Coronary heart disease is the abbreviation of coronary heart disease. Due to the atherosclerotic lesions of the coronary artery wall causing obstruction or narrowing of the lumen of the vessel, the coronary blood flow is blocked, the myocardial blood supply is insufficient, and the degree of obstruction is severe enough to cause myocardial infarction. Over the past 40 years, the incidence of coronary atherosclerotic heart disease has gradually increased in China. According to Shanghai Medical University statistics, in 1948-1958 hospitalized patients with heart disease, coronary heart disease accounted for only 6%; 1959-1971 accounted for 18%; 1972-1979 increased to 29%, and is now the first in all types of heart disease. Etiology
The pathogenesis of coronary atherosclerosis is complex, and is not yet fully understood. According to a large number of epidemiological and experimental research data, the main causative factors are: high-calorie, high-fat, high-sugar diet, smoking, hyperlipidemia, hypertension, diabetes mellitus, obesity, physical activity is too little, stressful mental labor, emotional agitation, mental stress, middle-aged and older men, low HDL, coagulation abnormality and so on. A few cases may have familial genetic factors. [Back to top]
Pathologic changes
Coronary artery anatomy: coronary arteries are blood vessels supplying myocardial blood and oxygen, and its anatomical form is quite variable. Under normal circumstances the coronary arteries have two branches, left and right, which open into the left and right coronary sinuses of the ascending aorta, and sometimes another smaller paracoronary artery is issued from the aorta.
The left coronary artery trunk has a diameter of about 4-5 mm and a length of about 0.5-2 cm, and is issued from the ascending aorta and then travels to the lower left side behind the common trunk of the pulmonary artery, and is divided into anterior descending and retrograde branches along the left atrioventricular groove in the left side between the common trunk of the pulmonary artery and the left auricle, forwards and downwards.
The anterior descending branch is a continuation of the main trunk of the left coronary artery, traveling down the anterior interventricular groove and then around the apical notch to reach the posterior wall of the heart, where it coincides with the posterior descending branch of the right coronary artery at the lower 1/3 of the posterior interventricular groove. The anterior descending branch gives off branches such as the left conic branch, the oblique branch, the left anterior ventricular branch, the right anterior ventricular branch, and the anterior interventricular septal branch, etc. The areas supplied with blood are the roots of the aorta and the pulmonary artery trunks, a part of the left atrial wall, the anterior wall of the left ventricle, a part of the anterior wall of the right ventricle, a part of the interventricular septum (the upper part and the anterior part), the apical area, and the anterior papillary muscles.
The circumflex branch emanates from the main trunk of the left coronary artery and travels along the anterior aspect of the left atrioventricular groove immediately below the base of the left auricle, traveling left and backward, and then down through the left border of the heart to the diaphragmatic surface. The branches emanating from the circumflex branch are quite variable, with the main branches being several left marginal branches, a posterior left ventricular branch, and an atrioventricular branch along the left atrioventricular groove. The atrioventricular branches are sometimes (about 10%) longer and give off posterior descending branches and the AV node artery from their ends. 30% of humans with a pirouette branch also give off the sinus node artery. The areas supplied by the rotary branch are the lateral and posterior walls of the left ventricle, the left atrium, and sometimes the ventricular diaphragm, the anterior papillary muscles, the posterior papillary muscles, a portion of the interventricular septum, the AV node, the atrioventricular bundle, and the sinoatrial node.
The right coronary artery emanates from the right coronary valvular sinus and then adheres to the base of the right auricle, traveling outward and downward along the right atrioventricular groove. It reaches the ventricles of the atrioventricular groove, the atria, and the posterior junction of the atrial septum and ventricular septum and divides into two branches, the right posterior descending branch in the posterior interventricular groove toward the apical region, and the other smaller atrioventricular node artery turned upward. The major branches of the right coronary artery are the right conus branch, right atrial branch, sinus node branch, right anterior ventricular branch, right posterior lateral ventricular branch, posterior interventricular septal branch, posterior descending branch, and AV nodal artery. The right coronary artery supply region includes the right atrium, the sinus node, the right ventricular outflow tract, the pulmonary cones, the anterior right ventricular wall, the posterior right ventricular wall, the inferior third of the interventricular septum, and the atrioventricular node. Patients with right coronary artery predominance also supply blood to part of the left ventricle and the apical portion of the heart. The distribution of the right and left coronary arteries in the myocardial diaphragm is quite variable, and when stenosis occurs in the coronary arteries that supply a larger area of blood, the myocardial ischemic injury is more extensive and more severe. [Back to top]
Typing
According to the cross area of the heart, i.e., the back wall of the heart on both sides of the ventricle, atrium and atrial septum junction of the source of blood supply, the distribution of the left and right coronary arteries can be divided into three main types:
1) right coronary artery dominance type This type is the most common, accounting for about 80%. The right coronary artery is thick and long, supplying blood to the posterior wall of the right ventricle and across the cardiac cross region by the posterior descending branch to part of the posterior wall of the left ventricle and the posterior part of the ventricular septum.
