In recent years, important progress has been made in the diagnosis and treatment of acute ST-segment elevation myocardial infarction (STEMI), with the publication of the third edition of the Global Definition of Myocardial Infarction, the revision of STEMI treatment guidelines by the European Society of Cardiology, the American College of Cardiology Foundation and the American Heart Association, and the publication of the European Guidelines for Myocardial Revascularization. At the same time, several relevant randomized controlled clinical trials have been completed in China and abroad. For this reason, the Atherosclerosis and Coronary Artery Disease Group of the Chinese Society of Cardiovascular Diseases organized experts to update the 2010 Chinese guidelines for the diagnosis and treatment of acute ST-segment elevation myocardial infarction.
The recommendations for treatment in this guideline are expressed in an internationally accepted manner: Class I recommendation means that a treatment measure or operation is proven and/or unanimously recognized as beneficial and effective and should be used; Class II recommendation means that the effectiveness of a treatment measure or operation is still debated, where Class IIa recommendation means that the relevant evidence and/or opinion tends to be effective and the application of the treatment measure or operation is appropriate, and Class IIb recommendation means that the relevant evidence and/or opinion is not yet sufficient to prove effectiveness and further research is needed; Class III recommendation means that a treatment measure or operation has been proven and/or unanimously recognized as useless and/or ineffective and may be harmful in some cases and is not recommended. Level A of evidence refers to information derived from multiple randomized clinical trials or meta-analyses; Level B refers to information derived from a single randomized clinical trial or multiple large-scale nonrandomized controlled studies; Level C refers to information derived from expert consensus and/or small clinical trials, retrospective studies, or registries.
I. Myocardial infarction staging
We recommend using the third edition of the “Global Definition of Myocardial Infarction”, which classifies myocardial infarction into 5 types.
Type 1: Spontaneous myocardial infarction
Due to rupture, ulceration, cracking, erosion or entrapment of atheromatous plaque, one or more coronary arteries are thrombosed, resulting in reduced myocardial blood flow or distal platelet embolism with myocardial necrosis. Most patients have severe coronary artery lesions, while a few patients have only mild or even normal coronary artery stenosis.
Type 2: Myocardial infarction secondary to imbalance in myocardial oxygen supply and demand
Conditions other than coronary artery disease cause an imbalance between myocardial oxygen demand and supply, resulting in myocardial injury and necrosis, such as abnormal coronary endothelial function, coronary artery spasm or embolism, tachycardia/bradyarrhythmia, anemia, respiratory failure, hypotension, and hypertension with or without left ventricular hypertrophy.
Type 3: Sudden cardiac death
Cardiac death with symptoms of myocardial ischemia and new ischemic electrocardiographic changes or left bundle branch block without myocardial injury marker test results.
Type 4a: percutaneous coronary intervention (PCI)-related myocardial infarction
Patients with normal baseline cardiac troponin (cTn) have a cTn elevation of more than 5 times the upper limit of normal after PCI; or patients with increased baseline cTn have a cTn elevation of ≥20% after PCI followed by a stable decline. Concurrent occurrence of (1) symptoms of myocardial ischemia; (2) electrocardiographic ischemic changes or new left bundle branch block; (3) imaging demonstrating obstruction or persistent slow or no recurrent flow or embolism in the main branches or branches of the coronary arteries; and (4) imaging demonstrating new loss of surviving myocardium or segmental ventricular wall motion abnormalities.
Type 4b: Myocardial infarction due to stent thrombosis
Coronary angiography or autopsy reveals thrombotic obstruction at the site of stent implantation, and the patient has symptoms of myocardial ischemia and/or at least 1 marker of myocardial injury above the upper limit of normal.
Type 5: Surgical coronary artery bypass grafting (CABG)-related myocardial infarction
Patients with normal baseline cTn and a post-CABG cTn elevation greater than 10 times the upper limit of normal, along with (1) new pathologic Q waves or left bundle branch block; (2) angiography suggestive of a new bridge vessel or own coronary artery obstruction; and (3) imaging evidence of new surviving myocardial loss or segmental ventricular wall motion abnormalities.
This guideline focuses on the diagnosis and treatment of type 1 myocardial infarction (i.e., ischemia-related spontaneous acute STEMI).
II. Diagnosis and risk stratification of STEMI
(A) Clinical assessment
1.History taking
2.Physical examination
(B) laboratory tests
1.Electrocardiogram
In patients with chest pain suspected of STEMI, a 12-lead ECG should be recorded within 10 min after the first medical contact (FMC) [additional leads V3R to V5R and V7 to V9 are required for inferior and/or posterior wall myocardial infarction]. A typical early STEMI ECG shows ST-segment arch-back elevation (unidirectional curve) with or without pathologic Q-wave and R-wave depression (ST-segment changes can be unremarkable in orthoposterior myocardial infarction). The super-acute ECG may show abnormally high and asymmetric T waves in both branches. If the diagnosis is not clear on the first ECG, it needs to be repeated after 10 to 30 min. Comparison with previous ECG is helpful for diagnosis. When myocardial infarction occurs in patients with left bundle branch block, ECG diagnosis is difficult and needs to be carefully determined in conjunction with the clinical situation. Early initiation of ECG monitoring is recommended to detect malignant arrhythmias.
