Acute coronary syndrome (ACS)

Introduction Acute coronary syndrome (ACS) is a group of clinical syndromes including acute ST-segment elevation myocardium based on rupture or invasion of coronary atherosclerotic plaque, secondary or complete or incomplete occlusive thrombosis. Infarction, acute non-ST-segment elevation myocardial infarction, and unstable angina (UA). ACS is a common serious cardiovascular disease and a serious type of coronary heart disease. Common in elderly, male and postmenopausal women, smoking, hypertension, diabetes, hyperlipidemia, abdominal obesity and patients with a family history of early onset coronary heart disease. Patients with ACS often present with symptoms such as paroxysmal chest pain and chest tightness, which can lead to arrhythmia, heart failure, and even sudden death, which seriously affect the quality of life and longevity of patients. If appropriate treatment is taken in time, the mortality rate can be greatly reduced, complications can be reduced, and the prognosis of patients can be improved. Most causes of ACS are the result of instability of coronary atherosclerotic plaque. Very few ACS are caused by non-atherosclerotic diseases (such as arteritis, trauma, dissection, thromboembolism, congenital anomalies, abuse of cocaine, or complications of cardiac intervention). When there is a contradiction between the blood supply of the coronary artery and the blood supply of the myocardium, the coronary blood flow can not meet the needs of myocardial metabolism, causing acute and temporary ischemia and hypoxia of the myocardium, and angina can occur. Coronary atherosclerosis can cause stenosis of one or more vascular lumens and insufficient blood supply to the myocardium. Once the blood supply is drastically reduced or interrupted, the acute and persistent acute ischemia of the myocardium can reach 20 to 30 minutes. Myocardial infarction (AMI). Symptoms are usually characterized by paroxysmal sternal pain, tightness or pressure, burning, and can be radiated to the left upper arm, lower jaw, neck, back, shoulder or left forearm ulnar, intermittent or continuous, accompanied by Sweating, nausea, difficulty breathing, suffocation, and even syncope, lasting for >10 to 20 minutes, AMI is often indicated when nitroglycerin is not completely relieved. Some patients have fatigue, chest discomfort, nausea, shortness of breath, irritability, angina and other prodromal symptoms during the first few days of AMI. Atypical manifestations include: toothache, sore throat, pain in the upper abdomen, indigestion, acupuncture-like pain in the chest, or difficulty breathing. These are common in elderly, female, diabetic, chronic renal insufficiency or dementia patients. The clinical lack of typical chest pain, especially when the ECG is normal or critical, is often overlooked and delayed treatment, should pay attention to continuous observation. Most ACS patients have no obvious signs. In severe cases, the skin may be wet and cold, pale, irritated, and jugular vein engorgement. The auscultation may smell lung vocal, arrhythmia, heart murmur, heart sound splitting, third heart sound, pericardial rubbing sound and galloping. Diagnostics can be diagnosed as angina when there is a typical ischemic chest pain or an electrocardiographic dynamic change without an elevated myocardial necrosis marker. Myocardial infarction can be diagnosed when any of the following is present. 1. The cardiac biomarker (preferably troponin) is increased or decreased, at least 1 time value exceeds the upper limit of normal, and there is at least one evidence of myocardial ischemia: (1) clinical symptoms of myocardial ischemia; (2) There is a new myocardial ischemia change in the electrocardiogram, that is, a new ST segment change or left bundle branch block (according to whether the ECG has ST segment elevation, divided into STEMI and NSTEMI); (3) Electrocardiogram shows pathological Q (4) Imaging evidence indicates a new loss of myocardial viability or regional wall motion abnormalities. 2. Sudden, unanticipated cardiac death, involving cardiac arrest, often accompanied by symptoms suggestive of myocardial ischemia, presumed to be new ST-segment elevation or left bundle branch block, coronary angiography or necropsy test Evidence of fresh blood clots, death occurs before blood samples can be obtained, or before cardiac biomarkers appear in the blood. 3. In patients with normal baseline troponin and undergoing percutaneous coronary intervention (PCI), elevated cardiac biomarkers above the upper limit of normal myocardial necrosis. Cardiac biomarkers rise more than three times the upper limit of the normal for PCI-associated myocardial infarction, including a subtype that has been shown to be associated with stent thrombosis. 