2) Left coronary artery dominant type The right coronary artery is smaller, and the left coronary artery gyratory branch sends a posterior descending branch to supply blood to the posterior wall of the left and right ventricles and to the posterior part of the ventricular septum.
3) Left and right coronary artery homogeneous type The left and right coronary arteries each send a descending branch to supply blood to the posterior wall of the left and right ventricles (1) right coronary artery dominant type (2) left coronary artery dominant type (3) left and right coronary arteries homogeneous type of the left and right coronary arteries distribution type
Pathologic anatomy: most of the atherosclerotic lesions of the coronary arteries in the proximal part of the main branches of coronary artery, about 5 cm from the aortic opening. When accompanied by hypertension or diabetes mellitus, the scope of the lesion is wide and may involve small branches of the coronary arteries. Atherosclerotic lesions mainly involve the coronary artery intima, in the early stage of the lesion, lipid and lipid-containing macrophages infiltrate the intima and mesangial cells, and the intima is thickened with yellow spots. With multiple causes of endothelial cell injury and increased endothelial permeability, lipid infiltration increased, and the spots gradually increased and expanded, forming plaques or streaks. Focal dense laminar collagen is also present in the endothelium, and lesions involving the entire periphery of the endothelium lead to stenosis or obstruction of the vessel lumen. The blood flow of the diseased coronary artery is reduced, and the local myocardial blood and oxygen supply is insufficient during exercise or even at rest, which can produce myocardial infarction in severe cases. Coronary atherosclerotic lesions can be complicated by bleeding, thrombosis and aneurysm. Atherosclerotic lesions rupture bleeding lipids into the vascular lumen, easy to cause distal vascular embolism and induced thrombosis, vascular wall hematoma and can gradually form granulation tissue and fibrosis. The acute phase of endothelial hemorrhage may prompt spasm of the coronary arteries and branches of the collateral circulation, aggravating the degree of myocardial ischemia. Thrombosis often exists in combination with hemorrhage, and may lead to distal vessel embolization and vessel wall fibrosis. Atherosclerotic plaques in the coronary artery endothelium under the middle layer of the vessel wall necrosis and aneurysm is very rare, most of the cases of aneurysm occurred in only one vessel, the diameter of up to 2.5cm, the lumen may contain blood clots, but the lumen of the vessel is still open. Coronary artery stenosis caused by atherosclerotic lesions, such as limited to only one branch of the coronary artery, and the development process is slow, the lesion of the vessel and the neighboring coronary arteries between the traffic branch is significantly expanded, the establishment of an effective collateral circulation, the affected area of the myocardium can still get enough blood supply. If the lesion involves more than one blood vessel, or if the stenosis progresses more rapidly and the collateral circulation is not sufficiently established, or if bleeding, hematoma, thrombosis, or vascular wall spasm occurs, severe myocardial ischemia or even myocardial infarction may result. Myocardial tissue in the diseased area may atrophy or even necrotic to the point of rupture or fibrous scarring later on, and myocardial contractile function may be severely impaired, resulting in arrhythmia or pumping failure. The greater the extent of myocardial ischemia, the more serious the harm caused. The left coronary artery supplies the most coronary blood flow, so heart disease caused by obstruction of the left coronary artery and its branches is more serious than the right coronary artery.
Pathophysiology: per 100g of myocardial blood flow per minute 60 ~ 80ml, compared with the whole body tissue per 100g of blood flow per minute 7ml about 10 times more. Another feature of the coronary circulation is that the arterial blood flow in diastole is the most, while in the systole of the heart due to myocardial vascular compression, coronary blood flow is reduced, while the other organs of the body in systole, the arterial perfusion pressure is the highest when the blood flow is the most. The myocardium has a high oxygen uptake capacity and can take up about 65-75% of the oxygen from the capillaries. Under normal conditions, every 100g of myocardial oxygen uptake of 8 to 10ml per minute, while the whole body organs and tissues can only take up 25% of the oxygen from the blood, every minute, every 100g of tissue oxygen uptake of only about 0.3ml. exercise, cardiac output increased significantly, the heart's workload increased, the myocardial oxygen demand increased, due to the further increase in the oxygen uptake from the blood of the margins are not much, the necessity of expanding the coronary arterial lumen to increase coronary blood flow to suit the oxygen demand, the coronary artery lumen is not enough. It is necessary to enlarge the lumen of the coronary arteries to increase the coronary blood flow in order to meet the requirements of the increase in oxygen demand. The coronary circulation has a sensitive regulating ability, the factors that regulate coronary blood flow are: arterial perfusion pressure, coronary vascular resistance, heart rate, cardiac diastolic time frame, blood co2 tension, O2 tension, acidity and alkalinity, as well as neurohumoral factors, etc.
