ischemic cardiomyopathy in the elderly
Introduction
Introduction to ischemic cardiomyopathy in the elderly Ischemic cardiomyopathy in the elderly refers to myocardial localization or diffuse fibrosis due to long-term myocardial ischemia, resulting in impaired contraction and/or diastolic function, causing heart enlargement or stiffness, congestive heart failure, arrhythmia, etc. A series of clinical manifestations of the syndrome. Its clinical manifestations are similar to those of primary hyperemia cardiomyopathy but intrinsic ischemic cardiomyopathy (ICM) is a severe myocardial dysfunction caused by a decrease in coronary blood supply. basic knowledge The proportion of illness: the incidence rate is about 0.03% - 0.04% Susceptible people: the elderly Mode of infection: non-infectious Complications: angina pectoris, acute myocardial infarction, sudden death
Cause
The cause of ischemic cardiomyopathy in the elderly
Coronary atherosclerosis (30%):
Is a common cause of myocardial ischemia, atherosclerosis is the result of a series of complex effects between the arterial wall cells, extracellular matrix, blood components, local hemodynamics, environmental and genetic factors, epidemiological studies have shown coronary The onset of atherosclerosis is affected by a combination of factors, including elevated blood pressure, hyperglycemia, hypercholesterolemia, elevated fibrinogen, and smoking, all of which are major risk factors for atherosclerosis. Diet, obesity or overweight, lack of physical activity, type A personality and family history of coronary heart disease are also risk factors for coronary heart disease.
ICM patients, especially congestive ischemic cardiomyopathy, often have significant atherosclerotic stenosis in multiple coronary arteries. It is reported that 72% of patients with 3 vascular lesions in this disease have 2 vascular lesions. 27%, single-vessel disease is rare, Atkinson found in 35 autopsy results of ischemic cardiomyopathy, the average of more than 2 cases of coronary artery stenosis more than 75%, of which 26 cases have evidence of myocardial infarction, Nine patients had no pathological manifestations of myocardial infarction, and Edward found that 100% of patients with ischemic cardiomyopathy had myocardial infarction at the autopsy. It was due to severe coronary artery stenosis that caused long-term hypoperfusion in a large range of myocardial infarction. Ischemic myocardial degeneration, necrosis, myocardial fibrosis, ventricular wall replaced by large scar tissue, ventricular hypertrophy, enlargement, decreased myocardial contractility and decreased ventricular compliance, leading to cardiac insufficiency.
Thrombosis (20%):
Recent studies have confirmed that coronary artery acute thrombosis is the main cause of acute coronary syndrome. On the basis of atherosclerotic plaque, acute thrombosis occurs, and about 3/4 of the plaque in the thrombus is broken. (or) bleeding, 31 cases of acute myocardial infarction in Beijing Fuwai Hospital, autopsy results, found in 21 patients with coronary artery thrombosis, autopsy proved that all thrombosis is blocked in the proximal branch of the coronary artery, the cumulative range of penetrating infarction is wider Left heart failure or cardiogenic shock complications are common. Some patients have thrombolytic recanalization, and a few patients have thrombosis, resulting in persistent stenosis or occlusion of the vascular lumen. In survivors after acute recovery, Most patients will have extensive wall motion diminished or disappeared, and the ventricular cavity is significantly enlarged.
Vasculitis (10%):
A variety of rheumatic diseases can accumulate coronary artery coronary artery disease, repeated inflammatory activities, repair, and mechanization can cause coronary stenosis, leading to myocardial ischemia, such as systemic lupus erythematosus, rheumatoid arthritis, knot Nodular polyarteritis, viral coronary arteritis, etc., nodular polyarteritis, also known as nodular periarteritis, is a major accumulation of necrotizing vasculitis of small arteries, lesions can be segmental It occurs at the bifurcation of the arteries, and extends to the small arteries, which is easy to form small aneurysms. About 60% of patients with nodular polyarteritis can develop coronary arteritis, cause myocardial ischemia, and induce angina or myocardial Infarction, and even cause ischemic cardiomyopathy.
Other (10%):
The factors that can cause chronic myocardial ischemia are coronary microvascular disease (X syndrome) and abnormal coronary structure, such as myocardial bridge, human coronary artery trunk and its large branches, mainly walking in the adipose tissue under the pericardial visceral layer. Or the deep surface of the visceral layer of the pericardium, sometimes covered by the superficial myocardium, and after walking a distance in the myocardium, it is shallow to the surface of the myocardium. This segment of the artery covered by the myocardium is called the wall coronary artery, and the coronary artery is covered. This part of the myocardium is called a myocardial bridge. When the myocardial bridge contracts, it compresses the coronary artery surrounded by it, which can lead to severe coronary stenosis, affecting local myocardial blood supply and causing myocardial ischemia.
