кардиосклероз фото Cardiosclerosis is a concept of morphological and signifies a pathological process that leads to diffuse or local expansion of connective tissue in the heart, followed by compaction of the organ. As a result of cardiosclerosis, functional units (cardiomyocytes) are replaced by nonfunctional tissue, and the heart loses its contractility, as well as the ability to conduct a signal from the sinus node. Any chronic inflammation occurring in the heart muscle can provoke cardiac cardiosclerosis.

Cardiosclerosis is incurable, and treatment is reduced to suppressing symptoms. In severe cardiosclerosis, cardiac transplantation is necessary, which gives a very small percentage of the population a chance.

Causes of cardiosclerosis

Morphologically, the following causes of cardiosclerosis: the outcome of an inflammatory process associated with an infectious agent, an allergic process, and, which is extremely rare, a foreign body; the result of rheumatic fever; the outcome of the organization of connective tissue at the site of necrosis, which originated in the place of acute ischemia; after mechanical damage to the heart tissue, rough scars from the connective tissue appear.

A large number of microorganisms cause myocardial damage, but not all cases of myocarditis will lead to cardiosclerosis. Sluggish chronic inflammation predisposes to the occurrence of cardiosclerosis.

Cardiosclerosis symptoms

Cardiosclerosis is a manifestation of chronic ischemic heart disease and can be atherosclerotic, diffuse, small-focal, or postinfarction large-focal, as a result of which chronic heart aneurysm is formed.

Cardiosclerosis occurs against the background of already existing pathology, and therefore the symptoms of cardiosclerosis overlap the symptoms of the concomitant disease. As a result of a decrease in the number of functioning myocytes, the myocardium loses the ability to effectively deliver oxygen to all tissues and organs in cardiosclerosis. Heart failure develops. For a long time the body manages to compensate for circulatory failure with the help of hypertrophy of a healthy area of ​​the myocardium. Thus, the first manifestations of heart failure in cardiosclerosis appear at a stage that is not amenable to treatment.

Depending on the localization of cardiosclerosis, right ventricular and left ventricular heart failure is isolated. The symptomatology of them is different. Left ventricular failure is manifested when the lungs "overflow" with blood. As a result, dyspnea occurs, the patient takes a forced position to improve breathing, there are attacks of suffocation, coughing. In the terminal phase of cardiosclerosis, there is pulmonary edema, which can lead to death. An attack of pulmonary edema can happen at night when the person is in a horizontal position. Skin pale, wet, suffocation makes the patient take a forced position, the pulse is frequent, breathing bubbling, sputum foamy pink color, blood pressure is lowered.

With right ventricular heart failure, swelling occurs on the legs, and with further progression of the disease, edema "rises" higher; the liver is enlarged; swollen veins on the neck; fluid accumulates in the abdominal, pleural cavities and pericardial cavity; swelling of the subcutaneous tissue.

There are several stages of heart failure.

I stage - shortness of breath and tachycardia appear only with physical work, but at rest a person feels satisfactory.

II A stage with left ventricular failure - shortness of breath, tachycardia appear with light load, moderate blueness of the extremities.

II A stage with right ventricular failure - edema on the feet and ankles appear in the evening, a moderate increase in heart rate, moderate cyanosis of the extremities (acrocyanosis).

II B stage - obvious stasis in both circles of blood circulation, liver enlargement is considerable, edema is constant, working capacity is reduced.

III stage - characterized by constant manifestations in the rest of the symptoms and terminal impairment of the functions of all systems and organs.

There is also a division into functional classes depending on the physical capabilities of the patient. The first functional class is characterized by the absence of restrictions in physical activity. II functional class - moderate limitation of ability to work with the appearance of dyspnea, palpitation during normal work. In patients with functional class III, symptoms of circulatory failure appear in any physical work. The fourth functional class is characterized by a constant presence of symptoms of heart failure.

In connection with the violation of the impulse from the sinus node due to the morphological changes in the myocardium in cardiosclerosis, there are various kinds of heart rhythm disturbances. Extrasystoles are most often detected only during preventive examinations, since with a small number of them, no subjective sensations arise.

With the progression of cardiosclerosis the patient complains of interruptions in the work of the heart, the "fading" of the heart. Danger is borne by the ventricular extrasystoles, especially in patients with ischemic heart disease.