Myocardial metabolism and cardiovascular function are the most important factors in the development of a healthy heart.
The base substances for myocardial metabolic energy are glucose, fatty acids, lactate, and so on. In the coronary blood supply is insufficient, myocardium is in hypoxic metabolism, fatty acid oxidation is reduced, carbohydrate oxidation is dominant, but in hypoxia, glucose and glycogen decomposition can supply only a small portion of the energy under aerobic metabolism. Sustained myocardial ischemia and hypoxia for more than 20 minutes can cause irreversible mitochondrial degeneration, necrosis of cardiomyocytes, loss of myocardial enzyme activity, and clinical symptoms such as angina pectoris, arrhythmia and heart failure. [Back to top]
Clinical manifestations
Symptoms: Typical symptoms of exertional angina pectoris, an imbalance of myocardial oxygen supply and demand caused by transient ischemia and angina pectoris, in the activity, emotional, full meal or cold when suddenly when the anterior precordial region of the crushing pain, the nature of the pain can be a severe colic, squeezing pain, pressure pain, tightly bound, or the pain is very light, only to feel the distension of the discomfort. Occasionally, the onset of severe pain is accompanied by sweating and a sense of fear of dying. In some patients, the pain radiates to the left shoulder, left upper arm, neck, throat and jaw, and usually lasts for 1 to 10 minutes, which can be relieved by resting or taking drugs such as nitroglycerin. Some of them are accompanied by chest tightness or mainly chest tightness, and in severe cases, the pain is heavier, lasts longer, and can come on during rest or sleep. History questions should pay attention to the triggers, the location of the pain, duration, the presence or absence of radiation, accompanying symptoms and mode of relief.
The cause of angina, the number of episodes, and the duration of the episodes are relatively stable, called stable angina. A part of the case of myocardial ischemia degree is more serious, from the typical stable angina pectoris to unstable angina pectoris, the main manifestation of angina pectoris frequent attacks, pain prolonged duration, degree of aggravation, or even rest also attack pain, the risk of acute myocardial infarction increased. Early onset of acute myocardial infarction can be nausea, vomiting, hiccups or epigastric distension, angina pectoris is severe, the duration can be up to several hours, rest or nitroglycerin tablets failed to relieve, often accompanied by shock, arrhythmia and heart failure.
Signs: Coronary atherosclerotic heart disease cases usually have no special signs, angina attack blood pressure can be slightly higher or lower, the heart rate can be normal, increased or slowed. If the pain is severe, the patient's expression is anxious, irritable, pale, sweating, and occasionally showing atrial or ventricular gallop rhythm. In cases with papillary muscle dysfunction, a systolic murmur may be heard in the apical region. In cases of myocardial infarction, the heart rate may increase or slow down, the blood pressure decreases, the heart murmur boundary may increase slightly, the 1st heart sound in the apical region is weakened, and sometimes there are 3rd and 4th heart sounds or diastolic prancing rhythm, and there may be all kinds of cardiac arrhythmias, shock, or signs of heart failure. [Back to top]
Auxiliary examination
X-ray examination: chest X-ray examination is generally no abnormal findings. Cases with hypertension may show enlargement of the left ventricle, aortic widening, enlargement, tortuous prolongation. In cases of heart failure, the heart is significantly enlarged and the lungs are depleted.
Electrocardiography: Electrocardiography is one of the most important ways to reflect myocardial ischemia. When angina attack, it often shows ST segment lowering, T wave flattening or inversion. It gradually recovers within a few minutes after the attack, and can sometimes be accompanied by arrhythmia. Patients who usually have no obvious abnormal changes in the ECG can undergo a load test to increase the cardiac load, increase myocardial oxygen consumption, and temporarily induce electrophysiologic changes of myocardial hypoxia. Electrocardiogram load test can be used to double two-step ladder exercise test, activity plate exercise test, stomping exercise test and glucose load test, etc. Holter ECG monitor can also be used to make dynamic electrocardiogram continuous recording. The electrocardiogram of acute myocardial infarction cases is characterized by deep Q or QS waves, marked ST-segment elevation, bow-back upward and T-wave inversion. A localized diagnosis of myocardial infarction can be made on the basis of the leads presenting these characteristic changes.
