Ischemic cardiomyopathy

Introduction to ischemic cardiomyopathy Ischemic cardiomyopathy (ICM) is a special type or advanced stage of coronary heart disease, which refers to long-term myocardial ischemia caused by coronary atherosclerosis, resulting in diffuse fibrosis of the myocardium, resulting in primary dilatation. Similar clinical syndromes of cardiomyopathy, with the increasing incidence of coronary heart disease, the harm caused by ICM to human health is also becoming more serious. In 1995, WHO/ISFC defined ischemic cardiomyopathy as: manifested as dilated cardiomyopathy with systolic dysfunction, but could not be explained by the degree of coronary artery disease and the degree of ischemic damage. basic knowledge The proportion of illness: 0.002% Susceptible people: no specific population Mode of infection: non-infectious Complications: heart failure, arrhythmia, shock

Causes of ischemic cardiomyopathy

(1) Causes of the disease

Common causes of ischemic cardiomyopathy are:

Coronary artery resistance lesion

(1) Coronary atherosclerosis: is the most common cause of myocardial ischemia, a series of factors between atherosclerosis, arterial wall cells, extracellular matrix, blood components, local hemodynamics, environmental and genetic factors As a result of complex effects, epidemiological studies have shown that the pathogenesis of coronary atherosclerosis is affected by a combination of factors such as elevated blood pressure, hyperglycemia, hypercholesterolemia, elevated fibrinogen, and smoking. Major risk factors for atherosclerosis, overeating, obesity or overweight, lack of physical activity, type A personality, and early family history of coronary heart disease are also risk factors for coronary heart disease. Under these risk factors, coronary artery Vascular endothelial injury or exfoliation, enhanced permeability of the endometrium, a small amount of plasma lipids invade into the subendothelial, monocytes appear around, mesangial smooth muscle cells proliferate and enter the intima, these proliferating monocytes and smooth muscle cells Subcutaneous phagocytosis of large amounts of lipids to form lipid-rich foam cells, followed by extensive enrichment of lipids due to invasion into the subendothelial Lipid foam cells are more and more, and gradually disintegrate, so that a large number of lipids are deposited under the intima to form a lipid pool. With the disintegration of foam cells and the release of lipids, the lipid pool is gradually enlarged. In addition to cholesterol, there are cholesterol crystals, neutral fats, phospholipids and disintegrating cell debris. Under the endothelium, lipid spots and lipid streaks gradually develop into atheromatous plaques. These atheromas stimulate the surrounding tissues to form fibrosis. The cap can also form calcification to make the plaque hard. When the atheromatous plaque protrudes into the lumen of the blood vessel, coronary atherosclerotic stenosis can gradually form, and the lipid and necrotic substances in the plaque can break into the endometrial surface. Collapse, the formation of atherosclerotic ulcers, bleeding or thrombosis may occur on the surface of the ulcer, causing further narrowing of the lumen resulting in myocardial ischemia and even infarction.

Patients with ischemic cardiomyopathy, especially congestive ischemic cardiomyopathy, often have significant atherosclerotic stenosis in multiple coronary arteries. It has been reported that 71 patients with 3 vascular lesions account for 71% of the disease. Vascular lesions accounted for 27%, single-vessel disease is rare, patients with ischemic cardiomyopathy have a history of multiple and/or multiple myocardial infarctions, and angina symptoms are more common, Atkinson in 35 ischemic myocardium In the autopsy results, an average of 2.2% of the coronary arteries with a stenosis of more than 75% were found, of which 26 had evidence of myocardial infarction, 9 had no pathological manifestations of myocardial infarction, and Edward found that 14 patients with ischemic cardiomyopathy were found at autopsy. 100% of patients have myocardial infarction, it is due to severe coronary stenosis caused by long-term perfusion of a large range of myocardial insufficiency, myocardial function decline, and even myocardial degeneration, necrosis, myocardial fibrosis, ventricular wall replaced by large scar tissue, ventricle Hypertrophy, enlargement, decreased myocardial contractility and decreased ventricular compliance, leading to cardiac insufficiency.

(2) Thrombosis: Recent studies have confirmed that coronary artery acute thrombosis is the main cause of acute transmural myocardial infarction, but thrombosis occurs on the basis of atherosclerotic plaque, local plaque of thrombus 3/4 had rupture and/or bleeding. Beijing Tongwai Hospital had an autopsy for 31 cases of acute myocardial infarction. Twenty-one patients with coronary artery thrombosis were found to have a thrombus detection rate of 74.1%. All autopsy proved that all thrombus All of them are blocked at the proximal end of the large branch of the coronary artery. The penetrating infarction has a wider range. The complications of left heart failure or cardiogenic shock are more common. Some patients have thrombolytic recanalization, and a few patients have thrombosis and cause blood vessels. In the persistent occlusion or stenosis of the cavity, in the survivors after the recovery of the acute phase, more patients will have extensive wall motion disappeared or weakened, and the ventricular cavity is obviously enlarged.

(3) vasculitis: a variety of rheumatic diseases can involve coronary arterial coronary artery disease, repeated activities, repair, mechanization can cause coronary stenosis, leading to myocardial ischemia, such as systemic lupus erythematosus, rheumatoid Arthritis, nodular polyarteritis, viral coronary arteritis, etc., especially nodular polyarteritis, also known as nodular periarteritis or polyarteritis, is a major involvement of small and medium arteries Necrotizing vasculitis, lesions can be segmental, occur in the bifurcation of the arteries, extending down to the small arteries, easy to form small aneurysms, inflammatory cell infiltration in all layers of the blood vessel wall, intimal hyperplasia, degeneration , necrosis and granulation formation, lumen shrinkage, occlusion, tube wall is often replaced by fibrous tissue, about 60% of patients with nodular polyarteritis can develop coronary arteritis, cause myocardial ischemia, can induce angina and (or) myocardial infarction And even cause ischemic cardiomyopathy.

