Different strategies for different times of acute ST-segment elevation myocardial infarction

Acute ST-segment elevation myocardial infarction (STEMI) is an important cause of acute death. In the United States, 600,000 people die from coronary heart disease each year, of which 60-65% die suddenly out of hospital. According to the epidemiological data of China’s interventional direct reporting system from 2009 to 2011, there are about 500,000 new STEMI patients in China each year. A, acute myocardial infarction (AMI) prognosis of the time correlation STEMI cause is usually in the coronary artery atherosclerosis unstable plaque lesions based on secondary thrombosis resulting in sustained, complete obstruction of the coronary vessels. A few myocardial cells supplied by the coronary artery are necrotic in 20-30 minutes of occlusion, 60% of myocardium can be necrotic at 180 minutes of flow blockage, and up to 70-80% of myocardium can be necrotic at 360 minutes of flow blockage. Animal studies have demonstrated that when reperfusion of coronary arteries was resumed within 15 minutes of complete ligation in dogs, there was no significant change in overall cardiac work and cardiac output, but after reperfusion for >2 hours, the indicators of overall cardiac systolic function decreased significantly. The time window between acute coronary artery occlusion and myocardial transmural necrosis is approximately 6 hours, and the efficacy of revascularization is time-dependent, i.e., the longer the time to onset, the lower or absent the efficacy. Reperfusion only prevents the occurrence of left ventricular remodeling and heart failure, and reperfusion therapy after 12 hours is basically unable to restore ischemic myocardial function. It is suggested that the earlier the blood flow is restored, the better the recovery of systolic and diastolic function of the myocardium. Therefore, the principle of STEMI treatment is to open the infarct-related vessels early, adequately and continuously to restore coronary blood flow and myocardial reperfusion and save the dying myocardium. Early opening of the infarct-related vessels (IRA) is the key to success and minimizes the risk of death, the later the time, the worse the outcome; adequate opening means achieving TIMI level 3 flow and ensuring myocardial level perfusion; continuous opening means preventing early re-occlusion and distant restenosis after IRA opening. Second, the time relevance of AMI reperfusion therapy In the past 30 years, a series of significant advances in the treatment of acute STEMI, a series of reperfusion therapy methods such as thrombolysis, percutaneous transluminal coronary angioplasty, stent implantation, etc., in which the preferred reperfusion therapy method has gradually over from thrombolysis to today’s emergency percutaneous coronary intervention (PCI). The earlier thrombolytic therapy is started, the better the outcome, and thrombolytic therapy at 1 hour of onset can save 35 more lives per 1000 people treated, while thrombolytic therapy at 7 to 12 hours of onset can save only 16 more lives per 1000 people treated. Since 1983, when Hartzler first reported direct PCI for AMI, direct PCI has been widely studied and most trials have shown its efficacy to be superior to thrombolytic therapy, and a summary of the MITRA registry and the MIR registry showed a significant improvement in the efficacy of direct PCI from 1994 to 1998, which may be related to the accumulation of experience, while the efficacy of thrombolysis remained essentially unchanged. The Zwolle trial, the APRICOT trial, the PAMI-I study, GUSTO-IIb, the Mayo Clinic trial, and a large body of evidence-based medicine have shown that direct PCI reduces major clinical events, including bleeding events, early compared with pharmacologic thrombolysis, with the same results obtained at long-term follow-up, and independent of the type of thrombolytic agent used. Although complete pain relief and ST-segment regression on ECG after thrombolytic therapy can determine coronary revascularization, it is not very reliable and the optimal time for coronary artery opening is easily missed. Compared with thrombolysis, direct PCI has a higher recanalization rate, less residual stenosis, higher left ventricular ejection fraction, more pronounced reduction in morbidity and mortality, less reinfarction, and less bleeding complications, and a more significant reduction in morbidity and mortality in high-risk patients. For example, in the GISSI study, streptokinase thrombolysis in patients with Killip class IV cardiac function still had a 70% mortality rate and intracoronary thrombolysis had a 67% mortality rate, while direct PCI reduced the mortality rate to less than 50%. The mechanisms by which direct PCI improves the prognosis of AMI are multiple. TIM I class 3 flow is known to be the most important determinant of survival and recovery of left ventricular function, with only 35% to 55% achieving TIMI class 3 flow after thrombolytic therapy, compared to more than 90% achieving TIMI class 3 with direct PCI. In addition, the rate of re-occlusion significantly affects the prognosis, with late imaging showing that only 60%-70% of vessels remain patent 3-6 months after successful thrombolysis, compared to 87%-91% after direct PCI. Emergency angiography also provides early clarification of coronary artery anatomy, which facilitates individualized treatment and more effective therapeutic measures, and also helps to reduce the morbidity and mortality rate. Within 2-3 hours of AMI onset, thrombolysis and emergency PCI are similar in efficacy and both can significantly reduce the area of myocardial necrosis or even prevent myocardial necrosis (“aborted myocardial infarction”), after 3-4 hours, thrombolysis begins to be less effective