Serum enzymes: in the early stage of acute myocardial infarction, serum ghrelin, creatine phosphokinase, and lactate dehydrogenase are elevated, and their dynamics can help determine the evolution of the disease.
Other diagnostic methods include echocardiography in the cross-section, radionuclide cardiac imaging, etc., which is valuable for the diagnosis of coronary artery disease and myocardial infarction, and for the understanding of the function of left ventricular motion.
Selective coronary angiography and left ventriculography: Selective coronary angiography can clearly show the left and right coronary arteries and their branches, which not only provides evidence for the diagnosis of coronary artery stenosis caused by atherosclerotic lesions, but also observes the exact location of the lesion, the scope of the lesion, the degree of stenosis of the lesion vessels, and the situation of collateral circulation. A reduction of 1/3 of the internal diameter of a diseased coronary artery branch reduces the lumen area by 50%; a reduction of 1/2 of the internal diameter reduces the lumen area by 75%; and a reduction of 2/3 of the internal diameter reduces the lumen area by 90%. Left ventriculography is used to visualize the normal, reduced, or absent contractile function of the ventricular wall in all parts of the left ventricle and to measure the left ventricular ejection fraction. Left ventriculography can also be used to diagnose myocardial infarction-induced ventricular wall aneurysms, ventricular septal defects, and mitral valve insufficiency. Selective coronary angiography and left ventriculography are necessary in cases of coronary artery disease in which surgical treatment is contemplated, in order to clarify the indications for surgery and to formulate a surgical plan. [Back to top]
Coronary heart disease prevention and treatment methods
Can be summarized as two categories of internal medicine and surgery. Internal medicine has a history of many years, the treatment measures are to adjust the diet and habits, pay attention to mental health, the application of drugs to reduce blood lipid content, inhibit platelet aggregation, control angina and so on. Surgical treatment of coronary artery disease has a history of more than 70 years, including the conceptual and methodological evolution of Jonnesco's excision of the cervical and thoracic sympathetic nerves for the treatment of angina pectoris in 1916, and the attempt to reduce the load on the ischemic myocardium by lowering the metabolism of the thyroid gland with a total thyroidectomy by Boas in 1926, and the fixation of the myocardium to the pectoralis major muscle and the myocardium by Beck and Tichy in 1935. In 1935, Beck and Tichy performed a fixation suture between the pectoralis major and the myocardium in the hope that the adhesions formed would supply blood to the myocardium. Since then, pericardium, greater omentum, lungs, jejunum, stomach, spleen and other tissues and organs have been used for fixation suture with myocardium. Some surgeons also applied talcum powder and asbestos powder to the pericardial cavity to promote the formation of pericardial adhesions. zola, cesa-Bianchi ligated the bilateral internal thoracic arteries in 1939, believing that the pericardial diaphragmatic arteries proximal to the ligated area could deliver more blood flow to the myocardium. vineberg implanted internal thoracic arteries into the myocardium in 1946. beck advocated the use of coronary artery ligation and partial ligation of venous sinus and the use of the coronary artery to the pericardium in 1955. In 1955, Beck advocated the use of partial ligation of the coronary sinus and coronary venous bypass with partial ligation of the coronary sinus in the arterial branches of the body circulation to perfuse the coronary circulation from the reverse direction. The above surgical treatments were all unsatisfactory and were abandoned. 1955 saw the beginning of research into direct surgery on the coronary arteries to improve myocardial blood supply. 1958 saw Longmire et al. perform endothelial debridement of diseased segments of coronary arteries to relieve luminal stenosis. 1961 saw Senning use a graft to mend the stenotic segment of the coronary artery under extracorporeal circulation. 1967 saw Gatrett use the saphenous vein to repair the stenotic segment of the coronary artery. In 1967, Gatrett performed a left anterior descending bypass graft with the saphenous vein, which remained patent for 7 years. Selective coronary angiography was widely used in the clinic and rapidly promoted the development of surgical treatment of coronary artery disease. 1967 Favaloro and Effler popularized the use of saphenous vein to perform ascending aorta-coronary artery bypass grafting and introduced the operation technique in 1969, and 741 operations were performed by 1971. 1968 Green reported that the internal thoracic artery-anterior descending coronary artery anastomosis was used for coronary artery bypass grafting. In 1968, Green reported an anterior descending coronary artery anastomosis, and in 1971, Flemma et al. reported a sequential grafting method, i.e., a saphenous vein was used to make multiple anastomoses with multiple branches of the coronary artery. Since then, the surgical treatment of coronary heart disease has entered a new stage. At present, countries around the world due to coronary heart disease vascular graft bypass surgery has reached more than 400,000, is the main method of surgical treatment of coronary heart disease. 1979 grüntzig and other reports, percutaneous transluminal coronary artery endoluminal angioplasty, this operation is relatively simple, do not need to open the chest, the medical cost is relatively small, but 6-9 months after the operation, the incidence of restenosis can be up to 30 ~ 40%. In recent years, there are percutaneous intracavitary coronary thrombolysis to treat myocardial infarction caused by early coronary artery embolism, and coronary artery intracavitary cold laser to eliminate atherosclerotic plaques and stenotic lesions of the new equipment, new technologies.
