becomes the direct cause of death.

Myocardial infarction is ischemic necrosis of the heart muscle. Typically this is

ischemic (white) infarction with a hemorrhagic rim. Myocardial infarction is usually classified according to a number of characteristics:

by the time of its occurrence;

by localization in various parts of the heart and cardiac muscle;

by prevalence;

with the flow.

Myocardial infarction is a temporary concept.

Primary (acute) myocardial infarction lasts approximately 8 weeks from the moment of myocardial ischemia. If myocardial infarction develops 8 weeks after the primary (acute) one, it is called a recurrent infarction. A heart attack that develops within 8 weeks of the primary (acute) is designated as a recurrent myocardial infarction.

Myocardial infarction is most often localized in the area of ​​the apex, anterior and lateral walls of the left ventricle and the anterior sections of the interventricular septum, i.e., in the basin of the anterior interventricular branch of the left coronary artery, which is functionally more burdened and more strongly affected by atherosclerosis than other branches. Less commonly, a heart attack occurs in the area of ​​the posterior wall of the left ventricle and the posterior sections of the interventricular septum, i.e., in the basin of the circumflex branch of the left coronary artery. When the main trunk of the left coronary artery and both of its branches are exposed to atherosclerotic occlusion, extensive myocardial infarction develops. In the right ventricle and

especially in the atria, infarction rarely develops. The topography and size of the infarction are determined not only by the degree of damage to certain branches of the coronary arteries, but also by the type of blood supply to the heart (left, right and middle types). Since atherosclerotic changes are usually more intense in a more developed and functionally burdened artery, myocardial infarction is more often observed with extreme types of blood supply - left or right. These features of the blood supply to the heart make it possible to understand why, for example, in case of thrombosis of the descending branch of the left coronary artery, in different cases the infarction has different localization (anterior or posterior wall of the left ventricle, anterior or posterior part of the interventricular septum). The size of the infarction is determined by the degree of stenosis of the coronary arteries, the functional capacity of collateral circulation, the level of closure (thrombosis, embolism) of the arterial trunk, and the functional state of the myocardium. With hypertension, accompanied by hypertrophy of the heart muscle, heart attacks are more common.

Topographically distinguished:

subendocardial infarction;

subepicardial infarction;

intramural infarction (localized in the middle part of the wall of the heart muscle);

transmural infarction (with necrosis of the entire thickness of the heart muscle.

When the endocardium is involved in the necrotic process (subendocardial and transmural infarctions), reactive inflammation develops in its tissue, and thrombotic deposits appear on the endothelium. With subepicardial and transmural infarctions, reactive inflammation of the outer lining of the heart is often observed - fibrinous pericarditis.

According to the prevalence of necrotic changes in the heart muscle, they are distinguished:

finely focal;

large-focal;

transmural myocardial infarction.

IN There are two stages in the course of myocardial infarction:

necrotic stage;

scarring stage.

At the necrotic stage, small areas of preserved cardiomyocytes are microscopically detected perivascularly. The area of ​​necrosis is delimited from the preserved myocardium by a zone of congestion and leukocyte infiltration (demarcation inflammation). Outside the focus of necrosis, uneven blood supply, hemorrhages, disappearance of glycogen from cardiomyocytes, the appearance of lipids in them, destruction of mitochondria and sarcoplasmic reticulum, and necrosis of single muscle cells are noted.

The stage of scarring (organization) of a heart attack begins essentially when macrophages and young fibroblastic cells replace leukocytes. Macrophages take part in the resorption of necrotic masses; lipids and tissue detritus products appear in their cytoplasm. Fibroblasts, having high enzymatic activity, participate in fibrillogenesis.

The organization of the infarction occurs both from the demarcation zone and from “islands” of preserved tissue in the necrosis zone. This process lasts 7–8 weeks, however, these periods are subject to fluctuations depending on the size of the infarction and the reactivity of the patient’s body. When a heart attack occurs, a dense scar forms in its place. In such cases we talk about

post-infarction macrofocal cardiosclerosis. The preserved myocardium, especially along the periphery of the scar, undergoes regenerative hypertrophy.

