Introduction
Acute coronary syndrome(ACS) is a group of clinical syndromes based on rupture or invasion of coronary atherosclerotic plaque, followed by complete or incomplete occlusive thrombosis, including acute ST-segment elevation myocardial 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.
Cause
The vast majority 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).
symptom
Typical manifestations of paroxysmal sternal pain, tightening pressure or pressure, burning sensation, can be radiated to the left upper arm, lower jaw, neck, back, shoulder or left forearm ulnar side, intermittent or continuous, accompanied by Sweat, nausea, difficulty breathing, suffocation, and even syncope, lasting for >10 to 20 minutes, AMI is not always relieved 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.
diagnosis
An angina can be diagnosed when there is a typical ischemic chest pain symptom 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 a left bundle branch block (according to whether the ECG has ST segment elevation, divided into STEMI and NSTEMI);
(3) pathological Q waves appear on the electrocardiogram;
(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.
complication
Patients with AMI can be concurrent:
Arrhythmia
Found in 75% to 95% of patients with AMI, mostly occurred in the first 1-2 days of onset, and most often 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 occurs within a few hours to several days after onset. It is found in about 20% of patients with AMI, mainly cardiogenic, which is caused by a wide range of myocardial necrosis (40%) and a sharp decrease in cardiac output.
3. Heart failure
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 infarction, and the incidence is about 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. Papillary muscle dysfunction or fracture
The total incidence 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
Rare, often appear within 1 week of onset, mostly rupture of the ventricular free wall, 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. Embolization
The incidence rate is 1% to 6%. It can be caused by the left ventricular wall thrombus due to 1-2 weeks after onset of the disease, causing arterial embolism of the brain, kidney, spleen or limbs. Pulmonary embolism can also occur due to partial shedding of venous thrombosis in the lower extremities.
7. Ventricular aneurysm
Mainly seen in the left ventricle, the incidence rate is 5% to 20%. A wall thrombus can occur in the tumor to cause embolism.
8. Post myocardial infarction syndrome
The incidence rate 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.
treatment
First-aid measures: 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 STEMI patients should be given oxygen and ECG, blood pressure and oxygen saturation monitoring immediately after admission to the hospital. Patients with severe hypoxemia should be masked with pressurized oxygen or tracheal intubation and mechanical Ventilation. 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.
Thrombolytic therapy was performed within 3 hours of onset, and its clinical efficacy was comparable to that of direct PCI. Thrombolytic therapy within 3 to 12 hours of onset is not as effective as direct PCI, but still benefits. Thrombolytic therapy is still effective if there is persistent or intermittent ischemic symptoms and persistent ST-segment elevation within 12 to 24 hours of onset. The sooner the vascular opening time after STEMI occurs, the more myocardium is saved. The goal is to start thrombolysis within 30 minutes of the arrival of the ambulance.
(3) Percutaneous coronary intervention (PCI) for PCI can quickly and effectively open infarct-related arteries, which is the first choice for acute STEMI.
1) Direct PCI1 is immediately feasible and can be performed in time (visiting-balloon expansion time <90min), STEMI (including positive posterior myocardial infarction) within 12 hours of symptom onset or accompanied by new or possibly new left bundle Patients with branch block should undergo direct PCI. 2 age <75 years old, shock occurred within 36 hours of onset, lesions suitable for revascularization, and can be completed within 18 hours of shock, should be direct PCI, unless the patient refuses, has contraindications and/or is not suitable Invasive treatment. 3 patients with symptomatic seizures for 12 hours, asymptomatic, hemodynamics and stable ECG should not be treated with direct PCI.
2) Patients with high-risk STEMI who are transferred to PCI are treated in hospitals without direct PCI conditions, especially those who have thrombolysis contraindications or have no thrombolysis contraindications but have been onset for >3 hours, and can be antithrombotic (antiplatelet or anticoagulation). At the same time, the patient should be transported as soon as possible to a hospital with a viable PCI.
(4) Antithrombotic therapy
1) Antiplatelet therapy 1aspirinAll patients should be given oral water-soluble aspirin or chewed enteric-coated aspirin 300mg as long as there is no contraindications, followed by long-term maintenance at 100mg/d. 2 thienopyridines: The initial loading of clopidogrel should be 300mg (600mg of direct PCI) before or at the time of PCI. All patients continued to take clopidogrel 75 mg/d during hospitalization. After discharge from the hospital, patients who have not been placed in the stent should be given clopidogrel 75 mg/d for at least 28 days, and conditions may be used for up to 1 year. Patients who underwent stenting for acute coronary syndrome were treated with clopidogrel 75 mg/d for at least 12 months. Patients with drug-eluting stents may consider clopidogrel 75 mg/d for more than 15 months. For those who are contraindicated in aspirin, clopidogrel can be taken for a long time. 3GPIIb/IIIa receptor antagonists: abciximab, eptifibatide, tirofiban, etc., can be selectively used in patients with severe thrombus burden and patients with thienopyridines not given appropriate loading.