Due to the complexity of the causative factors of coronary atherosclerotic heart disease, has not been fully understood; lesions involving the number of branches of the coronary arteries, the scope of the lesions, the development of the speed of the lesions, as well as the harm caused by the ventricular function, etc. There are more variations, therefore, according to the natural course of the various types of coronary artery disease, the in-depth comparison of the effect of internal medicine and surgical treatment, there is a long time to be investigated and gradually be enriched. The results have yet to be gradually enriched by a long period of research and study. According to the existing clinical experience, although the surgical treatment of coronary heart disease fails to change or reverse the process of coronary atherosclerosis, it can increase coronary blood flow and improve coronary circulation. After ascending aorta-coronary artery bypass grafting with the saphenous vein, the clinical follow-up of a large number of cases showed that it was effective for angina pectoris, and angina pectoris disappeared in 60-95% of the cases from 1 to 5 years after the operation. The electrocardiogram returned to normal, and the number of cases in which angina disappeared 10 years after the operation was reduced to 46% due to the lack of graft vascularization or the progression of coronary heart disease, while the rate of angina disappeared in cases without surgical treatment was only 3%. Physical activity endurance improved significantly from 3 to 10 years after surgery compared with non-surgical cases. Two years after surgery, 60% of the patients were able to perform their normal duties, while only 26% of the cases treated with internal medicine returned to work. [Back to top]
Coronary artery bypass grafting
Indications for surgical treatment of coronary artery atherosclerotic stenosis: the use of the saphenous vein to carry out ascending aorta-coronary artery bypass bypass grafting
The operation, commonly known as bypass grafting is the most commonly used surgical methods for the surgical treatment of coronary artery disease, surgical indications:
1. Stable angina The impact of stable angina is not only the development and prognostic factors, but also the development and prognostic factors. Factors affecting the development and prognosis of stable angina include: the number of coronary artery branch lesions, especially the left coronary artery trunk or anterior descending branch is involved, the left ventricular functional status, the degree of myocardial ischemia, the patient's gender and age, and whether or not there are other diseases. One or two coronary arteries obstructive lesions, and does not involve the left coronary artery trunk, the long-term efficacy of medical treatment and surgical treatment is close, it is appropriate to carry out medical treatment first, and regular review. However, if chronic stable angina pectoris fails to be treated with anti-angina drugs such as nitrate, β-blocker, calcium antagonist, etc., and the patient's work and life are seriously affected, selective coronary angiography should be carried out, and it is found that the lumen area of the blood vessel has been reduced to more than 50%, especially if the lesion involves the main stem of the left coronary artery, the anterior descending branch of the left coronary artery or the three branches of coronary arteries, surgical operation should be considered. The treatment is not limited to the main stem of the left coronary artery.
2. Unstable angina The vast majority of cases of coronary artery obstructive lesions of serious degree, some cases have a small piece of subendocardial or scattered myocardial infarction, and may be in the short term to develop into an acute myocardial infarction, the occurrence of serious arrhythmias or sudden death. Gazes et al. reported 1, 2 years and 10 years mortality rate of 18%, 25% and 50%, respectively. In this type of case, if angina is not controlled after 1 week of active medical treatment, selective coronary angiography should be performed, and surgery should be performed as soon as possible according to the results of the examination.
3. Acute myocardial infarction cases The opinions on the implementation of coronary artery bypass grafting are not unanimous, and those in favor of surgical treatment believe that the implementation of surgical treatment within 8 hours after the occurrence of myocardial embolism can reduce the area of myocardial infarction, and the formation of myocardial scar tissue in the future is relatively small, and the post-infarction complications such as left ventricular ventricular wall aneurysm, arrhythmia, heart failure, and sudden death occur at a lower rate, and the improvement of the function of the left ventricle is relatively obvious. The improvement of left ventricular function is more obvious. However, coronary artery bypass grafting in cases of acute myocardial infarction has a high operative mortality rate and a high incidence of postoperative complications, and the follow-up data on the long-term efficacy of the grafting have yet to be enriched. However, 2 weeks after myocardial infarction, active plate loading test ST-segment depression cases, follow-up 1 year mortality is 13 times higher than the test negative, such cases should be considered for surgical treatment.