Complications of a heart attack are cardiogenic shock, ventricular fibrillation, asystole, acute heart failure, myomalacia (melting of necrotic myocardium), acute aneurysm and cardiac rupture (hemopericardium and tamponade of its cavity), parietal thrombosis, pericarditis.

Death from myocardial infarction can be associated both with the myocardial infarction itself and with its complications. The immediate cause of death in the early period of a heart attack is

ventricular fibrillation, asystole, cardiogenic shock, acute heart failure.

Deadly complications of myocardial infarction in the later period are cardiac rupture

or its acute aneurysm with hemorrhage into the pericardial cavity, as well as thromboembolism (for example, cerebral vessels) from the cavities of the heart, when the source of thromboembolism becomes blood clots on the endocardium in the area of ​​infarction.

Cerebrovascular diseases Classification of cerebrovascular diseases

I. Brain diseases with ischemic damage

1. Ischemic encephalopathy

2. Ischemic cerebral infarction

3. Hemorrhagic cerebral infarction

II. Intracranial hemorrhages

1. Intracerebral

2. Subarachnoid

3. Mixed

III. Hypertensive cerebrovascular diseases

1. Lacunar changes

2. Subcortical leukoencephalopathy

3. Hypertensive encephalopathy

The following main groups of diseases are distinguished:

1) brain diseases associated with ischemic damage - ischemic encephalopathy, ischemic and hemorrhagic cerebral infarction;

2) intracranial hemorrhages;

3) hypertensive cerebrovascular diseases - lacunar changes, subcortical leukoencephalopathy, hypertensive encephalopathy.

The clinic uses the term stroke (from the Latin in-sultare - to jump), or brain stroke. Stroke can be represented by a variety of pathological processes: - hemorrhagic stroke

Hematoma, hemorrhagic impregnation, subarachnoid hemorrhage; - ischemic stroke - ischemic and hemorrhagic infarction.

Brain diseases caused by ischemic damage. Ischemic encephalopathy. Stenosing atherosclerosis of the cerebral arteries is accompanied by disturbances in maintaining a constant level of blood pressure in the vessels of the brain. Chronic ischemia occurs. The most sensitive to ischemia are neurons, primarily pyramidal cells of the cerebral cortex and piriform neurons (Purkinje cells) of the cerebellum, as well as neurons of the Zimmer zone of the hippocampus. These cells exhibit calcium damage with the development of coagulative necrosis and apoptosis. The mechanism may be due to the production of neurotransmitters (glutamate, aspartate) by these cells, which can cause acidosis and opening of ion channels. Ischemia also causes activation of c-fos genes in these cells, leading to apoptosis.

Morphologically, ischemic changes in neurons are characteristic - coagulation and eosinophilia of the cytoplasm, pyknosis of the nuclei. Gliosis develops in place of dead cells. The process does not affect all cells. When small groups of pyramidal cells of the cerebral cortex die, they speak of laminar necrosis. Most often, ischemic encephalopathy develops at the border of the anterior and middle cerebral arteries, where, due to the characteristics of angioarchitectonics, there are favorable conditions for hypoxia - weak anastomosis of vessels. Foci of coagulative necrosis, also called dehydrated infarcts, are sometimes found here. With the long-term existence of ischemic encephalopathy, atrophy of the cerebral cortex occurs. A coma with loss of cortical functions may develop.

Cerebral infarctions. The causes of cerebral infarction are similar to those of ischemic heart disease, but in some cases, ischemia can be caused by compression of the vessel by outgrowths of the dura mater during brain dislocation, as well as a drop in systemic blood pressure.

Ischemic cerebral infarction is characterized by the development of colliquation necrosis of irregular shape ("focus of softening") - Macroscopically determined only after 6-12 hours. After 48-72 hours, a zone of demarcation inflammation is formed, and then resorption of necrotic masses occurs and a cyst is formed. In rare cases, a glial scar develops at the site of small necrosis.

