What Is the Treatment for Ischemic Heart Disease?

[Overview]

[Overview]

Ischemic heart disease includes coronary obstruction or stenosis caused by atherosclerotic lesions. Left ventricular ventricular wall tumor caused by myocardial ischemia, ventricular septal defect after myocardial embolism, and mitral regurgitation due to papillary muscle ischemia are common acquired heart diseases in the elderly. This section focuses on coronary atherosclerotic obstruction or stenosis. Coronary artery wall atherosclerotic lesions lead to stenosis of the vascular cavity, obstruction of coronary circulation blood flow, insufficient myocardial blood supply, severe obstruction can cause myocardial infarction. In the past 40 years, the incidence of coronary atherosclerotic heart disease has gradually increased in China. According to statistics from Shanghai Medical University, coronary heart disease accounted for only 6% of inpatients with heart disease from 1948 to 1958; 18% from 1959 to 1971; it rose to 29% from 1972 to 1979, and currently ranks first among all types of heart diseases.

[Treatment]

The prevention and treatment of coronary heart disease can be summarized into two major categories of internal medicine and surgery. Medical treatment has many years of history. The treatment measures include adjusting diet and living habits, paying attention to mental health, applying drugs to reduce blood lipid levels, inhibiting platelet aggregation, and controlling angina pectoris. Surgical treatment of coronary heart disease has evolved in concept and method for more than 70 years. In 1916, Jonnesco removed cervical and chest sympathetic nerves to treat angina pectoris. In 1926, Boas performed a total thyroidectomy in an attempt to reduce the burden on the ischemic myocardium by reducing metabolism. In 1935, Beck and Tichy performed a pectoralis major and myocardial fixation suture, hoping that the adhesions formed could supply blood to the myocardium. Since then, tissues and organs such as the pericardium, greater omentum, lungs, jejunum, stomach, spleen, etc. have been used for fixed suture with the myocardium. Some surgeons also apply talc 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, and believed that the pericardial iliac artery at the proximal end of the ligation could transport more blood to the heart muscle. In 1946 Vineberg was implanted into the myocardial artery of the thorax. In 1955, Beck also advocated partial coronary artery sinus ligation and coronary artery shunt coronary artery shunt plus partial coronary sinus ligation to reverse coronary perfusion. The above-mentioned various surgical treatment methods have been unsatisfactory and have been abandoned. Since 1955, research has been performed directly on coronary arteries to improve myocardial blood supply. In 1958, Longmire et al. Performed endometrial ablation on the coronary arteries of the diseased segment to relieve stenosis of the lumen. In 1961, Senning underwent extracorporeal circulation to sew up the graft to enlarge the coronary stenosis. In 1967, Gatrett used the great saphenous vein to perform left anterior descending shunt transplantation and remained unobstructed after 7 years of follow-up. Selective coronary angiography has promoted the development of surgical treatment of coronary heart disease rapidly after its clinical application. In 1967, Favaloro and Effler promoted the use of the great saphenous vein for ascending aorta-coronary artery bypass grafting, and introduced the operation technique in 1969. By 1971, 741 operations had been performed. In 1968, Green reported anterior thoracic artery-anterior descending coronary anastomosis. In 1971, Flemma et al. Also reported the operation method of sequential transplantation, that is, using a large saphenous vein with multiple branches of the coronary artery to make multiple anastomoses. Since then, the surgical treatment of coronary heart disease has entered a new stage. At present, more than 400,000 people have undergone coronary artery bypass surgery for coronary heart disease, which is the main method for surgical treatment of coronary heart disease. Grüntzig et al. Reported in 1979 that percutaneous transluminal coronary angioplasty is relatively simple, does not require thoracotomy, and has less medical expenses, but the incidence of restenosis can reach 30 to 40 within 6 to 9 months after surgery. %. In recent years, there has been new equipment and new technology for percutaneous coronary coronary thrombolysis for the treatment of myocardial infarction caused by early coronary embolism, and cold laser in coronary lumen to eliminate atherosclerotic plaques and stenotic lesions.