In recent years, early myocardial embolism cases to carry out thrombolysis and percutaneous intracavitary coronary artery dilatation angioplasty and other therapeutic methods, these therapies and the long-term efficacy of bypass grafting and its comparison, there is still a lack of sufficient information, failed to draw conclusions.
4. Severe ventricular arrhythmias, myocardial infarction recovery or late presentation of severe ventricular arrhythmias, according to statistics, about 1 / 3 to 1 / 2 in the follow-up of 2 to 3 years in the period of sudden death. Therefore, myocardial ischemic ventricular arrhythmias should be considered as an indication for coronary artery bypass grafting.
Surgical techniques for coronary artery disease: Surgery to re-establish coronary blood flow can be performed using the saphenous vein or the internal thoracic artery. The saphenous vein has a large caliber and is easy to collect, so it has been used in the largest number of cases and has a relatively satisfactory effect. In recent years, the number of cases of end-to-end anastomosis between the internal thoracic artery and coronary arteries, especially the anterior descending branch of the left coronary artery, has been increasing. Atherosclerotic lesions rarely occur in the internal thoracic artery, and postoperative narrowing of the lumen due to intimal hyperplasia is rare, and the postoperative patency rate is higher than that of the saphenous vein. However, it is difficult to anatomically free the internal thoracic artery, and the complication rate of postoperative hemorrhage is higher, and freeing the internal thoracic arteries bilaterally may have an adverse impact on the healing of the sternum. Selective coronary angiography shows that the coronary artery branches are larger than 1.5 mm and the lumen diameter is reduced by more than 50%, all should be performed bypass surgery, in order to adequately re-establish myocardial blood flow. In cases of multi-branch coronary artery lesions, sometimes it is necessary to perform shunt surgery on 5 or more branches. In order to simplify the surgical operation and shorten the operation time, sequential anastomosis can be used, i.e., a section of saphenous vein should be used to make another 1 to 2 lateral anastomoses proximally to the end of end-lateral anastomosis, so that a section of the vein can only be used to shunt two or more coronary arteries, and to reduce the anastomotic port between the aorta and the saphenous vein. After the sequential anastomosis, the vascular patency rate is high and the blood flow rate is fast, but the operation needs to be careful and accurate, pay attention to avoid the twisting of the saphenous vein, and sometimes the thicker branch of the saphenous vein can be utilized to make a y-shaped anastomosis with the other coronary artery branch.
Preoperative preparation: lung, liver and kidney function should be checked before surgery, and digitalis and diuretics should be stopped 2 days before surgery, but nitroglycerin, beta-blockers and calcium antagonists should not be stopped.
Saphenous vein shunt grafting surgical operation techniques: endotracheal intubation general anesthesia, surgery in extracorporeal circulation combined with hypothermia, intraoperative monitoring of blood pressure, central venous pressure, electrocardiogram, body temperature, urine output. Skin preparation should include chest, abdomen, groin and bilateral lower limbs. The surgeons are divided into two groups to simultaneously open the chest and strip the saphenous vein. When freeing the saphenous vein, the operation must be gentle and must not pull the vein to cause injury. A long incision in the lower extremity is better than multiple small incisions to protect the vein from pulling injury. In the process of freeing the saphenous vein, do not clamp the vein with vascular clamps, and use tissue forceps to hold only the outer membrane of the vein wall, so as not to cause damage to the endothelium of the vein to rupture. When dealing with the branches of the vein, care should be taken to cut off the ligated branches at a distance from the main trunk of the vein, so as not to cause the wall of the vein to crumple, resulting in the reduction of the lumen of the vessel. The lower section of the saphenous vein near the ankle is more suitable for graft bypass than the upper section of the saphenous vein because of the lack of a venous valve and the better pressure resistance of the lumen. After removing a segment of the saphenous vein, a syringe with a smooth needle is inserted distally and ligated to identify the proximal and distal ends of the vein, and a small amount of cold heparin solution (10,000 u of heparin in 1,000 ml) may be injected to enlarge the lumen and to check for leakage through the wall of the vein. The removed vein is injected into the lumen with the solution, kept moderately dilated, and stored in a 10°C solution for backup. Topical application of dilute concentration of popovine (60 mg per 500 ml of saline) prevents venous spasm. While the saphenous vein is cut free, another group of surgeons makes a median sternotomy, splits the sternum longitudinally, cuts the pericardium, reveals the heart, inserts blood-draining and blood-giving catheters into the vena cava and the distal part of the ascending aorta, respectively, and puts a pressure-reducing drainage catheter into the left cardiac cavity to be connected to an artificial heart-lung machine to establish extracorporeal circulation. During the procedure, attention should be paid to protecting the myocardium, using measures such as blood cooling, local cooling of the myocardium and infusion of cold cardiac arrest fluid, and minimizing the time of blocking the ascending aorta. Generally, the distal saphenous vein and coronary artery branch anastomosis is