4. Patients with normal baseline troponin values and coronary artery bypass grafting (CABG), cardiac biomarkers rise above the upper limit of normal, suggesting perioperative myocardial necrosis. Increases cardiac biomarkers by more than 5 times the upper limit of normal and develops new pathological Q waves or new left bundle branch block, or coronary angiography confirms newly transplanted or autologous coronary occlusion, or myocardial viability Lost imaging evidence was defined as myocardial infarction associated with CABG. 5. There are pathological findings of AMI. Complications AMI patients can be complicated: 1. Arrhythmia is common in 75% to 95% of AMI patients, mostly in the onset of 1 to 2 days, and most commonly within 24 hours. Among a variety of arrhythmias, ventricular arrhythmias are the most common, especially ventricular premature contractions. Ventricular fibrillation is the main cause of death in the early stages of AMI, especially before admission. Atrioventricular block and bundle branch block are also more common, and supraventricular arrhythmia is less, mostly in heart failure. 2. Hypotension and shock shock occur more than a few hours to several days after onset. It is found in about 20% of patients with AMI, mainly cardiogenic, with extensive myocardial (more than 40%) necrosis and a sharp drop in cardiac output. To. 3. Heart failure is mainly acute left heart failure, which can occur in the first few days of onset of AMI, or in the stage of pain and shock improvement, which is caused by a significant decrease or inconsistency of heart contractility after infarction. 32% to 48%. Difficulty in breathing, cough, cyanosis, irritability and other symptoms, severe pulmonary edema can occur, followed by jugular vein engorgement, liver enlargement, edema and other right heart failure. Right ventricular AMI can show right heart failure at the beginning, with blood pressure drop. 4. The total incidence of dysfunction or fracture of the papillary muscle can be as high as 50%. Causes varying degrees of mitral valve prolapse and insufficiency, causing heart failure. Severe cases can die within a few days. 5. Heart rupture is rare, often occurs within 1 week of onset, mostly rupture of the free wall of the ventricle, causing sudden death. Occasionally, perforation of the ventricular septal rupture can cause heart failure and shock and die within a few days. Heart rupture can also be subacute, and patients can survive for months. 6. The incidence of embolism is 1% to 6%. It can be caused by the left ventricular wall thrombus after 1 to 2 weeks after onset, causing arterial embolism of brain, kidney, spleen or limbs. Pulmonary embolism can also occur due to partial shedding of venous thrombosis in the lower extremities. 7. Ventricular wall tumors are mainly found in the left ventricle, with an incidence of 5% to 20%. A wall thrombus can occur in the tumor to cause embolism. 8. The incidence of myocardial infarction syndrome is about 10%. It occurs several weeks to several months after AMI, and can occur repeatedly, manifested as pericarditis, pleurisy or pneumonia, with fever, chest pain and other symptoms. First-aid measures for treatment: Stop the activity, rest, and call the emergency center as soon as possible if symptoms of suspected acute ischemic chest pain occur. For patients with ACS without contraindications, nitroglycerin should be administered sublingually, repeated once every 5 minutes, and the total amount should not exceed 1.5 mg. "Time is the heart muscle, time is life." For patients with STEMI, the use of thrombolysis or interventional therapy (PCI) to open infarct-related arteries as early as possible can significantly reduce mortality, reduce complications, and improve patient outcomes. Treatment: drug treatment, surgical treatment, interventional therapy, other treatments, etc. 1. Treatment of STEMI (1) Initial treatment after hospitalization All patients with STEMI should be given oxygen and ECG, blood pressure and oxygen saturation monitoring immediately after admission to the hospital. Those with severe hypoxemia should be masked with oxygen or The trachea is intubated and mechanically ventilated. Analgesic treatment. (2) Thrombolytic therapy for STEMI in the acute phase of direct PCI has become the preferred method, but because there are not many hospitals that can carry out direct PCI, it is still difficult to apply universally. Thrombolytic therapy is fast, simple, economical and easy to operate. Intravenous thrombolysis is still a good choice. Read more...