Hemorrhagic cerebral infarction is often the result of embolism of the cerebral arteries and has a cortical localization. The hemorrhagic component develops due to diapedesis in the demarcation zone and is especially pronounced during anticoagulant therapy.

Intracranial hemorrhages. They are divided into intracerebral (hypertensive), subarachnoid (aneurysmal), mixed (parenchymal and subarachnoid - arteriovenous defects).

Intracerebral hemorrhages. They develop when microaneurysms rupture at the sites of bifurcations of intracerebral arteries in patients with hypertension (hematoma), as well as as a result

diapedesis (petechial hemorrhages, hemorrhagic impregnation). Hemorrhages

are most often localized in the subcortical ganglia of the brain and the cerebellum. The outcome is formed

cyst with rusty walls due to hemosiderin deposits.

Subarachnoid hemorrhages. Occur due to the rupture of large cerebral aneurysms

vessels not only atherosclerotic, but also inflammatory, congenital and traumatic

Hypertensive cerebrovascular diseases. Develop in people suffering

hypertension.

Lacunar changes. Presented by many small rusty cysts in the subcortical area

Subcortical leukoencephalopathy. Accompanied by subcortical axonal loss and

development of demyelination with gliosis and arteriolohyalinosis.

Hypertensive encephalopathy. Occurs in patients with a malignant form

hypertension and is accompanied by the development of fibrinoid necrosis of the vascular walls,

petechial hemorrhages and edema.

Complications of strokes. Paralysis, cerebral edema, brain dislocation with

herniations, breakthrough of blood in the cavities of the ventricles of the brain, leading to death

3. MICROPREPARATIONS

1. Atherosclerosis of the coronary arteries of the heart (environment hem., eos.).

Macroscopically: in the intima of the left coronary artery - atheromatous plaques - soft, mushy consistency, yellowish in color, bulging into the lumen of the vessel and narrowing it. The lumen of the artery is completely clogged with reddish-gray dry crumbling masses.

Microscopically: the center of the plaque is represented by amorphous atheromatous masses of pink color; the masses are delimited from the lumen of the vessel by connective tissue fibers - the plaque cap.

2. Myocardial infarction (environmental hem., eos.).

Macroscopically: by 24 hours from the moment of ischemia, the zone of necrosis (infarction) at autopsy becomes clearly defined: it is localized mainly in the myocardium of the left ventricle, has an irregular shape, a denser consistency than the surrounding tissues, a yellowish-gray color with a narrow perifocal zone of plethora and hemorrhages (hemorrhagic whisk).

Microscopically: the area of ​​myocardial infarction is represented by necrotic tissue, a sign of which is the absence of nuclei in cardiomyocytes. The area of ​​necrosis is delimited from the preserved myocardium by a zone of congestion and leukocyte infiltration (demarcation inflammation).

3. Organizing myocardial infarction (surrounding hem., eos.).

Macroscopically: yellowish-gray structureless masses localized in the thickness of the myocardium of the left ventricle are almost completely replaced from the periphery by dense whitish tissue.

Microscopically: in contrast to the previous drug, in the zone of demarcation inflammation, the development of granulation tissue is noted, consisting of a large number of newly formed thin-walled vessels, macrophages and fibroblasts. The growth of newly formed collagen fibers occurs into the infarction site both from the demarcation zone and from the “islands” of preserved tissue in the necrosis zone.

4. Myofibrosis of the heart, (environment according to Van Gieson).

Macroscopically: in the thickness of the myocardium of the left ventricle, a section reveals thin whitish layers that have a dense consistency and alternate with reddish-brown areas of muscle fibers.

Microscopically: in the preparation, between hypertrophied green cardiomyocytes there are small layers of red connective tissue. A synonym for cardiac myofibrosis is small-focal atherosclerotic cardiosclerosis.

5. Post-infarction cardiosclerosis (environment according to Van Gieson).

Macroscopically: by the sixth week of the disease, the area of ​​necrosis (infarction) is completely replaced by scar tissue. A section of the left ventricular myocardium reveals a compact focus of dense white tissue at the site of necrosis.