performed first, but there are cases in which the ascending aorta and saphenous vein anastomosis is performed first and then the distal anastomosis is performed. The coronary artery branches are exposed at the selected anastomosis site, the middle of the anterior wall of the artery is incised longitudinally with a sharp knife, and the coronary artery incision is enlarged with a curved pair of fine scissors to a length of approximately 6 to 8 mm. Sometimes a small triangular piece of the anterior wall of the coronary artery branch needs to be resected in order to facilitate the vascular anastomosis. The severed end of the saphenous vein for anastomosis is trimmed behind the peritoneum and cut obliquely to make a 45° incision so that the vessel does not twist after the anastomosis is completed. If necessary, a small section of the vein wall can be cut longitudinally to enlarge the anastomotic end. The length of the saphenous vein incision should be 10-20% longer than that of the coronary artery branch incision, and the anastomosis should be closed with 6-0 or 7-0 Prolene suture for continuous or interrupted suture, with a needle spacing of about 1 mm, slightly wider on the side of the saphenous vein, with the intima-media properly aligned, and with a small amount of heparin solution injected into the other end of the saphenous vein during the anastomotic process to help improve the visualization of the field. A small amount of heparin solution is injected through the other end of the saphenous vein during the anastomosis, which helps to improve the visualization of the surgical field. In the case of sequential anastomosis, the anastomosis is performed by making a longitudinal or transverse incision in the wall of the saphenous vein according to the direction of travel of the grafted saphenous vein and its anatomical relationship with another coronary artery branch after completion of the distal-most end-to-side anastomosis. Care must be taken to ensure that the saphenous vein is properly spaced between the incisions, that the anastomosis is not distorted, and that blood flow is smooth. Once the distal anastomosis is completed, the aortic clamp is relaxed and extracorporeal rewarming is initiated. With the saphenous vein kept filled, the anastomosis of the ascending aorta was selected, and the aortic wall was partially clamped with a noninvasive vascular clamp, and the aortic wall was incised with an aortic wall perforator with a diameter of about 5 mm at each anastomosis, and the saphenous vein was cut off diagonally to the cut end of the saphenous vein for the anastomosis, the venous anastomosis should be 10-20% larger than the incision of the aortic wall, and the anastomosis was closed with a continuous suture of 5-0 Prolene suture.
(1) Enlargement of the venous lumen with heparin solution
(2) Saphenous vein severed end is cut at 45° and then cut longitudinally
(3) Saphenous vein-coronary artery end-to-end anastomosis
(4) Sequential anastomosis: Saphenous vein incision may be longitudinal or transverse
Thoracic internal artery-coronary artery end-to-end anastomosis: The caliber of the internal thoracic artery is similar to the coronary artery. The caliber of the internal thoracic artery is similar to that of the coronary arteries, and the rate of patency is higher than that of the greater saphenous vein when the internal thoracic artery is used to perform the bypass operation, and a proximal aortic anastomosis is not necessary. However, due to its limited length and anatomic location, anastomosis with the left internal thoracic artery and the anterior descending or diagonal branch of the left coronary artery is generally only indicated. The right internal thoracic artery is smaller in caliber than the right coronary artery and is of insufficient length, so anastomosis of the right internal thoracic artery to the right coronary artery branch is rarely performed.
After splitting and spreading the sternum, before incising the pericardium and injecting heparin, the intrathoracic fascia is incised with an electric knife along both sides of the internal thoracic artery at a distance of about 1 cm from the vessel, and the internal thoracic artery and vein, as well as the surrounding adipose tissues, muscles, and pleura, are freed by going upward to the upper part of the sternum from the sixth intercostal space. The branches of the intercostal arteries were ligated and severed. The free internal thoracic artery and its surrounding tissues are carefully protected from trauma and wrapped in gauze impregnated with dilute poppy solution. After systemic heparinization before starting extracorporeal circulation, the internal thoracic artery is ligated at the level of the 6th intercostal space, and the proximal arterial cut-off end bleeds up to 120-240 ml per minute; if it bleeds less than 100 ml per minute, the quality of the blood vessel is poor, and it is not suitable for application. The left anterior descending branch was cut, the appropriate length of the distal section of the internal thoracic artery was stripped of the surrounding tissue, the length of the artery was revealed to be about 1 cm, the lumen could be gently enlarged with a dilator with a diameter of 1.0 to 1.5 mm and cut off obliquely, and the anterior descending branch incision was closed with a continuous or interrupted suture with a 7-0 Prolene stitch and the soft tissues around the internal thoracic artery were sutured and fixed with a number of interrupted sutures with the myocardium to reduce the tension of the anastomosis. The soft tissue around the internal thoracic artery is then secured to the myocardium with several interrupted sutures to minimize anastomotic tension, and the left pericardium is incised transversely to ensure an unobstructed pathway from the internal thoracic artery to the heart.