Paroxysmal tachycardia is characterized by a disturbance of the rhythm of the ectopic character with sudden acceleration of the frequency of contractions and a similar sudden decrease in rhythm. In connection with cardiosclerosis, the excitation wave is delayed in a certain part of the heart and "circulates" along this section. This is how the excitability of the myocardium increases. The patient complains of a heartbeat, the pulse rate is determined by a frequency of more than 150 per minute. There is shortness of breath, severe weakness. With the development of cardiogenic shock, blood pressure drops sharply, a cold sweat appears, the patient loses consciousness. Often there are pain in the heart.

Atrial fibrillation very often accompanies atherosclerotic, postinfarction and myocardial cardiosclerosis. Cardiosclerosis provokes the emergence of a circular excitation wave in the atria or ventricles. Such waves in the atria are layered on the main rhythm, and the frequency of the waves is 350-600 per minute. These waves are called fibrillation or atrial fibrillation. Subjective sensations at the same time are reduced to an unpleasant feeling of rhythm disturbance, dizziness, weakness when performing physical exertion. The prognosis for patients with cardiosclerosis in atrial fibrillation depends on the frequency of occurrence and the area of ​​the myocardium covered by cardiosclerosis.

Atrioventricular blockades occur as a result of involvement of myocytes in cardiosclerosis, which participate in the impulse from the atrioventricular node. If I - II degree does not give any clinical manifestations, then with complete blockade there is weakness, a rare heartbeat, dizziness , headaches, loss of consciousness. These symptoms indicate a decrease in blood supply to the brain.

Syndrome of weakness of the sinus node is also a manifestation of cardiosclerosis. Sclerotic changes lead to a decrease in the function of the sinus node, which leads to bradycardia and stopping rhythmic activity.

Tahi-bradyarrhythmic variant occurs when other structures begin to take part in the formation of rhythm. As a result, the transition to a permanent form of atrial fibrillation may occur. At the initial stages of the disease, a person does not make complaints. Then there are symptoms associated with a decrease in the blood circulation of the brain: weakness, dizziness, memory loss. Cardiac complaints include shortness of breath, angina pectoris. Insufficiency of blood circulation of the extremities in a patient is manifested by pain in calves, heaviness in the legs. For episodes of asystole are characterized by: "failure of memory", swallowing of the endings of words, there are cases of loss of consciousness (Morgagni-Adams-Stokes syndrome).

In addition to the patient's complaints, a diagnosis of cardiosclerosis is made on the basis of electrocardiography, echocardiography, and the determination of the patency of the coronary vessels. All diagnostic methods show the presence of a non-functioning part of the myocardium. The fraction of the discharge of blood decreases, coronary arteries are impassable. Depending on the type of cardiosclerosis, these or other symptoms may predominate.

Atherosclerotic cardiosclerosis

Atherosclerotic changes disrupt the blood flow through the coronary arteries due to the deposition of atherosclerotic plaques on the vessel walls and the formation of platelet aggregates and then a thrombus in the plaque area. This may affect the area of ​​blood supply to one or many branches of the coronary arteries. With long-term ischemia, organic changes occur in the muscle tissue of the heart, replacing it with a connective one. With this pathology, both small-focal cardiosclerosis and diffuse cardiosclerosis can develop. It depends on the coronary arteries involved in atherosclerosis.

The mechanism of development of atherosclerotic cardiosclerosis is ischemic and has symptoms of coronary heart disease. At the stages of the onset of cardiosclerosis the patient complains of angina pains that are stopped by nitrates, rhythm disturbance, weakness, edema, decreased ability to work. In coronary angiography, it is seen that arteries, blood supplying the heart are deformed and their lumen is closed by atherosclerotic overlays. When studying the composition of the blood, there is an increase in cholesterol, which is directly related to the progression of atherosclerosis.

The prognosis for this type of cardiosclerosis is determined by the extent of the lesion. Small-focal cardiosclerosis can not manifest itself throughout life, a diffuse variant causes very dangerous complications.

Postinfarction cardiosclerosis

Postinfarction cardiosclerosis is one of the manifestations of ischemic heart disease . Based on the name it is clear that this type of cardiosclerosis appeared on the site of damaged myocardial tissue as a result of a heart attack. At the site of the infarct, inflammation forms, which is soon replaced by a connective tissue scar.

The hearth of a heart attack can be of various sizes. Small-focal cardiosclerosis is formed with a small-focal infarction. Diffuse cardiosclerosis is typical for massive myocardial damage.