Microscopically: The preparation shows extensive fields of coarse fibrous connective tissue, stained red with picrofuchsin mixture. Around the scar, cardiomyocytes are increased in size, their nuclei are large and have a round shape - regenerative hypertrophy.

5. ILLUSTRATIVE MATERIAL (MACROPREPARATIONS)

Rice. 1 Pericarditis after myocardial infarction

Rice. 2 Hemopericardium as a result of rupture of the heart muscles during myocardial infarction

Lecture7

ISCHEMICDISEASEHEARTS. CEREBROVASCULARDISEASES

Coronary heart disease and cerebrovascular disease are widespread throughout the world, especially in economically developed countries. They are the main causes of death in people with cardiovascular pathology.

Cardiac ischemia(CHD) is a group of diseases caused by absolute or relative insufficiency of coronary circulation. In the vast majority of cases, IHD develops due to atherosclerosis of the coronary arteries, so there is a synonym for the name - coronary disease.

IHD was identified by WHO as an independent group of diseases in 1965 due to its great social significance. Until 1965, all cases of ischemic heart disease were described as a cardiac form of atherosclerosis or hypertension. The classification of IHD into an independent group was dictated by the epidemic increase in morbidity and mortality from its complications and the need to urgently develop measures to combat them.

Changes in the myocardium similar to ischemic heart disease develop much less frequently without atherosclerosis of the coronary arteries of the heart and are caused by other diseases leading to relative or absolute insufficiency of coronary circulation: congenital anomalies of the coronary arteries, arteritis, thromboembolism of the coronary arteries in thromendocarditis, impaired blood oxygenation in severe “cyanotic” defects heart disease, anemia, poisoning with carbon monoxide (II) CO, pulmonary failure, etc. Changes in the myocardium in the listed diseases do not relate to coronary artery disease, but are considered as complications of these diseases.

Epidemiology. IHD is the leading cause of death in many economically developed countries of the world. In the USA, for example, 5.4 million new cases of illness are registered every year, ] / 2 of which 550,000 are disabled and die. Since the late 60s, incidence rates of coronary artery disease among the working-age male population began to increase sharply, which led to talk of an epidemic of coronary artery disease. In recent years, in many countries there has been a tendency towards stabilization of morbidity and mortality rates from coronary artery disease, which is due to many reasons: smoking ban, reduction of cholesterol in food, correction of high blood pressure, surgical treatment, etc.

Etiology and pathogenesis. IHD has common etiological and pathogenetic factors with atherosclerosis and hypertension, which is not accidental, since IHD is actually a cardiac form of atherosclerosis and hypertension.

Pathogenetic factors of IHD are also called risk factors, since they determine the likelihood of developing the disease. According to the degree of significance, they are divided into first- and second-order factors. The most important first-order risk factors include: hyperlipidemia, tobacco smoking, arterial hypertension, decreased physical activity, obesity, nutritional factor (cholesterol diet), stress, decreased

glucose tolerance, male gender, alcohol consumption. Among the second-order risk factors are disturbances in the content of microelements (zinc), increased water hardness, increased levels of calcium and fibrinogen in the blood, hyperuric acid.

Hyperlipidemia. Hypercholesterolemia and hypertriglyceridemia are the most important pathogenetic factors in the development of atherosclerosis of the coronary arteries of the heart. A direct relationship has been established between blood cholesterol levels and mortality due to coronary artery disease. People with cholesterol concentrations less than 150 mg/L and relatively low levels of low-density lipoprotein (LDL) develop CHD relatively rarely. The independent significance of hypertriglyceridemia is controversial, but a correlation has been shown between an increase in their concentration in the blood in parallel with LDL. The frequent development of ischemic heart disease in patients with diabetes mellitus becomes clear.

Tobacco smoking, IHD develops 2.14 times more often in smokers than in non-smokers. The main effect of smoking is due to stimulation of the sympathetic part of the autonomic nervous system, accumulation of carbon monoxide (11) in the blood, immune damage to the vascular wall and activation of platelet aggregation. People who smoke more than 25 cigarettes per day have decreased levels of high-density lipoprotein (HDL) and increased levels of very low-density lipoprotein (VLDL). The risk of developing CHD increases with the number of

cigarettes smoked.