(4) Others: factors that can cause chronic myocardial ischemia include coronary microvascular disease (X syndrome) and abnormal coronary structure, such as muscle bridge, human coronary artery trunk and its large branches, mainly walking in pericardium In the lower adipose tissue or in the deep surface of the pericardial visceral layer, sometimes they are covered by the superficial myocardium. After walking a distance in the myocardium, they are shallow to the surface of the myocardium. This segment of the artery covered by the myocardium is called the wall coronary artery. The part of the myocardium that covers the coronary artery is called the muscle bridge. The intimal layer of the wall coronary artery is thinner than the proximal and distal endometrium, and there is little or almost no atherosclerotic lesion, but when the muscle bridge Compression of the coronary artery surrounded by contraction can lead to severe coronary stenosis, affecting local myocardial blood supply, resulting in myocardial ischemia.

2. Coronary artery dynamic lesions Under the action of humoral and neurological factors, vascular smooth muscle reactivity is abnormally enhanced, and vasospasm occurs. Especially in the presence of atherosclerosis, the extensive blood vessels often show a slow relaxation response. Can cause vasomotor dysfunction, leading to increased myocardial ischemia, when the formation of coronary atherosclerotic plaque, the stenosis area is not static, most of the human coronary atherosclerotic plaque is eccentric stenosis, which means There is still a part of the normal arterial wall in the stenosis, which will make the lumen smaller due to the contraction of smooth muscle. Due to the incompressibility of plaque tissue, if the outer diameter is reduced by the increase of vascular smooth muscle tension, the effect on the lumen will be It is very huge. For example, if the diameter of the lumen has been reduced by 50% due to plaque, if the diameter of the vascular smooth muscle tendon is reduced by 10%, the stenosis of the lumen will increase. By 80% to 85%, the stenosis of the transverse section will be more than 95%. Through research, many factors have been involved in the regulation of vascular smooth muscle contraction. For example, adrenergic alpha receptor agonism, local platelet aggregation and release of thromboxane A2 (TXA2), and hypercholesterolemia or local atherosclerotic lesions can cause abnormal vascular reactivity, and ergometrine is the most effective drug for inducing sputum. Both nitroglycerin and calcium channel antagonists can effectively alleviate this problem.

(two) pathogenesis

1. Myocardial blood oxygen supply and demand balance disorder Due to the non-stop systolic and diastolic activity of the heart, myocardial oxygen demand is relatively high, and the myocardium can not perform anaerobic exercise for a long time like skeletal muscle, and the oxygen bond generated is reserved for later repayment. Aerobic respiration must be performed, so even in a quiet state, the myocardium also takes up 75% of the available oxygen from the coronary circulation, which has reached the maximum oxygen uptake. The main pathogenesis of ischemic cardiomyopathy lies in Long-term myocardial ischemia, myocardial blood supply is affected by myocardial oxygen consumption and myocardial oxygen supply, while myocardial ischemia is insufficient for myocardial oxygen supply to meet myocardial oxygen demand, resulting in imbalance of blood oxygen supply and demand. A result.

(1) Factors determining myocardial oxygen consumption: The amount of myocardial oxygen consumption depends on the following six factors: ventricular wall tension during systole, continuous tension interval, myocardial contractility and basal metabolism, electrical activation and myocardial fiber shortening, among which The first three are the decisive factors determining the amount of myocardial oxygen consumption. The latter three are secondary factors, systolic wall tension = systolic ventricular volume × intraluminal pressure ÷ wall thickness; and tension duration = heart rate × Systolic ejection time, so when the left ventricular systolic pressure, volume or wall thickness increases; or heart rate increases; or myocardial contractility increases, myocardial oxygen consumption increases, in practical applications, measuring all these indicators is not easy, Therefore, the "double product" of systolic blood pressure and heart rate is commonly used as the myocardial oxygen consumption index in clinical practice. This method is simple and reliable.

(2) Factors determining myocardial oxygen supply: The oxygen supply of the myocardium depends on the oxygen uptake and delivery. The most important factor determining the oxygen supply of the myocardium is the blood flow of the coronary artery, because the myocardium has been extracted to the utmost extent. Oxygen in the coronary blood flow, so when the myocardial oxygen demand increases, it can only increase the oxygen uptake by increasing the coronary blood flow. The coronary blood flow and the perfusion pressure difference are the proximal coronary artery and the right atrium. The pressure difference is proportional to the coronary artery resistance. According to the difference of the main effects, the coronary artery can be divided into two sections, which are located on the surface of the pericardial visceral layer. The lumen of the blood vessel is thicker and mainly transmits blood flow. The effect, which produces only a small resistance, is called "transmission of blood vessels"; this part of the blood vessels gradually branches into smaller blood vessels into the anterior capillary vessels after entering the myocardium. This part of the blood vessel diameter changes from the resistance of the whole coronary circulation. The decisive role, called "resistance blood vessels", specifically, factors affecting coronary blood flow are:

1 Influenced by the cardiac cycle: The blood flow to the left ventricular myocardium is affected by the cardiac cycle, and the blood flow to the left ventricular myocardium during systole is only 7% to 45% of the diastolic phase, which is mainly due to myocardial infarction during left ventricular contraction. The resistance vessels are squeezed. Because the right ventricular ventricular muscle is relatively thin, it is less affected by the cardiac cycle, and the blood flow to the right ventricle is almost the same during the systolic and diastolic phases.