For the diagnosis of postinfarction cardiosclerosis, an anamnesis with a previous heart attack, symptoms of heart failure and rhythm disturbances are necessary.

The prognosis for this variant of cardiosclerosis is unfavorable, as it is often aggravated by repeated infarctions.

Diffuse cardiosclerosis

The term "diffuse" in this case means "uniformly distributed".

Diffuse cardiosclerosis is a concept that characterizes pathology in terms of the vastness of the affected myocardium. That is, the heart muscle is affected evenly and completely. There is such a cardiosclerosis most often against the background of coronary heart disease, when a large area of ​​the myocardium is affected, and with myocarditis.

Symptoms in the diffuse version of the course of cardiosclerosis are more severe and progress more rapidly. Therefore, immediate therapy of cardiosclerosis is required so that life-threatening complications do not arise.

Postmiocardial cardiosclerosis

Myocarditis is a polyethological disease. Inflammation of the myocardium can be a result of infections, systemic inflammatory diseases, allergic reaction, toxic effects, the effects of medications, etc. A huge number of pathogens cause inflammation of the myocardium. Bacteria, viruses, protozoa, helminths, rickettsia, spirochetes, fungi cause damage to the myocardium.

Cardiosclerosis develops more rapidly with myocarditis, mediated indirectly. Drugs cause myocarditis, which is based on an allergic reaction. In the treatment of cytotoxic drugs, antituberculosis drugs, antibiotics, anticonvulsants, non-steroidal anti-inflammatory drugs, diuretics, an immune reaction arises with involvement of the myocardium.

To cardiosclerosis also leads uremic myocarditis, which occurs as a result of toxic effects on the body, systemic lupus erythematosus , idiopathic dermatomyositis cause myocarditis. This causes damage to the endothelium of microvessels, which supply blood to the myocardium. As a result, blood cells come out of the bloodstream and impregnate the heart tissue. Full blood vessels can not fully supply the myocardium with oxygen, and eventually the muscle tissue is replaced by a connective tissue. This process leads to cardiosclerosis. Inflammation should be chronic.

The appearance of cardiac complaints in infectious myocarditis is preceded by symptoms of general intoxication. Most often, people aged 35-45 years are affected. After 1-2 weeks, after suffering an infectious disease, pains occur in the heart area in 85% of patients, a sense of disruption, shortness of breath during physical work, general weakness, sweating. At the same time, the intensity of the pain symptom increases, it is not stopped by nitrates.

Dyspnea with myocarditis manifests itself already at the stage of onset cardiosclerosis. Often patients with myocarditis complain of a fever. Myocarditis of an allergic nature can be manifested by rashes on the skin. When cardiosclerosis has already developed, rhythm disturbances occur. Thromboembolic complications are possible with both acute and chronic myocarditis, which has passed into cardiosclerosis. With the course of myocarditis are divided into acute, subacute, chronic, recurrent, latent. It is the chronic course that contributes to the onset of cardiosclerosis. Duration of the disease for more than 6 months indicates a chronic variant of the course.

Cardiosclerosis treatment

The treatment of cardiosclerosis is aimed at eliminating the main syndromes. Since cardiosclerosis is an altered myocardium in a different kind of tissue, there can be no question of regression. Therapy in the case of cardiosclerosis is aimed at slowing the process of reorganization and improving the work of the heart.

To slow down the process, the main disease is treated. If cardiosclerosis is caused by an infection, then antibiotic therapy, antiviral, antifungal, anthelmintic, antiprotozoal drugs are used.

Therapy of the most dangerous consequence of cardiosclerosis - heart failure, reduces to reducing the burden on the heart. The patient with cardiac failure in cardiosclerosis must comply with the protective regime, physical activity is calculated individually according to the functional class of the disease. Food for this pathology should be rich in protein, easy to digest, should contain a small amount of table salt. The use of liquid is reduced to 1.5 liters per day.

For patients of the first functional class, the physical load is reduced to daily work, but without unnecessary stress. II functional class implies the exclusion of physical education and hard work. For III and IV functional classes, cutting is limited to physical activity up to the semi-postal regime.

Drug therapy includes the following groups of drugs: cardiac glycosides, beta-blockers, angiotensin-converting enzyme inhibitors, diuretics, angiotensin II receptor antagonists and the first type, inotropic substances of a non-glycosidic nature, peripheral vasodilators.