Coronary artery bypass grafting can be accompanied by coronary endarterectomy if the lesion requires it.
Postoperative treatment: After coronary artery bypass grafting, blood pressure, central venous pressure, left atrial pressure, heart rate, heart rhythm, body temperature, thoracic drainage, urine output, blood gas analysis, blood pH and electrolyte levels should be closely monitored to prevent hypovolemia, hypoxia, acidosis and electrolyte disorders. Oral β-blockers can prevent arrhythmia. In the case of saphenous vein shunt grafting, postoperative aspirin and Pansentin can prevent thrombosis in the deep veins of the lower extremities. A small number of patients with postoperative complications of low blood volume syndrome and unsatisfactory drug therapy need to be treated with intra-aortic balloon counterpulsation.
Shunt graft efficacy: In recent years, the operative mortality rate has been reduced to less than 5%. The most common cause of death is acute heart failure. Factors affecting surgical mortality include: the extent of coronary artery branch lesions, the severity of angina pectoris, preoperative left ventricular function, the patient's age, gender, whether or not the myocardial infarction is complicated, the number of grafted blood vessels, the time of aortic obstruction, and whether or not the surgical operation is technically sound, and so on. Perioperative myocardial infarction is a common factor affecting outcome, with an incidence of 2-10%. In mild cases, it only manifests as abnormal serum enzymology, while in severe cases, it presents with electrocardiographic changes. Improved anesthesia techniques and intraoperative myocardial protection measures can reduce the incidence of myocardial infarction.
Long-term efficacy after shunt transplantation: after shunt surgery, angina pectoris was significantly reduced or disappeared, left ventricular function improved, cardiac output increased, and cardiac function improved significantly. About 2/3 patients can resume work after surgery, nearly 70% of cases can survive for more than 10 years after surgery. After single branch coronary artery lesions, the 10-year survival rate is 78%, two-vessel lesions become 69%, three-vessel lesions become 48%, and left coronary artery trunk lesions are 67%. After bypass grafting, the endothelium of the saphenous vein may proliferate, leading to luminal narrowing and poor blood flow. The incidence of saphenous vein intima-media hyperplasia of varying degrees can be 10-45% at 5 years after surgery. [Return to top]
Prevention of acute myocardial infarction
All kinds of physical or mental factors that can increase myocardial oxygen consumption or induce coronary artery spasm may cause coronary heart disease patients to have an acute myocardial infarction, and the common triggers are as follows: 1. Overwork: Doing incapable of physical labor, especially heavy stair climbing, excessive physical activities, and continuous stressful strain, etc., can make the burden on the heart significantly increased. The burden on the heart increased significantly, myocardial oxygen demand suddenly increased, and coronary artery of coronary artery disease patients have occurred hardening, narrowing, can not be fully expanded and cause myocardial ischemia within a short period of time. Ischemia and hypoxia can cause arterial spasm, which in turn aggravates myocardial hypoxia, leading to acute myocardial infarction in severe cases. 2. Excitement: Some patients with acute myocardial infarction are induced by intense emotional changes such as excitement, tension and anger. It is reported that there is a state in the United States, on average, every 10 ball games, there are 8 spectators have an acute myocardial infarction. 3. Overeating: many cases of myocardial infarction occur after overeating, both at home and abroad have information that the incidence of acute infarction on weekends and holidays is higher. After eating a lot of food containing high fat and high calorie, the blood lipid concentration suddenly rises, resulting in increased blood viscosity, platelet aggregation increases. Thrombus is formed on the basis of coronary artery stenosis, causing acute myocardial infarction. 4. Cold stimulation: sudden cold stimulation may induce acute myocardial infarction. This is the reason why doctors always advise patients with coronary heart disease to pay close attention to cold and warmth, but also one of the reasons why the incidence of acute myocardial infarction is higher in winter and spring cold season. 5. constipation: constipation is very common among the elderly, but its