Due to the complex pathogenic factors of coronary atherosclerotic heart disease, it has not been fully understood so far; there are many variations in the number and extent of coronary branches involved in lesions, the speed of lesion development, and the harm to ventricular function. The natural course of this type of coronary heart disease, in-depth comparison of the effects of medical and surgical treatment, has yet to be gradually enriched by long-term investigations. According to the existing clinical experience, although the surgical treatment of coronary heart disease fails to change or reverse the course of coronary atherosclerotic lesions, it can increase coronary blood flow and improve coronary circulation. After the ascending aorta-coronary artery bypass shunt was performed with the great saphenous vein, the clinical follow-up observation data of a large number of cases showed that the effect was good for angina pectoris, and 60 to 95% of the cases disappeared after 1 to 5 years. The electrocardiogram returned to normal, and the angina pectoris disappeared to 46% in 10 years after operation due to vascular obstruction or the progression of coronary heart disease, while the angina pectoris disappeared rate was only 3% in patients without surgical treatment. Physical activity endurance was significantly improved in 3 to 10 years after operation compared with non-surgical cases. 60% of patients were qualified for normal work 2 years after surgery, while only 26% of medically treated cases returned to work.

Indications for surgical treatment of coronary atherosclerotic stenosis: The ascending aorta-coronary artery bypass shunt is performed with a large saphenous vein, commonly known as bypass surgery is the most commonly used surgical method for coronary heart disease surgery. The surgical indications are:

1. The factors affecting the development and prognosis of stable angina pectoris include: the number of coronary artery branch lesions, especially whether the left coronary artery trunk or anterior descending branch is involved, the left ventricular function status, the severity of myocardial ischemia, and the gender of the patient And age, and whether there are other diseases. For patients with one or two coronary obstructive lesions that do not involve the left main coronary artery, the long-term efficacy of medical treatment is similar to that of surgical treatment. Medical treatment should be performed first and regularly reviewed. However, such as chronic stable angina pectoris medicine, nitrate, -blocker, calcium antagonist and other anti-angina pectoris medications have not been effective, and patients with severely affected work and life should undergo selective coronary angiography. It was found that the area of the blood vessel cavity was reduced to more than 50%, and especially those whose lesions involved the left main coronary artery, the left anterior descending coronary artery, or the three branches of the coronary artery should be considered for surgical treatment.

2. Most cases of unstable angina pectoris have severe coronary obstructive disease. Some cases have subendocardial patches or scattered myocardial infarction, and may develop into acute myocardial infarction in a short period of time, with severe arrhythmia or sudden death. Gazes et al reported that the 1, 2 and 10 year mortality rates were 18%, 25% and 50%, respectively. Patients with this type of angina who have not been controlled by active medical treatment for 1 week, should be treated with selective coronary angiography, and surgical treatment should be performed as soon as possible based on the test results.

3 Opinions on the implementation of coronary artery bypass grafting in patients with acute myocardial infarction are still inconsistent, and those who support the surgical treatment believe that the surgical treatment can reduce the area of myocardial infarction within 8 hours after the occurrence of myocardial embolism, and there will be less myocardial scar tissue in the future. The incidence of complications such as left ventricular ventricular aneurysm, arrhythmia, heart failure, and sudden death was low, and the improvement of left ventricular function was obvious. However, the mortality rate of coronary artery bypass grafting is higher in patients with acute myocardial infarction, and the incidence of postoperative paniculitis is also higher. The follow-up data of long-term efficacy need to be enriched. However, in the 2 weeks after myocardial infarction, the ST segment of the active plate load test was significantly depressed, and the mortality rate at follow-up for 1 year was 13 times higher than that of the test negative. Such cases should be considered for surgical treatment.

In recent years, treatment methods such as thrombolysis and percutaneous transluminal coronary angioplasty have been carried out in early myocardial embolism cases. The long-term efficacy of these therapies and their comparison with bypass grafting are currently insufficient. get conclusion.