In addition, under the action of humoral and neurological factors, the vascular smooth muscle response is abnormally enhanced, and vasospasm occurs. Especially in the presence of atherosclerosis, the extensive blood vessels often show a slow relaxation response, which can cause vasomotor vasomotion. Dysfunction leads to aggravation of myocardial ischemia. Many factors have been involved in the regulation of vascular smooth muscle tendon contraction, such as adrenergic alpha receptor agonism, local platelet aggregation and release of thromboxane A2 (TXA2), and hypercholesterolemia or topical porridge. The sclerosing lesions can cause abnormal vascular reactivity, and ergometrine is the most effective drug for inducing sputum, and nitroglycerin and calcium antagonists can effectively alleviate this sputum.
Pathogenesis
1. Myocardial oxygen supply aerobic balance imbalance
Cardiac oxygenation and aerobic imbalance lead to myocardial infarction, necrosis, apoptosis, myocardial fibrosis, myocardial scar and heart failure, lesions of the tendon and capillary network cause myocardial cell reduction and necrosis can be myocardial infarction The direct consequences can also be caused by chronic cumulative myocardial ischemia. Therefore, there may be a block-like necrotic area on the ventricular wall, or there may be non-continuous multiple focal myocardial damage.
Myocardium is constantly contracting and diastolic, myocardial oxygen demand, even in a quiet state, the myocardium should maximize the intake of 75% of available oxygen from the coronary circulation, and the myocardium can not be as long as skeletal muscle The anaerobic exercise, myocardial must have aerobic respiration, determine the amount of myocardial oxygen consumption depends on the following six factors: systolic wall tension, tension duration, myocardial contractility and basal metabolism, electrical activation and myocardial fiber shortening, before The three are the decisive factors determining the amount of myocardial oxygen consumption. The latter three are secondary factors. When the left ventricular systolic pressure, volume and wall thickness increase, or heart rate increases, myocardial contractility increases, myocardial oxygen consumption increases. Clinically, the "double product" of systolic blood pressure and heart rate is commonly used as the myocardial oxygen consumption index. When the myocardial oxygen demand increases, the coronary blood flow can be increased to increase oxygen intake, coronary blood flow and perfusion pressure. The step is proportional to the pressure difference between the proximal coronary artery and the right atrium, and inversely proportional to the coronary artery resistance. The coronary artery can be divided into two segments, located in the pericardial visceral layer. A section of the surface, the lumen of the blood vessel is relatively large, mainly for transmitting blood flow, and only produces a small resistance, called "transmission of blood vessels". This part of the blood vessel gradually branches into a smaller blood vessel until the capillary anterior blood vessel. This part of the change in vessel diameter plays a decisive role in the resistance of the entire coronary circulation, called "resistance blood vessels". The blood vessels in the myocardium are squeezed during contraction of the left ventricle, and the blood flow to the left ventricular myocardium during systole. The flow rate is only 7% to 45% of the diastolic phase, so when the diastolic phase is shortened, the coronary blood flow is reduced, and when the alpha receptor distributed on the coronary vessel wall is excited, the coronary artery including the main blood vessel and the transmitted blood vessel is caused. Contraction increases blood flow resistance, and excitatory beta receptors can increase coronary blood flow due to coronary dilation.
2. Cardiomyocyte energy metabolism disorder
Myocardial energy metabolism is mainly derived from high-energy phosphate compounds (phosphoric acid adenosine and phosphocreatine assisted system) produced by oxidative metabolism of glucose and fatty acids. The energy required for myocardial activity is almost always produced by oxidative metabolism of high-energy phosphate compounds in mitochondria. Because the myocardium cannot synthesize lactic acid, the adenosine triphosphate produced by glycolysis is not the main pathway of myocardial productivity, but when myocardial ischemia and hypoxia, glycolysis becomes the main source of energy for cardiomyocytes, which can make ischemic myocardium. The damage does not deteriorate rapidly, but the lactic acid synthesis in the myocardium increases in the local area, and the accumulation of lactic acid. If the myocardium continues to be hypoxic, it will cause irreversible damage to the myocardium. If the myocardial blood supply suddenly stops, the adenosine triphosphate and creatine phosphate in the myocardial tissue. The level is rapidly reduced, acidosis occurs in cardiomyocytes, the sensitivity of contractile proteins to calcium ions, and the accumulation of phosphates and lipids cause myocardial diastolic and systolic dysfunction to occur immediately.
3. The effect of ischemia on cardiac function
Ischemia damage to ventricular function can be acute, reversible, or chronic, or acute onset of chronic ventricular dysfunction usually caused by transient myocardial ischemia, chronic ventricular dysfunction often Caused by scattered or diffuse myocardial fibrosis caused by coronary sclerosing stenosis.