than emergency PCI, and after 6 hours, thrombolysis is significantly less effective than emergency PCI. Thrombolysis is generally not advocated after 12 hours of onset, but recent clinical studies have shown that emergency PCI can still be beneficial for patients with ischemic manifestations after more than 12 hours of onset, and the time can be relaxed to 48 to 72 hours later. PCI can also be beneficial in patients in shock within 36 hours of AM I onset and within 18 hours of shock onset. However, PCI should not be performed in the acute phase without evidence of myocardial ischemia if the onset is more than 12 hours old. The shift in concept from easy PCI to a combined pharmaco-invasive strategy Although thrombolysis is not adequately reperfused and has a high reinfarction rate and risk of cerebral hemorrhage, it is relatively simple and easy to perform compared with emergency PCI. Conversely, although it is well established that emergency PCI is superior to thrombolysis and has a high rate of vessel opening, it can only be performed in hospitals where it is available. The PRAGUE study compared the outcomes of three reperfusion treatment strategies in AMI patients attending hospitals without cardiac catheterization: (i) in situ intravenous thrombolysis, (ii) transfer for direct PCI (median time to PCI treatment 96 minutes), and (iii) transfer for PCI with streptokinase thrombolysis en route (median time to PC I 106 minutes). The results showed that transfer of AMI patients from a community hospital to a regional central hospital for direct PCI was safe, and that the combined 30-day endpoints (death, reinfarction, and stroke incidence) were lower in the direct PCI group than in the thrombolysis group, whereas the thrombolysis plus PCI group did not have better outcomes than thrombolysis alone. The early concept of easy PCI, in which drug therapy (full or half dose of thrombolytic agent, GP IIb/IIIa antagonist (GPI), or GP I + a small amount of thrombolytic agent) was administered before planned immediate PCI in the expectation of better immediate imaging and clinical outcomes, was not achieved in studies such as ASSENT-4 and FINESSE because of small clinical benefit and high risk of bleeding. The results may be related to the earlier intervention of this strategy after thrombolysis (within 2 to 3 hours). Recently, the concept of pharmaco-invasive strategy has been proposed, in which the patient is seen in a hospital without emergency PCI, and the transfer time is <120 minutes, and the patient is objectively not in a position to receive direct PCI as soon as possible, and is treated with thrombolysis (or combined with GPI) as the initial reperfusion therapy, and then transferred to a center with PCI as soon as possible. If the stenosis is <70% or 50-70% with signs of instability (thrombosis, ulceration, spontaneous entrapment), regardless of flow, then PCI is performed, and stenting is performed as soon as technically possible. These patients underwent thrombolysis because they were objectively unavailable for direct PCI (including untimely transport) or because of a relatively long delay, not because they were routinely treated with half or full doses of thrombolytic agents before waiting for direct PCI (easy PCI), and because the time interval between thrombolysis and intervention was large, >2-3 hours, not immediately after thrombolysis (immediate/easy PCI), not equivalent to easy PCI, and not equivalent to the earlier immediate PCI. It is not the same as immediate PCI, nor is it the same as immediate PCI in earlier years. The results of the Transfer AMI, CARESS-in-AMI, and GRACIA 2 studies suggest that this regimen has a good clinical benefit without a significant increase in bleeding events, which has implications for the reperfusion treatment of STEMI patients in remote areas where transfer delays are expected. Fourth, the choice of special lesions and treatment decisions STEMI emergency coronary angiography, in addition to the routine management of conventional lesions, often can encounter some special lesions and clinical situations, are categorized as follows: 1, severe thrombotic load lesions, including their own thick coronary vascular lesions, large lipid pool soft plaque rupture lesions, longer onset lesions (greater than 6-12 hours), in-stent thrombosis lesions , and thrombogenic lesions in grafted bridge vessels are the main causes of the no/slow flow phenomenon. Treatment should first emphasize intensive antithrombotic (aggressive GPI application) therapy and anti-inflammatory blunting plaque therapy (statin application), aggressive thrombus aspiration catheter application during PCI operation, restoration of TIMI grade 3 flow after thrombus aspiration or balloon dilation, stent implantation should not be too aggressive if the residual stenosis is less than 30~50%, and post-stent implantation should not be post-high pressure dilation as much as possible to On the contrary, if the flow recovery after repeated thrombus aspiration or balloon dilation does not reach TIMI grade 2-3 flow, further operation should be stopped immediately and intensive antithrombotic 7-10 days of elective coronary angiography and PCI intervention should be performed if necessary, especially for lesions with long onset time (>6-12 hours) and occluded lesions of graft bridge vessels. In addition, in-stent thrombotic lesions should be stented as much as possible under IVUS or OCT guidance, while saphenous vein bridge vascular lesions require more distal protection device assistance. 