4 Severe ventricular arrhythmias, cases of severe ventricular arrhythmias in the recovery phase or late stage after myocardial infarction, according to statistics, sudden death occurred in the follow-up 2 to 3 years. Therefore, myocardial ischemic ventricular arrhythmias should be considered as an indication for coronary artery bypass grafting.

Operation technique of coronary heart disease surgery: Surgical operation to reconstruct coronary circulation blood flow can use the great saphenous vein or internal thoracic artery. The large saphenous vein has a large caliber and is easy to obtain. The number of applied cases is the largest and the effect is satisfactory. In recent years, the use of pedicled internal thoracic artery and coronary arteries, especially the left anterior descending coronary artery for end-to-end anastomosis, has been increasing. Atherosclerotic lesions rarely occur in the internal thoracic artery, and stenosis of the vascular cavity due to endometrial hyperplasia is rare. Postoperative vascular patency is higher than that of the large saphenous vein. However, it is difficult to dissect the free internal thoracic artery. Bleeding complications are high, and free internal thoracic arteries may adversely affect sternal healing. Selective coronary angiography shows that coronary branches greater than 1.5 mm and lumen diameter reduced by more than 50% should be shunted to fully reconstruct myocardial blood flow. In patients with multiple coronary artery lesions, shunts are sometimes performed on 5 or more branches. In order to simplify the operation and shorten the operation time, sequential anastomosis can be used, that is, a large saphenous vein is used near the end-to-side anastomosis. One or two side-to-side anastomosis is performed at the other end, so that only one segment of the vein can be used to shunt two or more coronary arteries, reducing the anastomosis of the aorta with the great saphenous vein. After sequential anastomosis, the vascular patency is high and the blood flow is fast, but the operation needs to be detailed and accurate. Pay attention to avoid distortion of the great saphenous vein. Sometimes a thicker branch of the great saphenous vein and another coronary artery branch can be used for y-shaped anastomosis.

Preoperative preparation: Lung, liver, and kidney function should be checked before surgery. Digitalis and diuretics should be stopped on the 2nd day before surgery, but nitroglycerin, beta-blocker and calcium antagonist should not be stopped.