For nearly 40 years, people have been convinced that after severe myocardial ischemia, either irreversible myocardial damage or rapid recovery has occurred, however, since the 1980s it has been clear that it is severe but relatively short-lived (generally not After more than 20 minutes of myocardial ischemia, the myocardium will not be permanently damaged. The systolic function can return to normal level after a period of time. The length of recovery depends on the length and severity of the ischemic time and can be sustained. Minutes, hours or days, and then fully recovered, this ischemic heart dysfunction, called "myocardial stun", the myocardium has biochemical changes and morphological abnormalities, when the blood flow is blocked, the myocardial is missing The ATP concentration in the blood area was rapidly reduced. If the perfusion was resumed after 15 minutes of ischemia, the ATP concentration gradually increased after several days, and reached a normal level one week later.
The myocardium is different from the necrotic myocardium. It can survive and has a reserve of myocardial contractility. When the myocardial perfusion is chronically reduced, the myocardium can maintain tissue survival, but it is in a state of sustained left ventricular dysfunction, in order to reduce Myocardial oxygen consumption, the myocardium reduces the metabolism of the coronary arteries by reducing the metabolism, thereby achieving a new balance between myocardial oxygen supply and aerobics. In this state, the myocardium is called "hibernating myocardium". The state of less blood supply and less work is a self-protection mechanism of cardiomyocytes. The hibernating myocardium lasts for a long time, up to several weeks, months or even years. Similar to the myocardium, the hibernating myocardium also has the ability to contract. Reserve, after correction of chronic ischemia, heart function can return to normal.
Stunned myocardium can also occur after myocardial ischemia caused by coronary artery spasm, and can be limited to subendocardial myocardium. Myocardial hibernation is as common as myocardial stunning, especially those with coronary arterial stenosis and long-term chronic disease. Most patients with insufficient blood supply, however, if the ischemia persists and becomes severe, the myocardium and hibernating myocardium develop into necrotic myocardium. Moreover, accumulated myocardial ischemia can also cause myocardial necrosis, and the necrotic myocardium eventually becomes The scar tissue of the contractile function, its influence on the function of the whole ventricle depends on its size, shape and location. Under normal circumstances, the stiffness of the myocardium is more than 10 times larger than the diastolic phase in the systolic phase, which can resist expansion, and acute ischemia. The ventricular wall may have wall motion disorder such as contradictory movement during ischemia, indicating that the stiffness decreases, such as myocardial necrosis and scar formation in this part, and the stiffness also changes. Generally speaking, after myocardial infarction 3~ After 5 days, the infarct area has begun to become quite stiff, and the scar tissue will become more rigid after it is formed. This change is beneficial on the one hand. Prevents contradictions from contraction and reduces the adverse effects caused by uncoordinated movement of the lesion; on the other hand, it has an adverse effect on the diastolic phase of the ventricle.
The meaning of diastolic compliance and dilatation of the ventricle is similar in nature. It can be expressed by V/P, that is, the change in volume accompanying the change of unit or instantaneous pressure. Conversely, it can be expressed by P/V. Stiffness, and this pressure-volume relationship is a curve, the so-called "change in ventricular stiffness or compliance", which refers to the abnormality of the pressure-capacity relationship represented by the parallel movement or slope change of this curve, myocardial stiffness An increase in degree means that the diastolic pressure associated with an increase in any given diastolic volume exceeds normal.
Changes in the diastolic volume of the normal ventricle, almost no change in pressure, that is, the pressure-volume relationship curve is relatively flat, so that ventricular filling and stroke volume vary widely, while ventricular end-diastolic pressure and pulmonary artery The wedge pressure was maintained at a low level. In patients with coronary heart disease and myocardial infarction, the left ventricular diastolic pressure-capacity curve was shifted to the upper left and the ventricular stiffness increased, indicating myocardial ischemia of coronary heart disease. Or extensive myocardial fibrosis or scar formation caused by myocardial infarction can alter the passive mechanical properties and geometry of the myocardium, resulting in changes in the pressure-capacity relationship.
If the myocardial infarction range is large and significant ventricular dilatation occurs, the opposite effect of ventricular stiffness can be exerted, that is, the pressure-capacity relationship curve is shifted to the lower right. Otherwise, the increase of ventricular volume will increase the filling pressure and cause Pulmonary edema, of course, even if there is ventricular dilatation, pulmonary edema can still occur if the diastolic volume is very large.