2 Influenced by innervation: -receptors and -receptors are distributed on the wall of coronary vessels, and when the -receptors are excited, coronary artery contraction including resistance vessels and blood vessels is caused to cause blood flow. Increased resistance, and excitatory -receptors can cause coronary dilation, which increases coronary blood flow. If -receptor block, -receptor causes coronary artery contraction to be more obvious.

3 affected by myocardial metabolites: some metabolites produced during myocardial metabolism affect coronary blood flow, including oxygen, carbon dioxide, hydrogen ions, potassium ions, adenosine, lactic acid, etc., when myocardial metabolism increases or crown When arterial blood flow is reduced, the local concentration of one or a group of metabolites is increased, which makes the resistance vascular smooth muscle relax, reduces coronary resistance, and increases coronary blood flow.

4 by the blood vessel wall and platelet-derived bioactive substances: the blood vessel wall can synthesize prostacyclin (PGI2), which has obvious vasodilating effect; while platelets can release TXA2 during aggregation, which has a strong vasoconstriction effect. In general, the two substances are in a dynamic balance in the blood flow. If the balance between the two is broken, it will obviously affect the change of vascular tone. In addition, the endothelium released from the vascular endothelium (endothelium) -derived relaxing factor (EDRF) and endothelin (epithelin) also have strong biological activity in the cardiovascular system. Endothelium-derived relaxing factor dilates blood vessels, and endothelin is the strongest vasoconstrictor, and the growth and decline of these two substances are also Significantly affects the tension of the coronary arteries.

When the atherosclerosis of the larger coronary artery leads to occlusion of the lumen, the local blood flow resistance is significantly increased, and the vascular bed of the distal small artery is adjusted to achieve maximum expansion to reduce blood flow resistance and ensure sufficient blood flow. If the coronary vasodilator reserve is near the limit, when the myocardial oxygen consumption increases, the ability to increase blood flow through coronary artery expansion is very limited. Repeated regulation by the above various mechanisms can not meet the blood oxygen supply of the heart. Myocardial ischemia.

2. The effect of ischemia on the myocardium

(1) Effects on myocardial metabolism: Myocardial energy metabolism is mainly derived from high-energy phosphate compounds (adenosine triphosphate and phosphocreatine assisted system) produced by glucose and fatty acid oxidative metabolism. The energy required for myocardial activity is almost always high-energy phosphoric acid. The compound is produced by oxidative metabolism in the mitochondria. Since the myocardium cannot synthesize lactic acid under normal conditions, the production of triphosphate adenosine by glycolysis is not the main pathway of myocardial productivity. However, when myocardial ischemia and hypoxia, glycolysis becomes a cardiomyocyte. To obtain the main source of adenosine triphosphate, glycolysis can provide a small amount of high-energy phosphate compounds, which can slow down the level of high-energy phosphate compounds in ischemic myocardium, so that the ischemic myocardial injury does not deteriorate rapidly, but the local area of the myocardium Increased lactic acid synthesis causes lactic acid accumulation. If the myocardium continues to be hypoxic, it will cause irreversible damage to the myocardium.

(2) Effects on cardiac function: The direct source of energy required for cardiomyocytes is high-energy phosphate compounds, while the production of high-energy phosphate compounds is mainly based on aerobic metabolism. If myocardial blood supply suddenly stops, ATP and phosphate muscles in myocardial tissue The acid level is rapidly reduced, acidosis occurs in the cardiomyocytes, the sensitivity of the contractile protein to calcium ions is reduced, and the accumulation of phosphate and lipids causes myocardial diastolic and systolic dysfunction to occur immediately. First, the diastolic function is affected, which is expressed as -dp/ Dt decreased, ventricular end-diastolic pressure increased, compliance decreased; subsequent ventricular systolic function was impaired, +dp+dt progressive abnormality, and finally local myocardial systolic contraction, if the ischemic myocardium involved in a larger range, will reduce the stroke volume, Cardiac function indicators such as cardiac output and ventricular ejection fraction, short ischemic time, rapid recovery of blood flow, myocardial contraction and diastolic function can also recover quickly, severe ischemic but shorter, myocardium does not occur permanently Sexual damage, at this time under the electron microscope, no damage was observed in the cell membrane, and the high-energy phosphate compound was not lower than 70% of the control level. After the blood flow was restored, the cardiomyocytes were Adenylate gradually recovers, but the recovery of myocardial diastolic and systolic function takes a long time. This severe reversible damage to the myocardium is called myocardial stunning. The length of recovery depends on the length of ischemia. Depending on the severity, it can last for several minutes, several hours up to several days. Severe and long-lasting ischemia leads to irreversible myocardial cell damage, from subendocardial to pericardial dysplasia, and obvious cell membrane damage. In one case, due to the incomplete occlusion of the coronary artery stenosis, the blood flow to the myocardium is lower than normal. In order to reduce the oxygen consumption, the myocardium can reduce the blood flow by reducing the metabolism and reducing the work to achieve the myocardial oxygen supply. A new balance between aerobic conditions. In this state, the myocardium remains viable under low function. If the ischemia does not deteriorate further, the part of the myocardium will neither infarct nor cause clinical symptoms of ischemia. It is called hibernating myocardium. (hibernating myocardium), the state of less blood supply of hibernating myocardium is less self-protective. After waiting for myocardial blood flow is restored, the function of hibernating myocardium can be fully restored, if the balance in such a state of low blood supply is broken, converted to oxygen supply and demand balance in an unfavorable direction, ischemic signs and symptoms occur.