Surgical technique of great saphenous vein shunt transplantation: general anesthesia with endotracheal intubation, operation under extracorporeal circulation combined with low temperature, blood pressure, central venous pressure, electrocardiogram, body temperature, urine volume, etc. are monitored during the operation. Skin preparation should include the chest, abdomen, groin, and bilateral lower limbs. The surgeon performed the thoracotomy and the saphenous vein at the same time in two groups. The operation must be gentle when freeing the saphenous vein, and the injury of the vein should not be caused. When freeing the large saphenous vein, a long lower incision of the lower limbs can be used to better protect the blood vessels from traction damage than multiple small incisions that segment the free veins. During the process of freeing the great saphenous vein, it is forbidden to clamp the vein with vascular forceps. When using tissue forceps, only the adventitia of the vein wall can be clamped, so as not to cause damage to the lining of the vein. When dealing with venous branches, care should be taken to cut off the ligature branch farther from the main vein, so as not to cause shrinkage of the vein wall and contraction of the vascular cavity. The lower part of the great saphenous vein near the ankle is due to the lack of venous valves and the pressure resistance of the vascular cavity is better. It is more suitable for transplantation shunting than the upper part of the great saphenous vein. After taking out a large saphenous vein, insert a syringe with a smooth injection needle at its distal end and ligate it to identify the proximal and distal ends of the vein, and it can be used to inject a small amount of cold heparin solution (1000ml solution containing 10,000u heparin). To enlarge the vascular cavity and check the vein wall for leaks. The removed vein was injected with a solution into the cavity, and kept at a moderate expansion, and stored in a 10 ° C solution for later use. Topical application of dilute papaverine (60 mg per 500 ml of normal saline) can prevent venous spasm. While freely cutting the great saphenous vein, another group of surgeons made a midline incision of the sternum, splitting the sternum longitudinally, cutting the heart bag, and exposing the heart, and inserted a blood drainage and blood supply catheter into the vena cava and the distal ascending aorta, respectively. A lateral decompression drainage catheter is connected to the artificial heart-lung machine to establish extracorporeal circulation. During the operation, attention should be paid to protecting the myocardium. Measures such as blood cooling, local cooling of the myocardium, and perfusion of cold cardiac arrest fluid should be used, and the time to block the ascending aorta should be minimized. Generally, the distal saphenous vein and coronary artery anastomosis are performed first, but there is also an ascending aorta and great saphenous vein anastomosis followed by distal anastomosis. Coronary artery branches were exposed at the selected anastomosis site, and the middle part of the anterior wall of the artery was longitudinally cut with a sharp knife, and then the incision of the coronary artery was enlarged with curved scissors to a length of about 6 to 8 mm. Sometimes a small triangular branch of the anterior wall of the coronary artery is removed to facilitate vascular anastomosis. After the stump of the great saphenous vein for anastomosis is repaired with an excision membrane, a 45 ° incision is made obliquely so that the blood vessels do not distort after the anastomosis is completed. If necessary, a small segment of the venous wall can be cut longitudinally to enlarge the anastomotic end. The length of the saphenous vein incision should be 10 to 20% longer than that of the coronary branch incision. The anastomosis is sutured continuously or intermittently with 6-0 or 7-0 Prolene sutures. The needle pitch is generally about 1mm, and the side of the great saphenous vein is slightly wider. The endometrium of the blood vessel must be properly aligned. During the anastomosis, a small amount of heparin solution is dripped through the other end of the great saphenous vein to help improve the surgical field exposure. For those who need a sequential anastomosis, after completing the most distal end-to-side anastomosis, make a longitudinal incision on the wall of the great saphenous vein or the anatomical relationship between the transplanted great saphenous vein and another branch of the coronary artery. Transverse anastomosis was performed. It must be noted that the distance between the several incisions of the great saphenous vein is appropriate, the anastomosis does not produce distortion, and the blood flow is smooth. Once the distal anastomosis is complete, the aortic blocking forceps can be relaxed and the extracorporeal circulation rewarmed. With the great saphenous vein kept full, select the ascending aortic anastomosis, use a non-invasive vascular forceps to clamp the aortic wall, and cut a small hole with a diameter of about 5 mm with an aortic wall perforator at each anastomosis. To the cut end of the saphenous vein for anastomosis, the venous anastomosis should be 10-20% larger than the aortic wall incision, and the anastomosis is sutured continuously with 5-0 Prolene sutures.

Internal Thoracic Artery-Coronary End-to-Side Anastomosis: The internal thoracic artery has a similar caliber to the coronary arteries. The use of the internal thoracic artery to perform shunting has a greater vascular patency rate than the saphenous vein, and does not require a proximal aortic anastomosis. However, due to its limited length and anatomical location, it is generally only suitable for anastomosis with the left internal thoracic artery and the left anterior descending or diagonal branch. The diameter of the right internal thoracic artery is smaller than that of the right coronary artery, and the length is insufficient. Therefore, anastomosis of the right internal thoracic artery and the right coronary artery branch is rarely used.

After splitting and spreading the sternum, before cutting the sacral capsule and injecting heparin, use an electric knife to cut the thoracic fascia along the sides of the internal thoracic artery about 1 cm from the blood vessel, starting from the 6th intercostal space and up to the top of the sternum. Free internal thoracic arteries, veins and surrounding adipose tissue and muscle, pleura. The intercostal artery branches need to be ligated and cut off. The free internal thoracic artery and its surrounding tissue need to be carefully protected from trauma and wrapped with gauze impregnated with a dilute solution of papaverine. After heparinization of the whole body before the start of extracorporeal circulation, the internal thoracic artery was ligated and cut at the 6th intercostal level. The bleeding at the proximal end of the artery can reach 120-240ml per minute. If the bleeding is less than 100ml per minute, the blood vessel quality is not good. Not suitable for application. The left anterior descending branch is incised, and the tissues around the internal segment of the thoracic artery are removed at an appropriate length to expose the artery about 1 cm in length. The lumen can be gently expanded with a dilator with a diameter of 1.0 to 1.5 mm and then cut obliquely. 7 0Prolene suture and anterior descending incision are used for continuous or intermittent suture, and then the soft tissue around the internal thoracic artery and the myocardium are sutured with several needles to reduce the anastomotic tension, and the left pericardium is cut transversely to ensure the thoracic The internal arteries have unobstructed access to the heart.