The diastolic pressure-to-volume relationship can also be acutely altered, as evidenced by the effect of acute ischemia on stiffness, such as diastolic pressure-volume relationship shifts during acute myocardial ischemia caused by rapid cardiac pacemakers. To the left; when the ischemia is terminated and gradually returns to normal, the curve also moves back to the normal position. In addition, as with the functional recovery of the systolic phase after myocardial ischemia, the recovery of diastolic function is also affected by time, temporary myocardial After ischemia, this increase in myocardial stiffness will return to normal after a few days. Therefore, the myocardial and hibernating myocardium will also affect the diastolic function of the ventricle, but with necrotic myocardium and fibrosis. The myocardial tissue of the scar is different, and they gradually return to normal after the myocardial ischemia is corrected.
Due to myocardial ischemia, part of the myocardial cells are necrotic, the loss of contractility is reduced, the cardiac output and the amount of stroke are reduced, and the end-diastolic volume of the ventricle is increased. As a result, the ventricular volume at the time of systolic ventricular contraction is also increased. The wall pressure increases. According to Laplace's law, the wall tension is proportional to the intraventricular pressure and the ventricular radius, and inversely proportional to the thickness of the wall. The initial expansion of the ventricle increases the ventricular radius and wall tension, but the healing process of the necrotic myocardium In the non-necrotic area of the ventricular muscle, the progressive hypertrophic function can be reduced. At this time, the myocardial cell hypertrophy increases the myocardial thickness, and the wall tension can return to normal. After the large myocardial necrosis occurs in the left ventricle, right Cardiac hypertrophy occurs in the room, but the degree of right ventricular hypertrophy is lighter than that of the left ventricle where myocardial necrosis occurs. If the hypertrophied myocardium has sufficient blood supply, although a considerable part of the myocardium has lost function, the heart can still be stable. Compensatory state, if coronary artery lesions are diffuse, due to the persistence of chronic ischemia and indirect or acute The effect of ischemia, the myocardial is difficult to maintain a good compensation, so that the number of damaged or necrotic myocardial cells gradually increased, at this time the hypertrophic myocardial tissue also lacks a proportional growth of the capillary network, making myocardial ischemia further aggravated, lacking Blood myocardium is also prone to focal damage and fibrosis, which increases wall tension and stiffness, that is, myocardial cell necrosis, residual cardiomyocyte hypertrophy, fibrosis or scar formation, and increased myocardial interstitial collagen deposition. Almost a structural pattern of ischemic cardiomyopathy, and can lead to increased wall tension and abnormal wall stiffness, heart enlargement and heart failure.
4. The effect of ischemia on myocardial electrical activity
Ischemic cardiomyopathy is complicated and diverse, including the difference of cardiomyocyte hypertrophy, which is not proportional to the distribution of capillary network, microcirculatory disorder and viable myocardium and necrotic myocardium, stunned myocardium, doping of hibernating myocardium, etc. Leading to arrhythmia can also make certain clinical manifestations of ischemic cardiomyopathy and response to treatment different.
Myocardial ischemia affects the permeability of myocardial cell membrane to ions, resulting in loss of sodium pump activity, retention of sodium water in cells, acidosis due to anaerobic glycolysis in cardiomyocytes, and high potassium outside the cell. This change in ischemic myocardium affects the depolarization and repolarization of the ventricle, causing abnormalities in the release and conduction of cardiac impulses. Therefore, various severe arrhythmias can be caused in patients with ischemic cardiomyopathy.
5. Vascular endothelial dysfunction
In recent years, studies on vascular endothelium have found that endogenous vasodilators such as nitric oxide (NO) and prostaglandin (PGI2) are produced and released in patients with coronary heart disease, while a strong vasoconstrictor endothelium is present. In addition to vascular effects, endothelin and angiotensin II also promote cardiomyocyte hypertrophy, interstitial fibrosis and the expression of fetal contractile protein genes, directly involved in heart failure. Pathophysiological processes, this disorder of endothelial function, can stimulate the contraction of blood vessels, smooth muscle proliferation and lipid deposition in the blood vessel wall, and may promote coronary thrombosis, myocardial ischemia, lead to impaired left ventricular function, visible endothelium Dysfunction is also one of the important mechanisms leading to myocardial ischemia and heart failure. Recently, TREND (Trial on Reversing Endothelial Dysfunction) has demonstrated that angiotensin-converting enzyme inhibitors can reverse or improve endothelial dysfunction, and this blood vessel Hypothesis, also 4S (Scandinavian Simvastatin Survival Study) and CARE (Cholesterol) And Recurrent Event) The trial confirmed and provided some theoretical basis for the treatment of heart failure.