2) anticoagulant therapy 1 unfractionated heparin; 2 low molecular weight heparin; 3Fondaparinux4 bivalirudin; 5 oral anticoagulant therapy: after the acute phase of STMI, the following conditions require oral anticoagulant therapy: echocardiography suggests active thrombosis in the heart chamber, oral warfarin 3 to 6 months; Patients with atrial fibrillation; those who cannot tolerate aspirin and clopidogrel can take warfarin for a long time and maintain INR2-3. If you need to add warfarin to aspirin and clopidogrel, you should pay attention to the risk of bleeding, closely monitor the INR, and shorten the monitoring interval.
(5) Anti-myocardial ischemia and other treatments
1) Nitrate esters such as patients with systolic blood pressure below 90mmHg or lower than basic blood pressure >30%, severe bradycardia (heart rate) or tachycardia (heart rate >100 beats / min), diagnosed right ventricular infarction, should not Use nitrate drugs.
2) β-blockers reduce myocardial infarct size, reduce recurrent myocardial ischemia, re-infarction, ventricular fibrillation and other malignant arrhythmias, and have a positive effect on reducing acute mortality. If there is no contraindication to the drug, it should be routinely administered orally within 24 hours after the onset of the disease.
3) Angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB) can reduce the incidence of filling heart failure and reduce mortality. If there is no contraindication, all patients with STEMI should be given long-term treatment with ACEI. If the patient cannot tolerate ACEI, consider switching to ARB.
4) aldosterone receptor antagonists after left ventricular ejection fraction (LVEF) ≤ 0.4, with cardiac insufficiency or diabetes, no significant renal insufficiency (menstrual serum creatinine is less than or equal to 221μmol / L (2.5mg / dl), women are less than An aldosterone receptor antagonist should be administered to a patient equal to 177 μmol/L (2.0 mg/dl) and serum potassium 5 mmol/L or less.
5) Calcium antagonists do not recommend the use of short-acting dihydropyridine calcium antagonists.
6) In addition to lipid-lowering effects of statins, statins also have pleiotropic effects on anti-inflammatory, endothelial function, and inhibition of platelet aggregation. Therefore, all STEMI patients without contraindications should start statin therapy as soon as possible after admission. There is no need to consider cholesterol levels. The benefits of statin therapy are not only seen in patients with elevated cholesterol, but also in patients with coronary heart disease who have normal cholesterol. All patients with myocardial infarction should use statins to control low-density lipoprotein cholesterol levels below 2.6mmol/L (100mg/dl).
(6) Coronary artery bypass grafting (CABG) is not suitable for PCI in a small number of STEMI patients with cardiogenic shock. Emergency CABG can reduce the mortality rate. When mechanical complications (such as ventricular free wall rupture, papillary muscle rupture, ventricular septal perforation) cause cardiogenic shock, CABG and corresponding cardiac surgery are required in the acute phase.
(7) Treatment of complications
2. Treatment of NSTE-ACS
The NSTE-ACS treatment was designed to take appropriate medication and coronary revascularization strategies based on risk stratification (Table 1). Risk stratification of ischemic risk in patients with NSTE-ACS can be performed using the TIMI or GRACE integration system. Risk assessment of bleeding risk in patients with NSTE-ACS using the CRUSADE bleeding score system.
(1) Antithrombotic treatment is similar to STEMI.
(2) Anti-myocardial ischemia and other treatments are similar to STEMI.
(3) Thrombolytic therapy Because of the different pathogenesis and STEMI, NSTE-ACS does not recommend thrombolytic therapy.
(4) PCI treatment
1) High-risk patients with high-risk NSTE-ACS [including serum cTn or ECG ST-T wave changes, diabetes, renal insufficiency (eGFR <60ml/min・1.73m [1]), cardiac dysfunction (LVEF <40%) Patients with early post-infarction angina, recent PCI, previous CABG history, and moderate to high GRACE risk scores advocated diagnostic coronary angiography within the first 72 hours of symptom onset and then revascularization based on the condition. For patients at very high risk of myocardial ischemia, refractory angina with heart failure, life-threatening ventricular arrhythmia or hemodynamic instability, a viable emergency invasive strategy (140 incorporates several other high-risk factors (eg cTnT or ST-) Early (<24 hours) invasive strategies are recommended for patients with T-wave changes.
2) Early stable patients with NSTE-ACS who have a high risk of clinical events, if there is no serious comorbidities or contraindications for revascularization, should be early coronary angiography or revascularization. For patients with initially stable high-risk NSTE-ACS, early intervention should be performed (within 12 to 24 hours of admission). For patients with NSTE-ACS who are initially stable and have no severe comorbidities and contraindications to revascularization, conservative treatment may initially be considered, and subsequent treatment decisions (conservative or interventional) are determined by the physician based on the condition or patient's wishes.