When performing coronary artery bypass grafting, if the condition requires, coronary endarterectomy can be performed at the same time.

Postoperative management: After coronary artery bypass grafting, blood pressure, central venous pressure, left atrial pressure, heart rate, heart rate, body temperature, chest drainage, urine volume, blood gas analysis, blood pH and electrolyte content should be closely monitored to prevent blood Insufficient capacity, hypoxia, acidosis and electrolyte disturbances. Oral beta-blockers can prevent arrhythmias. In cases where the great saphenous vein is used for shunt transplantation, taking aspirin and persantin after surgery can prevent deep vein thrombosis in the lower limbs. A small number of patients are complicated by low blood volume syndrome after surgery, and those with unsatisfactory drug treatment need to be treated with intra-aortic balloon counterpulsation.

Efficacy of shunt transplantation: In recent years, surgical mortality has fallen below 5%. The most common cause of death is acute heart failure. Factors that affect the mortality of the operation are: the extent of coronary artery branch lesions, the severity of angina pectoris, the left ventricular function before surgery, the age and gender of the patient, whether there is concurrent myocardial infarction, the number of transplanted blood vessels, the aortic occlusion time, and whether the surgical technique is proper Wait. Perioperative myocardial infarction is a common factor affecting the efficacy, and its incidence is 2-10%. The lighter ones showed abnormal serum enzymes, while the more severe ones showed ECG changes. Improving anesthesia techniques and attaching importance to myocardial protection during surgery can reduce the incidence of myocardial infarction.

Long-term effects after shunt transplantation: After shunting, angina pectoris is significantly reduced or disappeared, left ventricular function is improved, cardiac output is increased, and cardiac function is significantly improved. About two-thirds of patients can return to work after surgery, and nearly 70% of cases can survive for more than 10 years. The 10-year survival rate was 78% for single coronary artery disease, 69% for two vascular disease, 48% for three vascular disease, and 67% for left coronary artery disease. After shunt transplantation, the intima of the great saphenous vein may proliferate, leading to narrowing of the vascular cavity and impeded blood flow. The incidence of intimal hyperplasia of the great saphenous vein within 5 years after operation can reach 10 to 45%.

Etiology

The pathogenesis of coronary atherosclerosis is complex and has not yet been 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, high blood lipids, hypertension, diabetes, obesity, too little physical activity, intense mental labor, and emotional excitement , Mental stress, middle-aged and older men, high-density lipoprotein is too low, abnormal blood coagulation and so on. Few cases may have familial genetic factors.

[Pathological changes]

Coronary Artery Anatomy: Coronary arteries are blood vessels that supply myocardial blood and oxygen, and their anatomical shapes vary widely. Under normal circumstances, there are two branches of the left and right coronary arteries, which are respectively opened in the left and right coronary valve sinuses of the ascending aorta, and sometimes another smaller accessory coronary artery is emitted from the aorta.

The left main coronary artery is about 4 to 5 mm in diameter and about 0.5 to 2 cm in length. After it is emitted from the ascending aorta, it walks in the lower left direction after the main pulmonary artery and runs along the left atrioventricular groove between the main pulmonary artery and the left atrial appendage. Forward and downward are divided into anterior descending branch and circumflex branch.

The anterior descending branch is a continuation of the left coronary artery trunk, descending along the anterior intersulcus, and then bypassing the apical notch to reach the posterior wall of the heart. It coincides with the posterior descending branch of the right coronary artery 1/3 below the posterior intersulcus. The anterior descending branch has branches such as the left conic branch, the oblique branch, the left ventricular anterior branch, the right ventricular anterior branch, and the anterior branch of the ventricular septum. Anterior wall of right ventricle, most ventricular septum (upper and anterior), apical area and anterior papillary muscles.