Pathology: ICM patients with enlarged heart, weight up to 450 ~ 830g, heart enlargement, mainly left ventricular cavity expansion, such as biventricular cavity is seriously enlarged, the heart can be spherical, the ventricular wall due to compensatory hypertrophy and local fibers Or scar formation and uneven thickness, compared with normal people, ICM patients with thin ventricular wall and ventricular wall thickness is not proportional to the enlarged heart, coronary artery often diffuse and severe atherosclerosis, leading to coronary artery Cavity stenosis and thrombosis, often with multiple coronary lesions, histological examination often has myocardial cell degeneration, necrosis and fibrous scar formation, large scar tissue often found in the ventricular wall, nearly half of patients with visible wall thrombus in the heart, under the microscope Observation, myocardial mitochondrial inner membrane destruction, sputum reduction, mitochondrial respiratory chain-related enzyme activity decreased, myocardial fiber visible I band widened, severe ischemic visible sac formation.
Prevention
Elderly ischemic cardiomyopathy prevention
Primary prevention
(1) Dietary structure: risk factors for coronary heart disease such as blood lipids, elevated blood pressure, overweight and obesity, coagulation, etc., are closely related to dietary nutrition factors. Improving dietary structure is one of the important measures to prevent coronary heart disease. According to China's longevity The survey of the elderly shows that the diet of long-lived elderly people is mostly vegetarian, not partial eclipse, not overeating. Epidemiological data show that eating less animal fat is beneficial to reduce the incidence and death of cardiovascular disease, and the physiological digestive function of the elderly is diminished. Reduce the secretion of digestive juice, should promote eating more digestible, low-fat animal fat food with certain nutrition, advocate smoking cessation, avoid heavy drinking, currently considered a small amount of alcohol consumption, daily alcohol intake is less than 28.34g, it is possible to increase blood density The level of lipoprotein cholesterol is good for health.
In the past 20 years, the survey of Chinese scientists shows that the traditional diet of Chinese people has advantages and disadvantages for the prevention of cardiovascular diseases. The characteristics of Chinese diet are mainly plant foods, especially cereals, vegetables, fruits and other non-staple foods. There are very few products and fish, and there are few milks. This kind of dietary structure is low in animal fat and low cholesterol, but less antioxidant vitamins, combined with high salt, low potassium, low calcium and low animal protein, which is conducive to promotion. High blood pressure and elevated blood pressure are important risk factors for coronary heart disease and stroke in Chinese population. Therefore, China's traditional diet needs to be improved, in order to improve health, prevent various chronic diseases, and address the deficiency of traditional diet, Chinese nutrition. The Society adopted a dietary guide for Chinese residents in 1997. The main principles are: 1 food is diverse, cereals are dominant, 2 eat more vegetables, fruits and potatoes, 3 often eat milk, beans or their products, 4 often eat the right amount Fish, eggs, lean meat, less fat and oyster sauce, 5 food and physical activity should be balanced, maintain a suitable weight, 6 eat light and salt-free diet , such as alcohol consumption to be limited, eat clean, not bad food, reasonable diet can reduce cardiovascular disease morbidity and mortality.
(2) control of hypertension: coronary heart disease is the most common clinical complication of hypertension, even if there is no clinical symptoms or only high blood pressure, but did not reach the diagnostic criteria for hypertension, the incidence of coronary heart disease has doubled, blood pressure drop To the normal range, the arteriosclerosis can be delayed. Firstly, the detection and control of hypertension should be strengthened. The low-salt diet, daily sodium intake is 2.4-6g, weight control, drug treatment combined with improved lifestyle, but in the treatment of the elderly In high blood pressure, avoid excessive blood pressure and cause insufficient blood supply to the target organs and orthostatic hypotension.
(3) Control of diabetes: long-term hyperglycemia can enhance the non-enzymatic glycation of the in vivo protein and the formation of glycation end products, and enhance the lipid peroxidation, which may accelerate the development of atherosclerosis, female After menopause, the effect of estrogen on coronary heart disease disappears. Therefore, coronary heart disease in elderly women with diabetes is four times higher than that in non-diabetics. In addition to diet and medication to control blood sugar, emphasis should be placed on early detection of prediabetes and diabetes. Early dietary guidance or hypoglycemic therapy can reduce the incidence of complications, improve the quality of life, and improve the prognosis.
(4) Physical activity: Physical activity can improve the risk factors of coronary heart disease by reducing obesity, such as improving body fat distribution and reducing the incidence of non-insulin-dependent diabetes. Medium-intensity physical activity is also beneficial for adjusting blood pressure and blood lipids. It has been recognized that people who regularly participate in physical activity have a lower rate of cardiovascular risk factors, so physical exercise is an important auxiliary treatment for improving risk factors. Adherence to physical exercise can prevent and treat hypertension, enhance insulin sensitivity, and make glucose utilization. Increase, reduce obesity, research, sports can also lower cholesterol, fibrinogen decline, reduce platelet activation, thereby reducing the formation of blood clots, in addition, sports can improve vascular endothelial function, improve parasympathetic activity, the elderly Sports should vary from person to person and adhere to long-term exercise to achieve the purpose of preventing and curing diseases.