(3) Effects on electrical activity: Myocardial ischemia affects the permeability of myocardial cell membrane to ions, resulting in loss of sodium pump activity, intracellular sodium, and water retention; due to enhanced anaerobic glycolysis in cardiomyocytes, intracellular Acidosis occurs; hyperkalemia occurs outside the cell, this change of ischemic myocardium affects the depolarization and repolarization of the ventricle, causing abnormalities in the release and conduction of cardiac impulses, thereby causing severe heart rhythm in patients with ischemic cardiomyopathy. Abnormal.

In patients with coronary arterial stenosis and long-term, chronic blood flow reduction, myocardial hibernation and myocardial stunning are common, resulting in long-term inhibition of left ventricular function, if multiple coronary arteries are severe Stenosis, when myocardial oxygen consumption increased significantly or severe myocardial ischemia multiple accumulation, can lead to irreversible necrosis of the myocardium, and the myocardium is often mixed with necrotic myocardial tissue, due to extensive or multiple infarction of ischemia Myocardium is difficult to maintain a good compensation, so that the number of damaged or necrotic cardiomyocytes gradually increases. The ischemic myocardium is affected by various factors, fibrosis, myocardial interstitial collagen deposition and scar formation after myocardial necrosis, making the wall Increased tension and stiffness, wall motion is generally weakened, the heart is significantly enlarged, and even congestive heart failure is caused, developing ischemic cardiomyopathy, but not with ventricular aneurysm.

Ischemic cardiomyopathy prevention

Because the main cause of ischemic cardiomyopathy is coronary atherosclerotic heart disease, it is important to prevent coronary heart disease in the prevention of this disease. The main measures are as follows:

1. Conduct health education for the population, improve citizens' self-care awareness, avoid or change bad habits, quit smoking, pay attention to reasonable diet, exercise properly, maintain psychological balance, etc., reduce the incidence of coronary heart disease, middle-aged and above, with a light diet It is advisable to reduce animal fat, quit smoking, drink a little alcohol, not drink or drink too much, exercise properly, and patients who have suffered from heartache should be treated for a long time. When heartache occurs, they should be treated promptly. Patients with myocardial infarction, after heartache Absolute bed rest for two weeks, then gradually resume activities, sit up on the bed, gradually extend the sitting time, one week later, you can go to the bedside activities, to recover physical strength, outdoor activities, for patients with myocardial infarction, give some liquid food in the first two weeks, or Semi-liquid food is suitable, but also pay attention to the smooth flow of the stool, when the solution is not available, for patients with myocardial infarction, it is necessary to closely observe the condition, when the condition changes, it should be treated in time.

2. Regular routine physical examination, early detection of high incidence of coronary heart disease, such as high blood pressure, high blood lipids, diabetes, obesity, smoking and family history of coronary heart disease, etc., give active control and treatment.

Ischemic cardiomyopathy Complications heart failure arrhythmia shock

1, heart failure

Heart failure is divided into left heart failure and right heart failure. Left heart failure is mainly characterized by fatigue and fatigue. It is difficult to breathe. It is labor-induced dyspnea at the beginning. It eventually evolves into difficulty breathing at rest. It can only sit and breathe, paroxysmal. Dyspnea is a typical manifestation of left heart failure, more than a sudden onset of sleep, chest tightness, shortness of breath, cough, wheezing, especially severe acute pulmonary edema and severe asthma, sitting breathing, extreme anxiety and cough Spit foamy sputum (typically pink foamy sputum), purpura and other symptoms of lung stagnation, right heart failure mainly manifested as lower extremity edema, jugular vein engorgement, loss of appetite, nausea and vomiting, oliguria, nocturia, Separation of drinking water and urination, etc., the main signs are the lung bottom wet rales or whole lung wet rales, the second sound of the pulmonary valve is hyperthyroidism, galloping and alternating veins, hepatomegaly, positive liver and neck reversal, X-ray examination to the left The ventricle or the left atrium was mainly enlarged. In the laboratory, the left heart failure had an extended period of the arm tongue. The floating catheter was used to measure the increase of the pulmonary artery capillary wedge pressure. The right heart failure had the prolongation of the arm lung and the venous pressure. Significantly higher.

2, arrhythmia

Arrhythmia: The normal heart rate is 60-100 beats per minute (adult). The rules are regular. Before the heart beats, the impulses are generated and transmitted. The origin of the heart's activation or the conduction of the agitation is abnormal, causing the whole or part of the heart. The activity becomes too fast, too slow or irregular, or the disorder of each part is disordered, causing a change in the rate or rhythm of the heart beat, which is called arrhythmia. Clinical manifestation is a sudden regular or irregular Palpitations, chest pain, dizziness, discomfort in the anterior region, nausea, shortness of breath, coldness and fainting of the hands and feet, and even unconsciousness, a small number of patients with arrhythmia can be asymptomatic, only ECG changes.

3, shock

Shock refers to a state in which the perfusion of the surrounding tissue is insufficient due to insufficient cardiac output or abnormal distribution of peripheral blood flow, and it is unable to maintain life. It usually has hypotension and oliguria. Symptoms and signs may be due to shock itself or its disease. Cause. Mind may remain awake, but indifferent, blurred consciousness, common sleepiness. Cold hands and feet, wet, often cyanosis and pale skin. Capillary filling time is prolonged, in extremely severe cases, large areas of mesh can occur Bleu. In addition to heart block or end-stage bradycardia, the pulse is usually fine. Sometimes, only the femoral or carotid artery can twitch and beat. There may be increased breathing and hyperventilation, when the brain is hypoperfused to the respiratory center. Apnea may occur during depletion, which may be terminal performance. The blood pressure measured by the airbag cuff at the time of shock is often low (systolic pressure <90 mmHg) or not measured, but the value directly measured from the arterial cannula is often compared. It is obviously high.