After the circumflex branch emanates from the left coronary artery trunk, it clings to the bottom of the left atrial appendage along the front of the left atrioventricular sulcus, walks left and back, and then descends through the left edge of the heart to the diaphragm. The branches from the circumflex branch are quite variable. The main branch has several branches on the left margin, the posterior branch of the left ventricle, and the atrioventricular branch along the left atrioventricular sulcus. The atrioventricular branch is sometimes (approximately 10%) long and emanates from the distal descending branch and atrioventricular node arteries. 30% of the human circumflex branches still have sinoatrial node arteries. The blood supply area of the circumflex branch includes the left ventricle side wall and the posterior wall, and the left atrium, and sometimes the blood supply to the ventricular diaphragm, anterior papillary muscle, posterior papillary muscle, part of the ventricular septum, atrioventricular node, atrioventricular bundle, and sinoatrial node.

After the right coronary artery is sent from the right coronary valve sinus, it is close to the bottom of the right atrial appendage and goes down the right atrioventricular groove. Reach the atrioventricular sulcus ventricle, atrium, and the junction of the atrial septum and the ventricular septum, divided into two branches, the right posterior descending branch in the posterior interventricular groove to the apical region, and the other smaller atrioventricular node artery turned upward. The main branches of the right coronary artery are the right conic branch, right atrial branch, sinoatrial node branch, anterior right ventricle branch, posterior lateral branch of right ventricle, posterior ventricular septal branch, posterior descending branch, and atrioventricular node artery. The right coronary artery blood supply area includes the right atrium, sinoatrial node, right ventricular outflow tract, pulmonary artery cone, anterior wall of right ventricle, posterior wall of right ventricle, 1/3 below ventricular septum, and atrioventricular node. Patients with a predominant right coronary artery are still supplying blood to parts of the left ventricle and apex. The distribution of left and right coronary arteries in the myocardial epiphyseal area is quite variable. When a narrow lesion of a coronary artery with a large blood supply range occurs, the area of myocardial ischemic injury is wider and the condition is more serious.

[Typing]

The distribution of left and right coronary arteries can be divided into three main types according to the source of blood supply at the intersection of the cardiac cross-section, the ventricle, the atrium and the atrioventricular septum on both sides of the posterior wall of the heart:

1) Right coronary artery predominant 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 supplying blood from the posterior descending branch across the cruciate zone to the posterior wall of the left ventricle and the posterior ventricular septum.

2) The dominant left coronary artery is smaller than the right coronary artery. The descending branch of the left coronary artery is supplied to the posterior wall of the left and right ventricles and the ventricular septum.

3) The left and right coronary arteries are evenly distributed. The left and right coronary arteries each issue a posterior descending branch to supply blood to the posterior wall of the left and right ventricles.