2. Acute left main stem lesions Unlike conventional emergency PCI, AMI combined with complete left main stem occlusion and non-complete left main stem occlusion are often clinically manifested as extensive anterior myocardial infarction or NSTEMI with ST-segment depression in extensive leads, often combined with signs and symptoms of cardiogenic shock, especially for patients without collateral circulation. During PCI, strong reperfusion reactions, including ventricular fibrillation, ventricular tachycardia, intense chest pain, or acute left heart failure, often occur when the guidewire or balloon is passed through the lesion and the blood flow is recanalized, and various drugs and devices should be actively applied, such as GPI, thrombus aspiration catheter, and stent placement after about half an hour of appropriate control of antegrade blood flow with a small balloon, so as to reduce reperfusion injury. Active noninvasive ventilator application is also required after PCI as well as vigilance against the occurrence of stress ulcers, active PPI-like agent application, infection control and heart failure. The best clinical outcome can be obtained. 3, combined CTO or multi-vessel lesions Patients with old myocardial infarction, diabetes mellitus or multiple PCI history, some patients with signs and symptoms of cardiogenic shock, often poor basal cardiac function, treatment also requires active IABP assistance, if the patient refuses CABG treatment, or the operator believes that the lesion requires emergency PCI treatment; treatment has three strategies: single-vessel intervention strategy ( Single-vessel PCI (culprit-only PCI), Multi-vessel PCI (onetime PCI, complete PCI), and Staged PCI strategies. Based on the results of the APEX-AMI study, the HORIZONS-AMI study, and the meta-analysis, the current guidelines recommend intervention in principle only in the infarct-related vessels, but in some non-CTO multivessel lesions when (i) the target vessel is difficult to determine; (ii) there are multiple infarct-related vessels and the patient has cardiogenic shock and very severe stenosis in the non-target vessel; and (iii) in some hemodynamically stable (iii) in the case of emergency PCI in partially hemodynamically stable STEMI patients; it is feasible to perform multiple vessel intervention strategies, especially in non-target vessels with unstable plaques and potential for collapse, provided that there is a very strong interventional experience and that the antithrombotic base and coronary lesions are not complex. 4.No obvious stenotic lesions Mostly due to severe and persistent spasm of coronary arteries or autolysis after thrombosis, which are low-risk lesions and can be treated conservatively with drugs. 5.Special patient populations include those with advanced age, low weight, active peptic ulcer, combined advanced malignancy or other bleeding-prone disorders, or diffuse complex coronary lesions refusing CABG surgery, when the balance between antithrombotic efficacy and bleeding risk needs to be fully evaluated in the long-term application of dual antiplatelet agents (DAPT) after stenting. A reasonable approach would be to first risk-stratify the patient, including risk stratification for thrombotic events and assessment of bleeding risk. If the patient is at low risk for thrombotic events and high risk for bleeding, the duration of DAPT can be relatively shortened, and the use of newer antiplatelet agents such as prasugrel or ticagrelor should be used with caution; if the patient is at low risk for thrombotic events and low risk for bleeding, DAPT is recommended for 12 months to reduce ischemic events, followed by lifelong single-agent antiplatelet therapy; if the patient is at high risk for thrombotic events and low risk for bleeding, PCI should be emphasized. Pre-procedural laboratory test results, vigilance to the occurrence of clinical antiplatelet drug resistance, active application of high-dose clopidogrel or new antiplatelet drugs, and appropriate prolongation of DAPT to minimize thrombotic events; those at high risk for both thrombotic events and bleeding should choose their treatment strategy carefully and try to adopt non-interventional interventional strategies, or at least not to adopt interventional treatment with complex, high-risk procedures, including Emphasis on the application of metal bare stents to reduce reliance on antiplatelet drug dosage and time course to minimize bleeding complications. If thrombolysis can be started immediately and interventional treatment needs to be delayed (D2B time < 90 minutes) or if conditions for immediate intervention are not available, thrombolysis should be started immediately, regardless of the success of thrombolysis, and coronary angiography should be performed 3 hours after thrombolysis, and PCI should be performed if necessary. 2.If the hospital has a skilled PCI center with experienced operators and teamwork, D2B time can be completed within 90 minutes; or high-risk patients, such as K illip R class III or cardiogenic shock, or those with contraindications to thrombolysis, especially those with onset time < 3 ~ 6 hours, and those with unclear diagnosis, emergency interventional consultation and treatment should be preferred. 3, for patients with onset time greater than 12 hours and still have ischemic manifestations, high-risk patients who are seen in hospitals without interventional treatment should be transferred to interventional treatment centers with fixed contact under conditions of hemodynamic support. 4, AMI reperfusion therapy regardless of whether to take thrombolysis or PCI, no matter how to perform PCI operation, the primary goal, is the early, sustained, and adequate restoration of antegrade blood flow. 5, anti-platelet therapy after PCI itself has conflicting effectiveness and safety. For those who are at high risk of bleeding but also have complex coronary lesions, more emphasis should be placed on the occurrence of bleeding risk in the assessment of the risk and benefit of invasive consultation.