Diuretics are the main means in unloading the heart muscle. At the first stages of heart failure in cardiosclerosis, Hypothiazide is used in a dose of 25-50 mg per day, followed by a rise in the dose to 75-100 mg per day. You can prescribe non-diasidic diuretics - Hygroton - 50-200 mg per day. To maintain a normal level potassium can be used together with these drugs to take Spironolactone or Triamteren.

If heart failure in more severe stages, then Furosemide is used - 20-40 mg per day, it is possible to increase the dose to 400 mg per day. Ectric acid is 25-50 mg per day, with the possibility of increasing the dose to 250 mg per day. Boumetamide 0.5-1.0 mg per day, followed by a maximum dose of 10 mg per day.

With a decrease in the response of the body to diuretics, two or more drugs should be combined. If the potassium content increases to 5.4 mmol / l against the background of the use of potassium-sparing diuretics, then their dose should be reduced.

Cardiac glycosides are also necessary for the treatment of cardiosclerosis. Their main function is to increase the strength of the heart muscle. In this case, the heart contractions are cut, the diastole lengthens. As a result, a better filling of the ventricles occurs, and the oxygen consumption of the myocardium does not increase. It is worth remembering that treatment with glycosides should occur with strict adherence to the dose and observation of the response to treatment, as the therapeutic dose and toxic are close in their values. With an overdose of glycosides, deadly conditions can occur, such as atrial fibrillation and bradycardia. There are the following indications for the appointment of cardiac glycosides: atrial fibrillation in tachysystolic form, patients with sinus rhythm in the absence of response to angiotensin-converting enzyme inhibitors, beta-blockers, diuretics. Начальная доза Дигоксина – 0,375-0,25 мг в д. в течение 5-7 дней, затем назначается по 0,125-0,25 мг в д. Если пациенту с кардиосклерозом более 70 лет, нарушены функции почек или низкая масса тела, то доза должна составлять 0,125 мг в д.

Ингибиторы ангиотензин-превращающего фермента очень эффективны для терапии кардиосклероза. Главным действием этих препаратов является сосудорасширение. При местном воздействии увеличивается сократительная возможность миокарда. Для начала терапии назначают Каптоприла – 6,25-12,5 мг, Эналаприл -2,5 мг, Лизиноприл – 2,5-5 мг, Периндоприл -2 мг. Спустя 3-7 дней стоит увеличивать дозу до следующих цифр: Каптоприл – 150 мг, Эналаприл – 20-40 мг, Лизинопррил – 20-40 мг, Периндоприл – 4-8 мг.

Динамическое наблюдение пациентов с кардиосклерозом за функцией почек и уровнем калия при лечении ингибиторами АПФ обязательно. Каптоприл принимают два раза в сутки, остальные препараты имеют более длительную продолжительность действия и принимаются один раз в сутки.

Бета-блокаторы применяются для снижения частоты сердечных сокращений, снижении степени ишемии миокарда, снижении частоты аритмий, улучшения сократительной способности сердца. Если в результате кардиосклероза возникла атриовентрикулярная блокада, то бета-блокаторы не назначаются. Начинать лечение следует со следующих доз: Карведилол – 3,125 мг два р/д., Бисопролол – 1,25 мг 1р/д., Метопролол – 12,5 мг 1 р/д. через 2-4 недели доза удваивается, если нет осложнений.

Блокаторы ангиотензина II уместны, когда у пациента возникли побочные реакции на применение ингибиторов ангиотензин-превращающего фермента при кардиосклерозе. Эти препараты лучше переносят больные, а эффект более выражен, чем у ингибиторов АПФ. Но в то же время блокаторы ангиотензина II способствуют деградации брадикинина. Но исследования по данным препаратам не выявили существенных преимуществ, поэтому их однозначно назначают пациентам с непереносимостью ингибиторов АПФ.

Нитраты в настоящее время применяются при наличии высокого артериального давления на фоне сердечной недостаточности при кардиосклерозе.

При лечении экстрасистолии при кардиосклерозе, нужно помнить, что редкие предсердные экстрасистолы не требуют медикаментозной терапии. Для лечения таких экстрасистол нормализуют режим, отдых, питание. Если экстрасистолы проявляются неприятными ощущениями, то необходимо начинать противоаритмическую терапию.