(5) Female coronary heart disease and hormone replacement therapy: Coronary heart disease is one of the important causes of death in postmenopausal women. Epidemiological data show that the incidence and mortality of coronary heart disease in postmenopausal women is four times that before menopause, and its incidence The age is delayed by about 10 years, suggesting that it is related to the protection of premenopausal estrogen. Hormone replacement therapy (HRT) can reduce the total mortality rate of postmenopausal women by 46% through beneficial protection of multiple systems. Patients with heart disease have the greatest benefit.
HRT not only morphologically controls the regression of atheromatous plaques, but also improves physiological conditions in the body, such as protection of endothelial function, recovery and maintenance of vasodilation, regulation of lipid metabolism and anti-oxidation, anti-thrombosis The hemodynamic characteristics are improved, the existing atherosclerotic lesions tend to be stable, and it is not easy to undergo degeneration or rupture, thereby reducing the incidence and mortality of clinical events of coronary heart disease, but how to use the drug, the dose must be strict in the doctor Under the guidance.
(6) Psychosocial factors: The meta-analysis of Lindon et al. showed that coronary heart disease is a psychosomatic disease, psychological factors and biological risk factors have a certain effect on the onset of coronary heart disease, and the outcome, prognosis and prevention of disease Both are closely related to psychosocial factors. The elderly should maintain emotional stability, optimism, and participate in social activities and group activities to reduce the occurrence of stress events related to coronary heart disease in work and life, and to ensure psychological and physiological health.
(7) Infectious factors: In recent years, more and more epidemiological, basic and clinical studies have suggested that inflammation of the coronary arteries or other parts is closely related to coronary heart disease. Microorganisms causing inflammation usually include Chlamydia pneumoniae, herpes simplex virus. , Helicobacter pylori, cytomegalovirus, etc., the main mechanism of infection caused by coronary heart disease may be that infection and inflammation initiate inflammatory cells and produce a variety of enzymes and inflammatory mediators, damage endothelial cells, promote the formation of atherosclerotic plaque , development and rupture, promote the formation of thrombosis, currently tend to believe that atherosclerosis has a chronic inflammatory change, infection or inflammation is one of the causes of coronary heart disease, especially unstable angina and acute coronary events, so the elderly should Enhance physical fitness, avoid the above-mentioned various pathogen infections, and reduce the chance of coronary heart disease.
2. Secondary prevention
Give medication based on lifestyle changes, exercise, weight control, etc., including prevention of angina pectoris, arrhythmia, etc.
(1) -blockers: slow down heart rate and prolong myocardial perfusion time, reduce blood pressure and myocardial contractility, reduce myocardial oxygen consumption, reduce plaque damage, rupture and thrombosis caused by acute coronary artery The event has anti-arrhythmia effect. The experiment proves that the continuous use of -blocker after AMI is 90 days, the incidence of re-infarction is reduced by 35%-40% in the first year, and the incidence of sudden death is reduced by 18%-39%. For heart failure, the application can also be considered, and the dosage varies from person to person.
(2) Nitrate: relax vascular smooth muscle, dilate coronary artery, increase coronary blood flow, or dilate peripheral arteriole to reduce peripheral vascular resistance, reduce cardiac afterload, reduce back heart volume and left ventricular preload to make myocardial energy The amount of oxygen is reduced to achieve an effect of improving myocardial ischemia and preventing the onset of angina pectoris.
(3) Calcium antagonists: The therapeutic effect on angina pectoris is significant, but there is still debate about the secondary prevention of myocardial infarction. It has been reported that short-acting agents are harmful to hypertension and coronary heart disease, and a new generation of long-acting calcium ion antagonists are short-term. Although the efficacy has been affirmed, but lack of large-scale clinical trial evaluation, calcium antagonists are more suitable for patients with coronary artery spasm and other vascular tone myocardial ischemia or complicated hypertension.
(4) Antiplatelet therapy: Studies have shown that the number and activity of platelets in the coronary arteries of patients with angina pectoris are increased, and platelets are easy to activate and aggregate, the patient's mental, emotional changes, psychological stress and environmental stress, personality, etc. Factors can affect platelet aggregation, plaque rupture and thrombosis, so antiplatelet drugs are especially important for the prevention of angina pectoris. Aspirin is commonly used at doses of 50-150 mg/d, and ticlopidine (according) has It inhibits the aggregation of platelets induced by exogenous and endogenous ADP, and blocks the receptors of fibrinogen on platelets, simultaneously inactivating substances related to aggregation. It is a broad-spectrum platelet inhibitor, commonly used. The dose is 0.25 ~ 0.5g / d, common side effects are nausea, vomiting, a small number of leukopenia and abnormal liver function, some people can cause aplastic anemia.