Symptoms of ischemic cardiomyopathy Common symptoms Cardiac structural abnormalities Cardiotrophy disorders Arrhythmias Pulmonary embolism Chest pain Myocardial infarction Labor dyspnea Heart stiffness Cardiac angina

According to the different clinical manifestations of patients, ischemic cardiomyopathy can be divided into two categories, namely, congestive ischemic cardiomyopathy and restricted ischemic cardiomyopathy. Their clinical manifestations are very similar to those in primary cardiomyopathy. Dilated cardiomyopathy and restrictive cardiomyopathy, however, are different in nature from ischemic cardiomyopathy and primary cardiomyopathy.

Patients with ischemic cardiomyopathy have different manifestations. Most patients may have symptoms of congestive cardiomyopathy or restrictive cardiomyopathy, while a small number of patients may have no obvious clinical symptoms. The following descriptions are based on different types of ischemic cardiomyopathy. Its corresponding clinical manifestations.

1. Congestive ischemic cardiomyopathy This type of patient with congestive cardiomyopathy accounts for the majority of cardiomyopathy, common in middle and old, mostly male patients, with a history of coronary heart disease, male: female is about 5 ~7:1, the symptoms generally occur gradually, the patient mainly manifests in the following aspects, (1) angina pectoris: angina pectoris is one of the main symptoms of patients, but with the appearance of heart failure, angina pectoris can be gradually reduced or even disappeared, ischemic myocardium The disease has a clear history of coronary heart disease, and the vast majority have more than one history of myocardial infarction. Angina is one of the common clinical symptoms of patients with ischemic cardiomyopathy. However, angina is not a necessary symptom for patients with myocardial ischemia. Some patients can also present only asymptomatic myocardial ischemia, no angina or myocardial infarction, about 72% to 92% of cases of ischemic cardiomyopathy have angina attacks, and some reported 1/3 ~1/2 of cases of myocardial infarction have been missed, and this recurrence and frequent asymptomatic myocardial ischemia or myocardial infarction can gradually cause hyperemic ischemic cardiomyopathy. The absence of angina in these patients may be due to the high pain threshold and the lack of angina as a protective alarm system. However, in such patients, asymptomatic myocardial ischemia persists and myocardial damage persists until In the presence of congestive heart failure, some people think that the clinical significance and harm of this asymptomatic myocardial ischemia is the same as that of myocardial ischemia with angina pectoris. The symptoms of angina pectoris in patients with angina may progress with the condition, congestive heart failure. Gradually worsened, the onset of angina pectoris gradually reduced or even disappeared, only manifested as chest tightness, fatigue, dizziness or difficulty breathing.

(2) Heart failure: Heart failure is often an inevitable manifestation of the development of ischemic cardiomyopathy to a certain stage. Early progress is slow. Once heart failure progresses rapidly, most patients have heart failure in the early stage of chest pain or myocardial infarction. This is due to myocardial diastolic and systolic dysfunction caused by acute myocardial ischemia. Current studies have shown that transient myocardial ischemia, mainly damage early diastolic function, that is, soothing performance; long-term recurrent myocardial ischemia, causing significant late diastolic function Abnormalities, ie, decreased left ventricular compliance, increased stiffness, large myocardial infarction disrupts the myocardial interstitial network, causing acute ventricular dilatation, increasing cardiac compliance; and focal focal myocardial infarction or fibrosis, Can cause increased stiffness of the heart chamber, decreased compliance, that is, ventricular dilatation after myocardial infarction, increased compliance, if myocardial ischemia occurs again, early left ventricular diastolic filling disorder and increased cardiac cavity, patients often show Labor dyspnea, in severe cases, can develop left ventricular function such as sitting breathing and paroxysmal dyspnea at night Full performance, accompanied by fatigue, weak symptoms, heart auscultation, first heart sounds weakened, audible and diastolic middle and late galloping, both lungs can be heard and scattered in the wet voice, late if combined with right ventricular failure, the patient appears Loss of appetite, peripheral edema and swelling of the right upper abdomen, physical examination showed jugular vein filling or anger, enlarged heart, liver enlargement, tenderness, positive sign of hepatic jugular venous return, this peripheral edema develops slowly and hides , for finger edema, often starting from the sagging site, and gradually develop upward.

(3) arrhythmia: long-term, chronic myocardial ischemia leads to myocardial necrosis, myocardial stunning, myocardial hibernation and focal or diffuse fibrosis until scar formation, leading to myocardial electrical activity disorders, including impulsive formation, release and conduction Can produce abnormalities, various types of arrhythmia can occur in the course of congestive ischemic cardiomyopathy, especially ventricular premature contraction, atrial fibrillation and bundle branch block are more common, in the same ischemic myocardium In patients with arrhythmia, the arrhythmia is complex and variable. The main reasons are: 1 the cause of arrhythmia is complex, such as myocardial necrosis, fibrosis, ischemia or other causes of myocardial damage; 2 the mechanism of arrhythmia formation is complex, including the mechanism of reentry , autonomic increase or trigger mechanism; 3 the type of arrhythmia is complex, the same patient can not only occur supraventricular and ventricular arrhythmia, but also can occur conduction block; 4 late arrhythmia type of transient changes, about half of the lack of Blood cardiomyopathy dies from a variety of severe arrhythmias.

(4) Thrombosis and embolism: cases of thrombosis and embolism in the heart chamber are more common in:

1 significantly enlarged heart chamber;

2 atrial fibrillation without anticoagulant therapy;

3 patients with significantly reduced cardiac output, patients who have been in bed for a long time without physical activity are prone to venous thrombosis of the lower extremities, pulmonary embolism occurs after shedding. It has been reported in the literature that the incidence of thrombosis in patients with ischemic cardiomyopathy is 14% to 24%.