Для правильного подбора препаратов пациентам с кардиосклерозом нужно назначить суточный мониторинг ЭКГ и пробные курсы. Если препарат приходится назначать эмпирически, то можно начать с Амиодарона – 0,6 г в сут. с последующим снижением дозы. Соталекс в дозе от 80 до 160 мг в сут. Пропафенон – 600-900 мг в сут. Этазициин – до 0,2 г в сут. Аймалин – до 0,3 г в сут. Дизопирамид – 0,6 г в сут. Аллапинин – 75-150 мг в сут. Если точно диагностирована желудочковая экстрасистолия, то добавляется Новокаинамид в суточной дозе 2-4г на 4-6 приемов, Этмозин – 0,6-0,8 г в сут, Дифенин – 0,117 г на 3-4 приема в сут, Мексилетин – 0,6 г в сут. При диагностированной наджелудочковой экстрасистоле на фоне кардиосклероза используют Хинидин в дозе 0,2г на 3-5 приемов в сут, бета-блокаторы (Пропранолол – 0,01-0,02 г на 3-4 приема в сут.), Верапамил – 40-80 мг на 3-4 приема в сут. Все препараты стоит принимать с минимальной начальной дозы, увеличивать дозу следует только после того, как убедились в отсутствии побочных действий. Препараты можно комбинировать. При смертельно опасных состояниях необходима неотложная помощь.

Пароксизмальная тахикардия при кардиосклерозе для начала должна подвергнуться немедикаментозной терапии. Глубокое дыхание, надавливание на глазные яблоки, натуживание, вызывание рвоты – способы купирования наджелудочковой пароксизмальной тахикардии. Если данные механические воздействия не приводят к желаемому результату, то прибегают к лекарственной терапии. Пропранолол в дозе 10-20 мг или Атенолол в дозе 25-50 мг совместно с Феназепамом – 1 мг или Клоназепамом – 2 мг. Верапамил не следует назначать при пароксизмальной тахикардии неизвестного происхождения. Когда происхождение тахикардии установлено, то внутривенно назначают АТФ, Верапамил – 2-4 мл 2,5%-го раствора, Новокаинамид – 10 мг 10%ого раствора, Пропранолол – 5-10 мг 0,1%-го раствора, Пропафенон -1 мг на кг. При отсутствии эффекта от лечения можно повторить введение Амиодарона. Если и это не приносит результатов, то пациента подвергают электроимпульсной терапии. Желудочковая пароксизмальная тахикардия является опасным для жизни состоянием, тем более на фоне кардиосклероза. Необходима экстренная помощь в виде электроимпульсной терапии на фоне внутривенного введения Лидокаина, Амиодарона.

Основная цель лечения мерцательной аритмии при кардиосклерозе – купирование приступов и препятствие возникновению новых. С профилактической целью вводится Гепарин. Кардиоверсия применима при явной нестабильности кровообращения. Приступ купируют Амиодароном в дозе 300-450 мг, Новокаинамидом в дозе 1000 мг. Возможно применение Нибентана – 10-15 мг, Пропафенона – 2 мг на кг. При постоянной форме мерцательной аритмии применим Хинидин с увеличивающейся дозой от 0,6 до 4 г в сут, а также кардиоверсия. При отсутствии нужного эффекта назначают Дигиталис. Он урежает сердечные сокращения, при этом сила сокращений увеличивается, и кровоснабжение становится эффективнее. При постоянной форме аритмии терапию проводят пожизненно. Для профилактики тромботических осложнений назначают Аспирин – 300-325 мг.

В зависимости от степени атриовентрикулярной блокады применяется медикаментозное или оперативное лечение. Блокада I степени не требует лекарственной терапии. При блокаде второй степени назначают Атропин в каплях, Изадрин по 2,5 мг 4-6 раз в сут. Более тяжелое течение требует немедленной госпитализации во избежание значительного нарушения гемодинамики. В этом случае методом лечения является имплантация электрокардиостимулятора.

Синдром слабости синусового узла при кардиосклерозе может лечиться оперативно и медикаментозно. Назначают успокоительные препараты, для ускорения ритма используют Атропин капельно 4 раза в сут, Изадрин таблетированно 4-6 раз в сут, Эуфиллин, Нифедипин. При тяжелом варианте протекания кардиосклероза потребуется установка кардиостимулятора.

Радикальным методом лечения кардиосклероза является пересадка сердца. Количество пациентов, которым провели такие операции, весьма ограничено. Для этого необходимо соответствия донора и реципиента по многим критериям.