Pathological anatomy: Most coronary atherosclerotic lesions occur in the proximal section of the main branch of the coronary artery, which is about 5 cm away from the aortic opening. It is often located in the atrioventricular sulcus and is surrounded by the main branch of the coronary artery with fatty tissue. The lesions provide favorable conditions for surgical treatment. Patients with hypertension or diabetes have a wide range of lesions and can involve small branches of the coronary arteries. Atherosclerotic lesions mainly involve the intima of the coronary arteries. Lipids and lipid-containing macrophages infiltrate in the intima and middle layers of cells at the early stage of the lesion, and the intima thickens with yellow spots. With multiple causes of endometrial cell damage and increased intimal permeability, lipid infiltration increases, spots gradually increase and expand, and plaques or stripes form. The endometrium also appears as focal dense lamellar collagen, and lesions involving the entire periphery of the intima cause narrowing or obstruction of the vascular cavity. Coronary arterial blood flow is reduced, local myocardial blood supply and oxygen supply are insufficient during exercise or even at rest, and severe cases can cause myocardial infarction. Coronary atherosclerotic lesions can be accompanied by blood, thrombosis, and aneurysms. When atherosclerotic lesions rupture and bleed, lipids enter the vascular cavity, which can easily cause distal vascular embolism and induce thrombosis, and vascular wall hematomas can gradually form granulation tissue and fibrosis. The acute phase of endometrial hemorrhage may cause coronary artery and collateral branch spasm and increase the degree of myocardial ischemia. Thrombosis is often associated with bleeding cakes, which can also cause distal vascular embolism and vascular wall fibrosis. Coronary endometrial atherosclerotic plaques with middle-layer necrosis of the vascular wall and aneurysms are very rare. In most cases, aneurysms occur in only one vessel, with a diameter of up to 2.5 cm. The lumen may contain blood clots, but the blood vessel lumen remains. unobstructed. Coronary artery stenosis caused by atherosclerotic lesions. If only limited to one branch of the coronary artery and the development process is slow, the communication branch between the diseased blood vessel and the adjacent coronary artery will significantly expand, and an effective collateral circulation can be established. The heart muscle can still get enough blood supply. Lesions involving multiple blood vessels, or stenotic lesions progress rapidly, collateral circulation is not fully established or blood, hematoma, thrombosis, vasospasm, etc. can cause severe myocardial ischemia or even myocardial infarction. Myocardial tissue atrophy, or even necrosis, rupture or form fibrous scars in the diseased area, and myocardial contractile function is severely damaged, arrhythmia or cardiac pump failure may occur. The larger the scope of myocardial ischemia, the more serious the harm. The left coronary artery supplies the most coronary blood flow, so heart disease caused by obstruction of the left coronary artery and its branches becomes more severe than that of the right coronary artery.

Pathophysiology: The blood flow per minute is 60-80ml per 100g of myocardium, which is about 10 times more than the blood flow of 7ml per 100g per minute. Another feature of coronary circulation is that the arterial blood flow is the largest during diastole, while the coronary blood flow is reduced during the systole due to the compression of myocardial blood vessels, while other organs of the body have the highest blood flow during the systole when the arterial perfusion pressure is highest. . Myocardium has a strong oxygen uptake capacity, and can take up about 65 to 75% of oxygen from capillaries. Under normal circumstances, oxygen is taken from 8 to 10 ml per minute per 100 g of myocardium, while whole body organs and tissues can only take in 25% oxygen from the blood, and only 0.3 ml per 100 g of tissue per minute. During exercise, cardiac output is significantly increased, cardiac workload is increased, and myocardial oxygen demand is increased. Since there is not much room to further increase oxygen uptake from the blood, it is necessary to expand the coronary lumen to increase coronary blood flow. Suitable for increased oxygen demand. Coronary circulation has a sensitive regulation ability. Factors that regulate coronary blood flow include: arterial perfusion pressure, coronary vascular resistance, heart rate, cardiac diastolic time limit, blood co2 tension, O2 tension, pH, and neurohumoral factors.

The basic substances of myocardial metabolic energy include glucose, fatty acids, and lactic acid. Under the condition of insufficient coronary blood supply and myocardial hypoxia metabolism, the oxidation of fatty acids is reduced, and the oxidation of carbohydrates is dominant. However, under hypoxic conditions, the energy that can be supplied after the decomposition of glucose and glycogen is only A small fraction under aerobic metabolism. Continuous myocardial ischemia and hypoxia for more than 20 minutes can cause irreversible deterioration of mitochondria, myocardial cell necrosis, loss of myocardial enzyme activity, clinical symptoms such as angina pectoris, arrhythmia, and heart failure.

[Clinical manifestations]