(5) lipid-lowering drugs: lipid-lowering therapy should start from improving diet, which is the basis of lipid-lowering therapy. After a certain period of time, active dietary treatment is not satisfactory, and lipid-lowering drugs can be added on the basis of dietary therapy. In 1997, in Japan. In the arteriosclerosis society, the target values of low-density lipoprotein cholesterol and total cholesterol were determined according to the influence of coronary heart disease and risk factors: it is recommended that there should be less than 3.6mmol/L and 5.7mmol/L in the absence of coronary heart disease and risk factors, respectively. Coronary heart disease, but there are risk factors, the former should be less than 3.1mmol / L, the latter should be less than 5.2mmol / L, if you have coronary heart disease should be less than 2.6mmol / L and 4.7mmol / L respectively There are four types of first-line lipid-lowering drugs commonly used in clinical practice: clofibrate, such as bezafibrate, fenofibrate, gemfibrozil, etc., HMG-CoA reductase inhibitors such as pravastatin, simvastatin Statins, lovastatin, atorvastatin calcium (Lipitor), niacin, bile acid-binding resin, should be different according to the condition, different lipid-lowering drugs, HMG-CoA reductase inhibitors It can lower cholesterol, triacylglycerol, and raise high-density lipoprotein. When there is an anti-atherosclerotic effect.
(6) Angiotensin-converting enzyme inhibitor (ACEI): ACEI is safe and effective as a secondary prevention for ischemic cardiomyopathy. Since SAVE, SOLVD, CONSENSUS and other large clinical trials, it has been used for heart failure. And the treatment of patients with low left ventricular function through clinical research, some scholars believe that ACEI can be applied two days after the onset of myocardial infarction, can prevent ventricular remodeling and improve left ventricular function.
3. Three levels of prevention
(1) anti-arrhythmia: coronary heart disease patients may have a variety of arrhythmia, ventricular arrhythmia, especially ventricular tachycardia and ventricular fibrillation can cause sudden death, it has been the focus of clinical prevention, in myocardial ischemia, Sympathetic excitatory myocardial catecholamine concentration and platelet activation may be involved in the occurrence of ventricular arrhythmia, the main goal of prevention and treatment of arrhythmia is to reduce and eliminate symptoms, prevent heart function deterioration, preventive measures: generally use beta blockers, but pay attention to Indications, do not advocate the use of Class I antiarrhythmic drugs, because CAST study, long-term oral administration of IA and IC drugs, although can reduce pre-systolic contraction, but increased mortality may be related to the drug's arrhythmogenic effect, if repeated Seizure ventricular tachycardia, lidocaine and amiodarone can be used. Patients with worsening circulatory condition should immediately synchronize with DC cardioversion. There is atrial fibrillation or repeated authoring. Long-term use of digoxin and amiodarone can be used.
(2) Correct heart failure:
1 Dietary control of total calories, dietary structure and fat constitute a reasonable, daily salt 0.2 ~ 2.0g, and quit smoking, limit alcohol, develop good habits, eat more vegetables, fruits, prevent constipation.
2 exercise: physical activity is conducive to coronary artery expansion and collateral circulation formation and improve cardiac compensatory ability, reduce platelet aggregation and increase fibrinolytic activity, patients with ischemic cardiomyopathy should emphasize rest, but also pay attention to physical activity, on the condition In severe cases, it is necessary to extend bed rest and sleep time. Severe patients should stay in bed completely. Resting is conducive to the discharge of sodium and water and the regression of edema. When heart failure is relieved, the condition varies from light to light and gradually increases. It is advisable not to have discomfort, such as active limbs, walking, doing gymnastics and tai chi.
3 drug treatment: diuretics and ACEI is the basic treatment of heart failure, furosemide is preferred, the drug is well absorbed orally, will not be affected by intestinal congestion, with the patient's body weight fluctuation as an indicator, each increase or decrease 40mg, but must Pay attention to maintaining the balance between water and electrolytes, especially when the dosage is more than 80mg/d. ACEI should be used for the elderly. The drugs with slow start-up time and long duration, such as perindopril, should be used starting from small doses. Common side effects are Hypotension, dry cough, and less common angioedema may be associated with increased bradykinin. Reduced dose may help reduce cough. Angiotensin II receptor antagonists reduce the incidence of cough and are easily tolerated by patients. For patients with severe heart failure, triple therapy should be used, such as cardiotonic, diuretic, and ACEI treatment. It must be excluded to cause deterioration of heart function, predisposing factors (infection, overwork, excessive infusion, etc.) or improper combination.