It should be noted that although the common clinical manifestation of congestive ischemic cardiomyopathy is congestive heart failure, there are also some patients with severe symptoms and the degree of damage to left ventricular function and myocardial abnormal changes are often not proportional, which may be related to myocardial The size of the infarct is related to the size of the site. In some patients, the myocardial infarction occurs in multiple locations and is distributed in more than two coronary arteries. The extent of necrosis may not be large in terms of a single infarct. However, myocardial necrosis in multiple sites has a much greater impact on ventricular function than those in a part of the myocardium that have the same size of myocardial necrosis. In addition, the average wall thickness of the heart in patients with ischemic cardiomyopathy It is thinner than the ventricular wall of patients with congestive dilated cardiomyopathy or valvular heart disease who have recurrent myocardial infarction but no congestive ischemic cardiomyopathy. This may be due to extensive coronary artery disease, which severely limits blood. Supply, so that the non-necrotic myocardium can not be moderately hypertrophied or the myocardial temporary hypertrophy eventually shrinks due to ischemia.

2. Restricted ischemic cardiomyopathy Although most patients with ischemic cardiomyopathy behaves like dilated cardiomyopathy, the clinical manifestations of a small number of patients are mainly left ventricular diastolic dysfunction, while myocardial contractile function is normal or only light. Abnormalities, similar to the symptoms and signs of restrictive cardiomyopathy, are called restricted ischemic cardiomyopathy or stiff heart syndrome. Patients often have exertional dyspnea and/or angina pectoris. Limited mobility, these patients often see patients with recurrent pulmonary edema, patients can have no history of myocardial infarction, the heart often does not expand, the patient's left ventricular end-diastolic pressure increases, end-diastolic volume increases and the ejection fraction is only slightly reduced, even In the case of acute myocardial infarction, some patients may have pulmonary hemorrhage and even pulmonary edema, but they may have a near-normal left ventricular ejection fraction, which fully indicates that the cardiac dysfunction of these patients is mainly due to diastolic dysfunction. Patients with ischemic cardiomyopathy often have abnormal pressure-volume curves. When the patient is at rest, the left ventricular end-diastolic pressure is also higher than normal. When ischemic attack, a further decline in ventricular compliance (i.e., a further increase in the stiffness of the heart) so that the left ventricular end diastolic pressure, increased pulmonary edema, and systolic function may be normal or only mildly impaired.

Examination of ischemic cardiomyopathy

There are several ways to check for ischemic cardiomyopathy:

1. Electrocardiogram examination : mainly manifested as left ventricular hypertrophy, ST segment depression, T wave changes, abnormal Q wave and various arrhythmias, such as sinus tachycardia, atrial premature beats, ventricular premature beats, ventricular tachycardia, atrium The tremor and heart block, and the ST-T change leads are often distributed according to the coronary artery innervation area, which has the value of localization diagnosis.

2. Chest X-ray examination : the main manifestations of increased heart shadow, and most of the aortic heart (mainly left ventricular enlargement, right ventricular majority), a small number of heart shadows are large, and can be seen as ascending aorta Wide and aortic calcification, etc., most patients have different degrees of pulmonary congestion, but the pulmonary artery segment changes are not obvious, chest X-ray examination of patients with congestive ischemic cardiomyopathy shows that the heart can have signs of whole heart or left heart enlargement, and Restricted ischemic cardiomyopathy X-ray examination of the heart is not large, there is no heart cavity dilatation, may have pulmonary congestion, pulmonary interstitial edema and pleural effusion and other signs, sometimes visible coronary and aortic calcification.

3. Ultrasonography of the heart : The inner diameter of the heart chamber is enlarged, and the left atrium and left ventricle are enlarged. The segmental motion of the wall is weakened or disappeared, and the left ventricular ejection fraction is significantly reduced. Most patients have mitral valve mouth. Reflux, and aortic valve thickening and calcification can be seen. Congestive ischemic cardiomyopathy suggests a general enlargement of the heart, often with left ventricular enlargement, with increased end-diastolic and end-systolic ventricular lumen diameter and left ventricular ejection. The blood fraction decreases, the wall of the wall often shows a multi-segmental exercise weakening, disappearing or stiffening. Unlike dilated cardiomyopathy, the wall motion is often a generalized weakening change, and sometimes the thrombus formation in the heart chamber is visible. Type Ischemic cardiomyopathy often manifests as diastolic limitation, ventricular myocardium is generally mildly contractile, and ejection fraction is only slightly decreased. Generally, no ventricular aneurysm or local wall motion disorder is seen.

4. Coronary angiography: patients often have multiple vascular stenosis lesions. Some people have statistics on two or more coronary artery lesions accounting for more than 98% of all statistical cases, and all have left anterior descending artery involvement, restricted type Coronary angiography of ischemic cardiomyopathy often has more than two diffuse vasculopathy. Ventricular angiography shows a general mild contractility of the ventricle, no ventricular aneurysm, local wall motion disorder and mitral regurgitation.

5. Ventricular nucleus angiography showed enlargement of the heart chamber, wall motion disorder and cardiac dysfunction. Myocardial imaging showed multi-segment myocardial radionuclide perfusion abnormalities.