2.Serum myocardial injury markers
cTn is the most specific and sensitive myocardial injury marker of choice for the diagnosis of myocardial necrosis. cTn is usually elevated 2-4 h after the onset of STEMI symptoms, peaks at 10-24 h, and can remain elevated for 7-14 d. The clinical specificity of creatine kinase isoenzyme (CK-MB) for the determination of myocardial necrosis is high, and its measured value exceeds the upper limit of normal and has dynamic changes during STEMI. CK-MB measurements are also useful in the diagnosis of recurrent myocardial infarction. Myoglobin measurement is useful for early diagnosis of STEMI, but its specificity is poor.
3.Imaging
Imaging tests such as echocardiography are useful for differential diagnosis and risk stratification of patients with acute chest pain (I, C).
It must be noted that patients whose symptoms and ECG allow a clear diagnosis of STEMI do not need to wait for myocardial injury markers and/or imaging findings, but should be given reperfusion and other related treatments as soon as possible.
STEMI should be differentiated from chest pain caused by aortic coarctation, acute pericarditis, acute pulmonary embolism, pneumothorax, and gastrointestinal disease (e.g., reflux esophagitis). Severe tearing pain radiating to the back with dyspnea or syncope, but without typical STEMI ECG changes, should alert for aortic coarctation. Acute pericarditis presents with fever, pleural irritation pain radiating to the shoulder, relieved by sitting in a forward leaning position, some patients can hear pericardial friction sounds, and the ECG shows PR segment depression and ST segment elevation in an arch-back-down pattern without mirror image changes. Pulmonary embolism often manifests as dyspnea, decreased blood pressure, and hypoxemia. Pneumothorax may present with acute dyspnea, chest pain, and decreased breath sounds on the affected side. Peptic ulcer may have pain in the chest or upper abdomen, sometimes radiating to the back, and may be accompanied by syncope, vomiting blood or black stool. Acute cholecystitis may have STEMI-like symptoms but with right upper abdominal tenderness. None of these diseases present with the electrocardiographic features and evolution of STEMI.
(iii) Risk stratification
Risk stratification is a continuous process that requires continuous updating of the initial assessment according to the clinical situation. Advanced age, female gender, Killip class II-IV, history of previous myocardial infarction, atrial fibrillation (AF), anterior myocardial infarction, pulmonary woven mat (6) 100 mmHg, heart rate >100 beats/min, diabetes mellitus, and significantly elevated cTn are independent risk factors for increased risk of death in patients with STEMI. Patients with inferior wall STEMI who failed thrombolytic therapy, with right ventricular infarction and hemodynamic abnormalities had increased morbidity and mortality. Patients with STEMI with combined mechanical complications are at increased risk of death. Coronary angiography may provide important information for STEMI risk stratification.
Third, the emergency procedure of STEMI
Early, rapid and complete opening of the infarct-related artery is the key to improving the prognosis of STEMI patients.
1. Shortening the time from onset to FMC should be done through health education and media campaigns to make the public aware of the early symptoms of acute myocardial infarction. Educate patients to call “120” emergency center as soon as possible after the onset of suspected symptoms of myocardial infarction (chest pain) and seek medical attention in a timely manner to avoid delaying treatment due to self-medication or multiple assessments of symptoms over time. Shortening the time from onset to FMC and arriving at the hospital under medical protection can significantly improve the prognosis of STEMI (I, A).
2. Shortening the time from FMC to opening the infarct-related artery Establishing a regional collaborative treatment network and standardized chest pain center is an effective means to shorten the time from FMC to opening the infarct-related artery (I, B).
When possible, the first ECG recording should be completed within 10 min after FMC, and the ECG should be notified by phone in advance or transmitted to the relevant hospital via remote wireless system (I, B).
After diagnosis, patients with STEMI within 12 h of onset should be triaged quickly and sent to hospitals where direct PCI is feasible (especially if direct PCI can be performed within 90 min after FMC) (I, A), and patients should be sent directly to the cardiac catheterization laboratory for direct PCI, bypassing the emergency room and coronary care unit or general cardiac ward whenever possible.
For patients who have already arrived at a hospital without direct PCI, if transport PCI can be completed within 120 min after FMC, the patient should be transported to a hospital where direct PCI is feasible (I, B).
A qualified physician may also be asked to perform direct PCI at a hospital that is equipped for PCI but cannot perform PCI independently (IIb, B).
Knowledge of myocardial reperfusion therapy should be disseminated among the public to reduce hesitation and delay in signing the informed consent for the procedure.
IV. General management after hospital admission
All STEMI patients should be given immediate oxygen and ECG, blood pressure and oxygen saturation monitoring for timely detection and management of arrhythmias, hemodynamic abnormalities and hypoxemia. Patients with combined left heart failure (pulmonary edema) and/or mechanical complications often have severe hypoxemia and require mask-applied oxygen or tracheal intubation with mechanical ventilation (I, C). patients with STEMI with severe chest pain should be given rapid and effective analgesia, such as intravenous morphine 3 mg, repeated at 5 min intervals if necessary, and the total amount should not exceed 15 mg. but morphine can cause hypotension and respiratory depression, and However, morphine can cause hypotension and respiratory depression, and reduce the antiplatelet effect of P2Y12 receptor antagonists. Take care to keep the patient’s bowels open and use laxatives if necessary to avoid cardiac rupture, arrhythmia or heart failure due to forceful defecation.