In addition, long-term use of aspirin should prevent platelet aggregation and thrombosis. In severe heart failure, vasodilators, sodium nitroprusside, etc. should be used intermittently to apply dobutamine to transition to a specific treatment, such as laser myocardial blood. Reconstruction and heart transplantation.
4. Community intervention
Community medical staff should provide medical and health education and awareness to patients with ischemic cardiomyopathy and their relatives, so that they can establish a correct understanding of the disease, eliminate psychological stress factors, anxiety, fear, etc., cooperate with doctors' treatment, and guide and develop non- Drug treatment, smoking cessation, alcohol withdrawal, balanced and reasonable dietary structure, regular inspection and follow-up of the coronary heart disease patients in the community, timely detection of high-risk individuals with ischemic cardiomyopathy, and taking targeted preventive measures to correct their high Risk factors such as obesity, hypertension, hyperglycemia, hyperlipidemia, etc., especially for the elderly, because the incidence is relatively hidden, symptoms and signs are not typical, the course of disease should be noted early, early diagnosis, early treatment, in The small area should carry out appropriate physical activities, especially for patients with ischemic cardiomyopathy, such as low-intensity Tai Chi, gymnastics, etc., to improve the tolerance of the heart and the body, improve the quality of life, and at the same time, the community medical staff Should guide the drug treatment of patients with ischemic cardiomyopathy, rational use of drugs, prevent drug abuse, reduce the side effects of drugs, The situation changes, should timely guidance they seek medical treatment to prevent disease progression and reduce the incidence of sudden death.
Complication
Complications of ischemic cardiomyopathy in the elderly Complications, angina pectoris, acute myocardial infarction, sudden death
Can be complicated by angina pectoris, acute myocardial infarction and sudden cardiac death.
Symptom
Symptoms of ischemic cardiomyopathy in the elderly Common symptoms Electrocardiogram abnormal appetite loss fatigue arrhythmia vertigo fatigue right heart failure dyspnea congestion congestion labor dyspnea
The different effects of myocardial ischemia and myocardial infarction or necrosis on the ventricle make ischemic cardiomyopathy have various clinical manifestations. According to the different manifestations of patients, ischemic cardiomyopathy can be divided into two types, namely, hyperemia. Ischemic cardiomyopathy and restricted ischemic cardiomyopathy, their clinical manifestations are very similar to dilated and restrictive cardiomyopathy in primary cardiomyopathy, but in nature, ischemic cardiomyopathy and primary Cardiomyopathy is different. The pathogenesis of ischemic cardiomyopathy is mainly due to coronary atherosclerotic stenosis, occlusion, sputum and even myocardial capillary network lesions, causing imbalance between myocardial oxygen supply and aerobics. And cause myocardial cell degeneration, necrosis, myocardial fibrosis, myocardial scar formation, heart failure, arrhythmia and enlargement of the heart chamber, manifested as a clinical syndrome of congestive cardiomyopathy, and a small number of patients with ischemic cardiomyopathy Mainly manifested as changes in ventricular diastolic function, abnormal ventricular wall stiffness.
Congestive ischemic cardiomyopathy
Congestive ischemic cardiomyopathy accounts for the vast majority of ischemic cardiomyopathy. It is common in the elderly. The elderly are mostly male patients. The male to female ratio is about 5:1 to 7:1. The symptoms are generally gradual. The performance mainly has the following aspects:
(1) angina pectoris: angina pectoris is one of the common clinical symptoms of patients with ischemic cardiomyopathy. However, angina pectoris is not a necessary symptom for patients with ischemic cardiomyopathy. As the symptoms of heart failure become more and more prominent, the onset of angina is gradually reduced or even completely Disappeared, only manifested as chest tightness, fatigue, dizziness or difficulty in breathing, angina is not an accurate indicator of myocardial ischemia, nor is it an accurate indicator of cardiac dysfunction in dyspnea when tired, some elderly patients may not have from the beginning The history of angina pectoris and myocardial infarction, because they lack a protective "heart warning system", may be due to higher pain thresholds in elderly patients, in fact the clinical significance and harm of this asymptomatic myocardial ischemia with angina72%92%1 /31/2
(2);
(3)
(4)14%24%
()()
4%8%15%
401/31/250%
2.
(stiff heart syndrome)-
Examine
1.
(1)ST-TQQQ
(2)XX
(3)
(4)
(5)
(6)70%371%227%2%88%79%
2.
(1)X
(2)
(3)
(4)
(5)2
Diagnosis
Diagnostic criteria
35%
Differential diagnosis
1.
42%92%64%85%10%20%10%XCT
Iskandrian9030%69215930%500.571.07
2.
PQRST
T3T4131I131I
3. Hypertensive heart disease
XX
4.