6. Left ventricular end-diastolic pressure, left atrial pressure and pulmonary wedge pressure increased in patients with cardiac catheterization and ischemic cardiomyopathy. Left ventricular ejection fraction was significantly reduced by ventriculography, left ventricular enlargement and multi-segment, multi-regional Ventricular dyskinesia and mitral regurgitation, patients with restricted ischemic cardiomyopathy, even after pulmonary edema subsided, showed a slight increase in left ventricular end-diastolic pressure, increased end-diastolic volume and a slight decrease in ejection fraction. There are mitral regurgitation and so on.

Diagnosis and diagnosis of ischemic cardiomyopathy

diagnosis

To diagnose this disease, you must have 3 positive conditions and 2 negative conditions. The 3 positive conditions are: 1 have a clear history of coronary heart disease, at least 1 or more myocardial infarction (Q-wave or no Q-wave myocardial infarction); 2 heart Significantly expanded; 3 cardiac dysfunction signs and/or laboratory basis; 2 negative conditions are: 1 exclude certain complications of coronary heart disease such as interventricular septal perforation, ventricular aneurysm and papillary muscle dysfunction due to mitral regurgitation Incomplete, because these complications can also cause heart enlargement and cardiac insufficiency, but the main reason is that the above mechanical complications lead to cardiac hemodynamic disorder, although the ejection fraction is decreased, but less < 0.35, not the result of long-term hypoxia, ischemia and myocardial fibrosis, can not be called ischemic cardiomyopathy, the above is a complication of myocardial infarction and coronary heart disease, the main treatment is surgical correction, and ischemia Cardiomyopathy is mainly medical treatment, there is a big difference between the two, 2 except for other heart disease or other causes of heart enlargement and heart failure.

Differential diagnosis

The most common cause of ischemic cardiomyopathy is coronary heart disease, which is mainly caused by coronary atherosclerotic stenosis, occlusion, sputum and other diseases, and a few are caused by congenital abnormalities of coronary arteries and coronary arteritis.

(a) dilated cardiomyopathy

Dilated cardiomyopathy is an unexplained cardiomyopathy characterized by unilateral or bilateral cardiac expansion, myocardial systolic dysfunction, clinical manifestations of recurrent congestive heart failure and arrhythmia, and its clinical features and ICM. Very similar, differential diagnosis is also very difficult, especially in patients over the age of 50, if accompanied by angina, it is easily misdiagnosed as ICM, because the principle of treatment of dilated cardiomyopathy and ICM is very different, so the correct identification of the two has The important clinical significance, while mastering the following points, will help to identify the two.

1. The age of onset of dilated cardiomyopathy is relatively mild, often with a history of myocarditis; while ICM is older, most have a history of angina or myocardial infarction, often accompanied by hypertension, hyperlipidemia and diabetes.

2. Electrocardiogram examination: electrocardiogram of patients with dilated cardiomyopathy and ICM can be expressed as left ventricular hypertrophy with strain, abnormal Q wave and arrhythmia, etc., difficult to identify, but dilated cardiomyopathy often accompanied by complete left bundle branch block The ECG ST-T changes are also mostly non-specific and have no diagnostic value for localization.

3. Chest X-ray examination: the heart shadow of patients with dilated cardiomyopathy is large, the ratio of cardiothoracic to more than 0.6. Above the perspective, the heart beat is obviously weakened. In the late stage, there are often pleural effusions, pericardial effusion or signs of pulmonary embolism. Although ICM patients have a significant increase in heart shadow, most of them have aortic heart, accompanied by ascending aorta widening and aortic calcification.

4. Identification of dilated cardiomyopathy and ICM during echocardiography:

(1) Morphological comparison of heart: Dilated cardiomyopathy is widely affected by myocardium, and it is often manifested that 4 heart chambers are generally significantly enlarged; while ICM is often characterized by left atrial and left ventricular enlargement, often accompanied by aortic valve and Thickening of the annulus, calcification,

(2) Comparison of wall thickness and movement status: the wall thickness of patients with dilated cardiomyopathy is diffusely thinned, and the wall motion is diffusely weakened; while the myocardial ischemia site of ICM patients is closely related to the distribution of coronary artery lesions, severe ischemic At the site, the wall of the chamber is thinned and the movement is weakened. Therefore, the thickness of the common wall is limited, and the wall motion is weakened or disappeared.

(3) Hemodynamic changes: patients with dilated cardiomyopathy have a generalized enlargement of the heart, often secondary to changes in the structure of the valve and valve support, resulting in significant regurgitation of multiple valves; and ICM patients with left atrium and The left ventricle is enlarged, often accompanied by mitral valve regurgitation.

(4) patients with dilated cardiomyopathy have a wide range of myocardial lesions, left ventricular enlargement and myocardial contraction, so the cardiac systolic function is significantly reduced; while ICM patients have reduced left ventricular ejection fraction and short axis shortening rate, but The degree is relatively lighter than dilated cardiomyopathy.

5. Peripheral artery ultrasound exploration: It is currently believed that the use of peripheral arterial ultrasound to explore the carotid artery and femoral artery can be used as a window to reveal coronary lesions, and can help differential diagnosis of dilated cardiomyopathy and ICM. Studies have shown that Only a few patients with dilated cardiomyopathy have positive carotid and femoral plaques; while ICM patients have positive carotid and femoral plaques, although carotid and femoral plaques in patients with dilated cardiomyopathy are not absolutely negative, but Carotid and femoral plaque negative can be used as an important condition to rule out the diagnosis of ICM.