3) Non-invasive myocardial ischemia assessment in patients with low to intermediate risk and asymptomatic recurrence in patients with low to intermediate risk. The myocardial revascularization strategy (PCI or CABG) should be based on clinical symptoms and severity of coronary lesions.
4) Patients with severe comorbidities in patients with liver function and pulmonary failure or cancer do not advocate early diagnosis of coronary angiography and revascularization.
(5) CABG
(6) treatment of complications
prevention
Non-pharmacological intervention
(1) Quit smoking
(2) Exercise ACS patients should be assessed for exercise tolerance before discharge and develop individualized physical exercise programs. For all patients with stable disease, it is recommended to perform 30 to 60 minutes of moderate-intensity aerobic exercise (such as walking fast, etc.) for at least 5 days per week. In addition, it is also recommended to perform 1 or 2 resistance trainings per week. Physical exercise should be gradual and avoid causing discomfort such as angina.
(3) Weight control should be monitored before and after discharge from the hospital. It is recommended to control the body mass index to 24kg/m [1] by controlling diet and increasing exercise.
2. Drug prevention
(1) Antiplatelet therapy If there is no contraindication, all ACS patients should be treated with aspirin (75-150 mg/d) for a long time after discharge. Patients who cannot apply aspirin due to contraindications may be replaced with clopidogrel (75 mg/d). Patients receiving PCI need to be combined with aspirin and clopidogrel.
(2) If there are no contraindications for ACEI and ARB drugs, all patients with STEMI with heart failure (LVEF < 0.45), hypertension, diabetes or chronic kidney disease should take ACEI for a long time. Patients with low-risk STEMI (ie, those with normal LVEF, successful revascularization, and satisfactory cardiovascular risk factors) may also be considered for ACEI. Patients with indications but not tolerated with ACEI can be treated with ARBs.
(3) β-blockers If there is no contraindication, all patients with STEMI should be treated with β-blockers for a long time, and individualized therapeutic doses should be determined according to the patient's tolerance.
(4) aldosterone antagonist patients with no obvious renal dysfunction and hyperkalemia after myocardial infarction, after an effective dose of ACEI and β blockers after treatment of LVEF <0.4, may consider the use of aldosterone antagonist treatment, but Close observation of the occurrence of related adverse reactions (especially hyperkalemia).
3. Control cardiovascular risk factors
(1) Control blood pressure should control its blood pressure to <140/90mmHg, and those with chronic kidney disease should control blood pressure to <130/80mmHg. Such patients should be treated with beta blockers and/or ACEI, and if necessary, small doses of thiazide diuretics may be considered.
(2) lipid-lowering therapy should be adhered to the use of statins after discharge, LDL-C control <2.60mmol / L (100mg / dl), and can be considered to achieve a lower target value [LDL-C <2.08mmol / L (80mg/dl)]; For patients with diabetes, LDL-C should be controlled below L (80mg/dl). Do not stop the drug after reaching the standard, and should not blindly reduce the dose. When LDL-C is not up to standard, a combination of cholesterol absorption inhibitors or other lipid-lowering drugs is used. After the LDL-C is up to standard, if the triglyceride is > 2.26 mmol/l, a fibrate or a nicotinic drug is used in combination. When the triglyceride is > 1.70 mmol/l and the lifestyle treatment is still high after 3 months, a fibrate or a niacin should be added.
(3) Blood glucose management If the patient's general health status is good, the diabetes history is short, and the age is light, the glycated hemoglobin can be controlled below 7%; if the patient's general health condition is poor, the diabetes history is longer, and the age is older It is advisable to control glycated hemoglobin from 7% to 8%.
(4) Implantable cardiac defibrillator (ICD) The following two types of patients can significantly benefit from ICD: 1LVEF is less than or equal to 0.4, and is accompanied by spontaneous non-sustained ventricular tachycardia, and/or electrical stimulation can induce Patients with persistent ventricular tachycardia; 2 patients with heart failure after at least 40 days of myocardial infarction (NYHA cardiac function and II-1V), and LVEF less than or equal to 0.30. IUD may also be considered for patients with mild heart failure after symptomatic AMI (NYHA class I) and LVEF less than or equal to 0.35.
(5) Rehabilitation treatment After discharge from hospital, regular physical exercise can help control cardiovascular risk factors such as obesity, hypertension, dyslipidemia and hyperglycemia, and increase cardiovascular reserve function, thus having a beneficial effect on its prognosis. Programmatic rehabilitation based on physical activity may have a better effect than general physical exercise. Meta-analysis showed that patients with coronary heart disease received rehabilitation treatment can reduce the overall mortality rate by 20% to 30%, and reduce the cardiac mortality rate by about 30%.
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