Arterial hypertension. It aggravates the course of atherosclerosis, promotes the development of hyalinosis of arterioles and causes hypertrophy of the left ventricular myocardium. All these factors together increase ischemic damage in the myocardium

The role of atherosclerosis of the coronary arteries. More than 90% of patients with coronary artery disease have stenotic atherosclerosis of the coronary arteries with stenosis of 75% of at least one main artery. The results of experimental and clinical observations show that 75% of coronary artery stenosis cannot meet the oxygen needs of the heart muscle even with a light load Immediate reasons ischemic damage to the myocardium during coronary artery disease are thrombosis of the coronary arteries, thromboembolism, prolonged spasm, functional overstrain of the myocardium in conditions of stenotic atherosclerosis of the coronary arteries and insufficient collateral circulation. Thrombosis of the coronary arteries is found in 90% of cases of transmural myocardial infarction - one of the most severe forms of coronary artery disease. The thrombus is usually localized in the ulcerated area

atherosclerotic plaque. The genesis of a thrombus is associated with platelet aggregation at the site of plaque ulceration, where the subendothelial layer is exposed and tissue thromboplastin is released. In turn, platelet aggregation leads to the release of agents that cause vasospasm - thromboxane A2, serotonin, histamine, etc. Aspirin reduces the synthesis of thromboxane A2 and inhibits platelet aggregation and vasospasm.

Thromboembolism in the coronary arteries usually occurs when thrombotic masses are separated from their proximal sections, as well as from the cavity of the left ventricle.

Prolonged spasm of the coronary arteries was proven by angiographic data. Spasm develops in the main trunks of the coronary arteries affected by atherosclerosis. The mechanism of vasospasm is complex, caused by the local release of vasoactive substances formed during platelet aggregation on the surface of atherosclerotic plaques. After resolution of prolonged vasospasm, blood circulation in the myocardium is restored, but this often leads to additional damage associated with reperfusion - reperfusion injury. Vasospasm can also result in coronary artery thrombosis. The mechanism of thrombosis may be due to damage to the atherosclerotic plaque during spasm, which especially often occurs with atherocalcinosis.

Functional overstrain in conditions of insufficiency of collateral circulation in atherosclerosis of the coronary arteries can also lead to ischemic damage to the myocardium. At the same time, the importance of the degree of stenosis and the prevalence of atherosclerosis has been proven. Stenosis of more than 75% of at least one main trunk of the coronary artery is considered significant.

Morphogenesis. In IHD, ischemic myocardial damage and regeneration processes develop in stages.

The mechanism of ischemic myocardial damage is complex and is caused by the cessation of oxygen supply to myocardiocytes, impaired oxidative phosphorylation and, consequently, the occurrence of ATP deficiency. As a result, the functioning of ion pumps is disrupted, and excess amounts of sodium and water enter the cells, while at the same time the cells lose potassium. All this leads to edema and swelling of mitochondria and the cells themselves. An excess amount of calcium also enters the cell, causing activation of Ca 2+ -dependent proteases

calpains, dissociation of actin microfilaments. activation of phospholipase A 2. In myocardiocytes, anaerobic glycolysis increases, glycogen reserves are broken down, which leads to thyroidosis. Under conditions of oxygen deficiency, reactive oxygen species and lipid peroxides are formed. Then comes destruction

When membrane structures, primarily mitochondrial ones, become damaged, irreversible damage occurs.

Typically, ischemic myocardial damage follows the path of coagulation and apoptosis. In this case, immediately reacting genes are activated, primarily c-fos, and the program of “programmed death” - apoptosis - is activated. Calcium mechanisms of damage are of great importance. During apoptosis, calcium endonucleases are activated with DNA hydrolysis into single-stranded fragments.

In peripheral areas, ischemic injury usually ends in liquefaction necrosis with cellular edema and myocytolysis, which is especially typical for reperfusion injuries.