6. Radionuclide examination: The distribution of nuclide in the myocardium is not only related to blood flow, but also closely related to the function and fibrosis of cardiomyocytes. It is generally believed that ICM is more severe than fibrotic in patients with dilated cardiomyopathy. To a higher degree, therefore, 99m Tc-methoxyisobutyl isocyanide (M IB I) myocardial perfusion imaging examination, dilated cardiomyopathy mostly showed no segmental distribution, scattered sparse areas, a small range, The degree is light, showing more small piece defects or variegated changes; while ICM patients are mostly segmental perfusion abnormalities distributed by coronary artery, myocardial perfusion damage is heavy, and the range is large; when the perfusion defect is larger than the left 40% of the ventricular wall has a higher value for the diagnosis of ICM.

7. Cardiac catheterization and cardiovascular angiography: left ventricular end-diastolic pressure, left atrial pressure and pulmonary capillary wedge pressure increase, cardiac output and stroke volume decreased, ejection fraction decreased in patients with dilated cardiomyopathy Left ventricular angiography showed a dilated left ventricular cavity and a weakened left ventricular wall motion; however, coronary angiography was normal.

(two) alcoholic cardiomyopathy

Alcoholic cardiomyopathy refers to myocardial lesions caused by long-term heavy drinking, mainly manifested as cardiac enlargement, heart failure and arrhythmia. There are many similarities between clinical and expanded ICM, and identification is more difficult. Compared with ICM, The following characteristics of alcoholic cardiomyopathy contribute to the identification of the two:

(1) There is a long history of heavy drinking,

(2) Most of the men are 30 to 50 years old, and most of them are accompanied by alcoholic cirrhosis.

(3) After stopping drinking for 3 to 6 months, the condition may gradually reverse or stop worsening, and the enlarged heart may be reduced.

(4) Electrocardiogram examination: visible non-specific ST-T changes (no diagnostic value); those who stopped drinking early in the course of the disease, ST-T changes can return to normal after a few months; if the disease is advanced, even if drinking is stopped, its ST- T changes are also difficult to return to normal,

(5) Chest X-ray examination: the heart shadow is large, the heart-thorax ratio is more than 0.6. Above, the heart beat is weakened, there is no ascending aortic widening and aortic calcification signs, (6) cardiac ultrasound examination: The chambers of the heart were enlarged, but the left atrium and left ventricle were enlarged. The wall motion was diffusely weakened, and the left ventricular ejection fraction was significantly reduced. The mitral valve was often combined with tricuspid regurgitation, but no Segmental wall motion abnormalities and aortic valve thickening, calcification signs, in addition, dynamic observation of patients after stopping drinking, showing a significant reduction in the left atrium and left ventricular diameter.

(c) Keshan disease

Keshan disease is an endemic cardiomyopathy of unknown cause. It is clinically classified into acute type, sub-acute type, slow type and latent type IV according to its rapid onset and cardiac function. Slow Keshan disease The patient's main manifestations are cardiac enlargement and congestive heart failure. His electrocardiogram, echocardiography and chest X-ray findings have many similarities with dilated ICM, but the following clinical features of Keshan disease contribute to both Differential diagnosis:

(1) There are obvious regionalities, and the ward is distributed in the low provinces including Hei, Ji, Liao, Inner Mongolia, Jin, Yi, Lu, Yu, Shan, Gan, Sichuan, Yunnan, Tibet, Guizhou, and Hubei. On the selenium zone,

(2) It has the characteristics of frequent populations. The vast majority of patients are women in the agricultural population and pre-weaning preschool children, while ICM is more common in the elderly.

(3) Electrocardiogram examination showed that most patients with Keshan disease had ECG changes, among which ventricular premature beats were the most common, followed by ST-T changes and atrioventricular block, but ST-T changed to non-specific, no Positioning diagnostic value,

(4) Chest X-ray examination showed that the majority of patients had a large heart shadow, a small number of mitral valve or aortic type; the pulsation was significantly weakened under fluoroscopy; no ascending aortic widening and aortic calcification signs,

(5) Cardiac ultrasonography: The heart of patients with Keshan disease is generally enlarged, the diffuse movement of the wall is weakened, the myocardial contraction is weak, the systolic function of the heart is significantly reduced, and the valvular regurgitation is accompanied by multiple valves; and the ICM patient room The wall is a segmental dyskinesia, and often combined with aortic valve thickening and calcification.

(4) Myocarditis

Viral-induced myocarditis is common, often a part of systemic infection, mostly after acute viral infection, patients often have respiratory tract inflammation or gastrointestinal inflammation, clinical manifestations vary in severity, lighter only chest tightness, Pain in the precordial area, palpitations and fatigue; severe heart enlargement, heart failure or severe arrhythmia such as complete atrioventricular block, ventricular tachycardia, and even ventricular fibrillation, a small number of patients in the acute phase After the heart gradually increased, resulting in progressive heart failure, its electrocardiogram, echocardiography and nuclear myocardial imaging changes similar to the corresponding changes in patients with ischemic cardiomyopathy, but myocarditis patients are mostly adolescents or middle-aged, serum viral infection The related antibodies are increased, and the virus is isolated from the throat swab or feces. The endocardial or myocardial tissue biopsy shows myocardial necrosis, inflammatory cell infiltration, and the isolation of the pathogenic virus from the myocardium may contribute to the disease. The identification, coronary angiography is generally no coronary stenosis.

(5) hypothyroid heart disease

In patients with hypothyroid heart disease, the heart is enlarged and the myocardial tension is weakened. There are mucin and mucopolysaccharide deposits in the cardiomyocytes, which are pseudohypertrophy. In severe cases, the myocardial fibers are broken and necrotic. The interstitial has obvious edema. The edema fluid contains a large amount. Mucin, clinically, there are obvious manifestations of hypothyroidism, such as cold, apathy, slow movement, sparse hair and mucous edema, may have difficulty breathing after fatigue, fatigue and angina, generally have obviousPQRST T4T3131I131I

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