Symptoms: The main symptom of coronary atherosclerotic heart disease is angina pectoris caused by temporary ischemia caused by imbalance of myocardial oxygen supply and demand. Most of them occur suddenly during labor, emotional excitement, full meal or cold. The common pain site is the posterior or anterior cardiac region, which can radiate to the inside of the left arm, shoulder, interscapular region, neck, throat, and jaw, and sometimes in the upper abdomen. The nature of the pain can be severe colic, cramping pain, oppression pain, tightening pain, or the pain is very mild, only feeling bloated and uncomfortable. Occasional or severe pain accompanied by sweating and dying fear. The pain usually lasts 1 to 10 minutes and disappears after rest or with nitroglycerin tablets. Angina pectoris is more stable in terms of its cause, frequency and duration. In some cases, the severity of myocardial ischemia can be changed from typical stable angina pectoris to unstable angina pectoris, which is mainly manifested by frequent episodes of angina pectoris, prolonged pain duration, severity, or even pain at rest, and acute myocardial infarction. Increased risk. Early onset of acute myocardial infarction may be nausea, vomiting, hiccups or epigastric pain, severe angina pectoris, duration can be up to several hours, rest or taking nitroglycerin tablets failed to relieve, often accompanied by shock, arrhythmia and heart effort Exhaustion.

Signs: There are usually no special signs in patients with coronary atherosclerotic heart disease. Blood pressure may increase or decrease slightly during angina pectoris, and the heart rate may be normal, increase or decrease. Those with severe pain expressed anxiety, irritability, pale complexion, and sweating, and occasionally showed atrial or ventricular running rhythm. With papillary muscle dysfunction, systolic murmurs can be heard in the apical region. In cases of myocardial infarction, the heart rate may increase or decrease, blood pressure may decrease, the heart dullness may slightly increase, the first heart sound in the apical region may weaken, and sometimes the third and fourth heart sounds or diastolic rhythm may occur, and various arrhythmias may occur. , Shock, or signs of heart failure.

[Auxiliary inspection]

X-ray examination: X-ray examination of the chest is generally found no abnormalities. Cases with hypertension can show enlarged left ventricle, widened, enlarged aorta and prolonged tortuosity. Patients with concomitant heart failure have a significantly enlarged heart and congested lungs.

Electrocardiogram: Electrocardiogram is one of the important ways to reflect myocardial ischemia. Angina pectoris attacks often show a decrease in ST segment and a flat or inverted T wave. It gradually recovers within minutes after the attack, sometimes with arrhythmia. Patients with no obvious abnormal changes in ECG can be used for stress test to increase cardiac load, increase myocardial oxygen consumption, and temporarily induce electrophysiological changes of myocardial hypoxia. The ECG stress test can be performed by the double secondary ladder exercise test, the treadmill exercise test, the pedal exercise test, and the glucose load test. Holter ECG monitors can also be used for continuous ECG recording. The electrocardiogram of patients with acute myocardial infarction is characterized by deep Q waves or QS waves, ST segments are significantly elevated, dorsal arch upwards and T waves inverted. Based on the leads showing the characteristic changes described above, a localized diagnosis of myocardial infarction can be made.

Serum enzyme examination: In the early stage of acute myocardial infarction, serum aspartate aminotransferase, creatine phosphokinase, and lactate dehydrogenase all increased, and its dynamic changes were helpful to judge the evolution of the disease.

Other diagnostic methods include cross-section echocardiography and radionuclide cardiac imaging, which are of great value in diagnosing coronary heart disease and myocardial infarction and understanding left ventricular motor function.

Selective coronary angiography and left ventricular angiography: Selective coronary angiography can clearly show the left and right coronary arteries and their branches, which can not only provide evidence for the diagnosis of coronary stenosis caused by atherosclerotic lesions, but also observe the lesions. The exact location and extent of the disease, the degree of stenosis of the diseased vessels, and the condition of the collateral circulation The inner diameter of the diseased coronary artery branches was reduced by 1/3, and the area of the vascular cavity was reduced by 50%; the internal diameter was reduced by 1/2, and the lumen area was reduced by 75%; the internal diameter was reduced by 2-3, and the lumen area was reduced by 90%. Left ventricular angiography can observe whether the systolic function of the ventricular wall in various parts of the left ventricle is normal, decreases or disappears, and measures the left ventricular ejection fraction. Left ventricular angiography can also be used to diagnose wall tumors, ventricular septal defects and mitral regurgitation caused by myocardial infarction. For patients with coronary heart considering surgical treatment, selective coronary angiography and left ventricular angiography must be performed before surgery to identify surgical indications and formulate a surgical plan.