Ischemic myocardial damage can be reversible or irreversible.

Reversible ischemic damage develop in the first 20-30 minutes of ischemia and, if the influence of the factor causing them ceases, completely disappear.

Morphological changes are detected mainly by electron microscopy (EM) and histochemical studies. EM makes it possible to detect swelling of mitochondria, deformation of their cristae, and relaxation of myofibrils.

Histochemically, a decrease in the activity of dehydrogenases and phosphorylases, a decrease in glycogen reserves, intracellular potassium and an increase in the concentration of intracellular sodium and calcium are detected. Some authors note that light microscopy reveals wavy muscle fibers at the periphery of the ischemic zone.

- coagulation - localized in the central zone, cardiomyocytes are elongated, characterized by karyopyknosis and calcium accumulation. Coagulative necrosis is actually a manifestation of apoptosis; necrotic masses are removed by phagocytosis by macrophages;

Coagulation followed by myocytolysis - necrosis of muscle bundles with the phenomena of overcontraction and coagulation necrosis, as well as the accumulation of calcium in the cells, but with subsequent lysis of necrotic masses. This necrosis is located in the peripheral parts of the infarction and is caused by the action of ischemia and reperfusion;

- myocytolysis - liquefaction necrosis - swelling and destruction of mitochondria, accumulation of sodium and water in the cell, development of hydropic dystrophy.

Necrotic masses are eliminated by lysis and phagocytosis.

Around the zone of necrosis, a zone of demarcation inflammation is formed, represented in the first days by full-blooded vessels with diapedesis of erythrocytes and leukocyte infiltration. Subsequently, a change in cellular cooperation occurs, and macrophages and fibroblasts, as well as newly formed vessels, begin to predominate in the inflammation zone. By the 6th week, the necrosis zone is replaced by young connective tissue. After a myocardial infarction, a focus of sclerosis forms at the site of former necrosis.

ClassificationA patient who has suffered an acute catastrophe is left with chronic heart disease in the form of post-infarction cardiosclerosis and stenosing atherosclerosis of the coronary arteries.

Classification.

IHD flows in waves, accompanied by coronary crises, i.e. with episodes of acute (absolute) and/or chronic (relative) coronary insufficiency.

In this regard, acute ischemic heart disease and chronic ischemic heart disease are distinguished. Acute IHD is characterized by the development of acute ischemic damage in the myocardium, chronic IHD is characterized by cardiosclerosis as a result of ischemic damage.

IHD

ACUTE IHD

Sudden cardiac death

Acute focal ischemic dystrophy of the myocardium

Myocardial infarction

CHRONIC IHD

Large focal cardiosclerosis

instantly or within minutes, several hours after the onset of symptoms of heart damage. In most cases (up to 80%), it occurs in patients with coronary artery disease with atherosclerosis of the coronary arteries. However, it should be remembered that sudden cardiac death can also develop in other diseases.

Sudden cardiac death in acute ischemic heart disease is considered death in the first 6 hours of acute myocardial ischemia. During this period, 74-80% of patients show changes in teeth Q, G, S-T interval, lethal arrhythmias (ventricular fibrillation, asystole) on the ECG, but blood enzymes do not yet change in this time interval.

Morphological changes may correspond to the early stages of ischemic damage against the background of unchanged myocardium, but more often - against the background of cardiosclerosis or previously developed myocardial infarction. In this case, damage is often localized in the area of ​​the conduction system, which is associated with the development of arrhythmias. In the foci of acute ischemic injuries that caused sudden death, macroscopic changes are not detected. Microscopically, wave-like changes in muscle fibers and initial manifestations of coagulation necrosis in the peripheral parts can be detected. EM reveals damage to mitochondria, calcium deposits in them, ruptures of the sarcolemma, chromatin margination, histochemically - a decrease in the activity of dehydrogenases, and the disappearance of glycogen.

Acute occlusion of the coronary arteries by a thrombus or thromboembolism is found only in 40-50% of autopsies of people who died from sudden cardiac death. The relative low incidence of thrombosis can be explained by developing fibrinolysis as well as the possible role of vasospasm and functional myocardial overstrain under conditions of coronary circulation deficiency in the genesis of sudden cardiac death.

Thanatogenesis (mechanism of dying) in sudden cardiac death is caused by the development of lethal arrhythmias.

Acute focal ischemic dystrophy of the myocardium. A form of acute ischemic heart disease that develops in the first 6-18 hours after the onset of acute myocardial ischemia. Characteristic changes are recorded on the ECG. An increase in the content of enzymes coming from the damaged myocardium - muscle-type creatinine kinase and glutamate noxaloacetate transaminase - may be detected in the blood. With EM and with the help of histochemical reactions, the same changes are recorded as with sudden cardiac death, corresponding to early ischemic damage, but more pronounced. In addition, with EM, one can observe the phenomena of apoptosis and marginal necrosis in areas of overcontraction of muscle fibers.

At the section table, early ischemic injuries are diagnosed using potassium tellurite and tetrazolium salts, which do not stain the ischemic zone due to the lack of oxygen in it and a decrease in the activity of dehydrogenases.

Myocardial infarction. A form of acute ischemic heart disease, characterized by the development of ischemic myocardial necrosis. It develops 18 hours after the onset of ischemia, when the necrosis zone becomes visible micro- and macroscopically. In addition to ECG changes, it is characterized by fermentemia.

Macroscopically, the infarction is irregular in shape, white with a hemorrhagic rim. Microscopically, a zone of necrosis is determined, surrounded by a zone of demarcation inflammation, separating the first from the intact myocardial tissue. In the necrosis zone, coagulation necrosis in the center, coagulation myocytolysis and liquefaction necrosis along the periphery are determined.

The zone of demarcation inflammation in the first days of a heart attack is represented by a leukocyte shaft and full-blooded vessels with diapedesis, and from the 7-10th day - by young connective tissue, gradually replacing the necrosis zone and maturing. Scarring of the infarction occurs by the 6th week.

During a heart attack, two stages are distinguished: necrosis and scarring.

Classificationheart attackmyocardium

I. By time of occurrence

Primary (first appeared)

Recurrent (developing within 6 weeks after the previous one)

Repeated (developed more than 6 weeks after the previous one)

II. By localization

The anterior wall of the left ventricle and the anterior sections of the interventricular septum

Posterior wall of the left ventricle

Lateral wall of the left ventricle

Interventricular septum

Extensive heart attack

III. By prevalence

Subendocardial

Intramural

Subendocardial

Transmural

Depending on the time of occurrence There are primary infarctions (which occurred for the first time), recurrent (developed within 6 weeks after the previous one), and repeated (developed after 6 weeks after the previous one). For recurrent

infarction, foci of scarring infarction and fresh foci of necrosis are detected.

If repeated, there are old post-infarction scars and foci of necrosis. By localization

If repeated, there are old post-infarction scars and foci of necrosis. isolated infarction of the anterior wall of the left ventricle, the apex and anterior sections of the interventricular septum - 40-50% of cases, develops with obstruction, stenosis of the left descending artery; posterior wall of the left ventricle - 30-40% of cases, with obstruction, stenosis of the right coronary artery; lateral wall of the left ventricle - 15-20% of cases, with obstruction, stenosis of the circumflex branch of the left coronary artery.

An isolated infarction of the interventricular septum develops less frequently - 7-17% of cases, as well as an extensive infarction - with obstruction of the main trunk of the left coronary artery. prevalence

subendocardial, intramural, subepicardial and transmural infarctions are distinguished. % ECG diagnostics allows to differentiate subendocardial and transmural infarction. It is believed that transmural infarction always begins with damage to the subepicardial sections due to the characteristics of their blood supply.

Large-focal (post-infarction) cardiosclerosis.

It develops as a result of a heart attack and is represented by fibrous tissue. The preserved myocardium undergoes regenerative hypertrophy. If large-focal cardiosclerosis occurs after a transmural myocardial infarction, a complication may develop - a chronic cardiac aneurysm. Death occurs from chronic heart failure or thromboembolic complications. Diffuse small-focal cardiosclerosis. As a form of chronic ischemic heart disease, diffuse small-focal cardiosclerosis develops as a result of relative coronary insufficiency with the development of small foci of ischemia. May be accompanied by atrophy and lipofuscinosis of cardiomyocytes.

ClassificationCerebrovascular diseases(allocated into a separate group - WHO in 1977) are characterized by acute disorders of cerebral circulation, the background for the development of which is atherosclerosis and hypertension. Patients with cerebrovascular diseases make up more than 50% of patients in neurological hospitals.

cerebrovascular

diseases

I. Brain diseases with ischemic damage

Ischemic encephalopathy

Ischemic cerebral infarction

Hemorrhagic cerebral infarction

II. Intracranial hemorrhages

Intracerebral

Subarachnoid

Mixed

III. Hypertensive cerebrovascular diseases

Lacunar changes

Subcortical leukoencephalopathy

Hypertensive encephalopathy The following main groups of diseases are distinguished: 1) brain diseases associated with ischemic damage - ischemic encephalopathy, ischemic and hemorrhagic cerebral infarction; 2) intracranial hemorrhages;

3) hypertensive cerebrovascular diseases - lacunar changes, subcortical leukoencephalopathy, hypertensive encephalopathy.The clinic uses the term stroke (from the Latin in-sultare - to jump), or brain stroke. Stroke can be represented by a variety of pathological processes: - Ischemic encephalopathy.

Stenosing atherosclerosis of the cerebral arteries is accompanied by disturbances in maintaining a constant level of blood pressure in the vessels of the brain. Chronic ischemia occurs Mia. The most sensitive to ischemia are neurons, primarily pyramidal cells of the cerebral cortex and piriform neurons (Purkinje cells) of the cerebellum, as well as neurons of the Zimmer zone of the hippocampus. Calcium damage with the development of coagulative necrosis is recorded in these cells

And

apoptosis.

The mechanism may be due to the production of neurotransmitters (glutamate, aspartate) by these cells, which can cause acidosis and opening of ion channels. Ischemia also causes activation of c-fos genes in these cells, leading to apoptosis. Mia. Morphologically, ischemic changes in neurons are characteristic - coagulation and eosinophilia of the cytoplasm, pyknosis of the nuclei. Gliosis develops in place of dead cells. The process does not affect all cells. When small groups of pyramidal cells of the cerebral cortex die, they speak of laminar necrosis. Most often, ischemic encephalopathy develops at the border of the anterior and middle cerebral arteries, where, due to the characteristics of angioarchitectonics, there are favorable conditions for hypoxia - weak anastomosis of vessels.

Hemorrhagic cerebral infarction is often the result of embolism of the cerebral arteries and has a cortical localization. The hemorrhagic component develops due to diapedesis in the demarcation zone and is especially pronounced during anticoagulant therapy.

Intracranial hemorrhages. They are divided into intracerebral (hypertensive), subarachnoid (aneurysmal), mixed (parenchymal and subarachnoid - arteriovenous defects).

Intracerebral hemorrhages.

They develop when microaneurysms rupture at the sites of intracerebral bifurcations.

arteries in patients with hypertension (hematoma), as well as as a result of diapedesis (petechial hemorrhages, hemorrhagic impregnation). Hemorrhages are most often localized in the subcortical ganglia of the brain and the cerebellum. As a result, a cyst with rusty walls is formed due to hemosiderin deposits.

Subarachnoid hemorrhages. They arise due to the rupture of aneurysms of large cerebral vessels, not only of atherosclerotic, but also of inflammatory, congenital and traumatic origin.

Hypertensive cerebrovascular diseases.

Develops in people suffering from hypertension.

Lacunar changes. They are represented by many small rusty cysts in the area of ​​the subcortical nuclei. Subcortical leukoencephalopathy.

Accompanied by subcortical axonal loss and the development of demyelination with gliosis and arteriolohyalinosis. Hypertensive encephalopathy. Arises