STEMI strikes about 500,000 Americans annually.
ST-segment elevation myocardial infarction (STEMI) is a subset of myocardial infarction with characteristic symptoms of myocardial ischemia, ST segment elevation or new or presumed new left bundle branch block.
Due to coronary arterial thrombosis most commonly from plaque rupture, erosion, or calcified nodule resulting in acute ischemia symtoms and EKG of ST-segment elevation.
Approximately 29% of patients with MI present with STEMI.
Myocardial cell cell injury occurs after 20-30 minutes of ischemia, and it takes several hours for transmural myocardial process to develop: the goal of reperfusion therapy with fibrinolytic drugs or PCI is to restore blood flow to ischemic, but still viable myocardium and reduce infarct size.
Reduced blood flow is associated with reperfusion injury which can lead to arrhythmias, contractile dysfunction, microvascular impairment, and irreversible myocardial damage.
Reduced myocardial perfusion is associated with heart failure and death.
Acute ST-segment elevation myocardial infarction (STEMI) often caused by intracoronary thrombus with blockage of the ante grade coronary flow leading to myocardial ischemia and cell death
Thrombus burden, reduced coronary blood flow, and reduced myocardial perfusion are predictors of poor clinical outcomes including recurrence of myocardial infarction, thrombosis of stents and death.
It occurs when thrombosis completely includes the coronary artery.
However, complete vessel occlusion does not always result in ST segment elevation in vessels supplying the lateral wall of the left ventricle myocardium, such as the left circumflex artery or a large diagonal branch arising from the left anterior descending artery may result in less characteristic changes, such as ST segment depression.
The primary goal in the management of an STEMI in the ED is to speed the time to coronary revascularization procedures.
Percutaneous coronary intervention is the preferred management for treating such myocardial infarctions.
Typically ST elevations are convex in shape and localized to an anatomical distribution.
Prompt treatment increases the likelihood of patient survival.
Immediate treatment with reperfusion techniques reduces myocardial damage and risk of developing left ventricular dysfunction.
Thrombus aspiration from coronary artery’s before PCI produces a thrombus burden and improves ST-segment resolution and coronary flow in patients with STEMI.
Randomized controlled studies of thrombus aspiration before PCI in patients with STEMI does not reduce the rate of death from any cause, or the composite of death for any cause, rehospitalization for myocardial infarction, or stent thrombosis at one year (Lagerqvist B et al).
Fibrinolysis is particularly effective in patient with anterior STEMI if it ministered within 60 Minutes of onset.
For patients with STEMI, fibrinolytic therapy should simultaneously be accompanied by anti-thrombotic therapy such as heparin and dual antiplatelet therapies.
Urgent angiography should be pursued with a rescue PCI if there is less than 50% resolution ST segment elevation 90 minutes after administration of the fibrinolytic agent.
If ST segment elevation is present emergency coronary angiography should be performed within two hours to confirm the diagnosis of STEMI and treat with percutaneous intervention.
STEMI should be treated with immediate coronary catheterization and coronary angiography followed by PCI with drug eluting stent implantation: rapid reperfusion with primary PCI within 120 minutes reduces mortality by 2% from 9 to 7% compared with fibrinolytic therapy.
Resolution of chest pain in the presence or absence of re-perfusion arrhythmias are useful mrkers of a successful reperfusion process.
Patient should be given for 90 minutes have to fibrinolytic therapy before being taken to the catheterization laboratory because percutaneous intervention after fibfinolysis can worsen the outcomes.
Results in left ventricular dysfunction in up to 50% of patients, an approximately 20-40% develop heart failure some time after STEMI.
Heart failure after STEMI. increases mortality risk by 3-4 times and left ventricular dysfunction is the strongest predictor of adverse outcome after STEMI.
All patients should receive aspirin, generally 325 mg by mouth at the recognition of the diagnosis.
In the emergency department further antiplatelet therapy with Ticagrelor, pasugrel or clopidogrel can be administered.
In a review of 100,000 patients with first myocardial infarction use of aspirin, B-blockers, ACE inhibitors or statins associated with decreased risk of presenting with a STEMI, and the risk decreases with the number of such medications (Bjorck L).
A delay in primary percutaneous coronary intervention of 0-60 minutes corresponded to a long-term mortality rate of 15.4%, a delay of 61-120 minutes to a rate of 23.3% , a delay 121 through 180 minutes to rate of 28.1%, a delay 181 through 360 minutes for other predictors of mortality noted in a historical follow-up of a Danish population based study: system delay independently associated with mortality. (Terklson CJ).
High risk patients tend to present early, whereas patients who present later have already survived the early hours:they are at highest risk-survivor-cohort effect makes analysis difficult for the mortality benefit of earlier reperfusion therapy.
Survivor-cohort effect demonstrated in the pre-fibrinolytic era that 88% of patients with acute myocardial infarction who contacted the health care system within one hour of chest pain died during the pre-hospital phase or in the hospital, while patients who contacted the health care system 1 to 24 hours after symptom onset only 43% died during the pre-hospital phase or in the hospital (Lowell H).
Early presenters have the highest risk scores and the largest ST segment elevations(Aquaro GD, Nallamothu BK).
In a study of 482,327 patients with STEMI mean delay in time to hospital presentation is 114 minutes, and subgroups of women, older age, Hispanic, Blacks, and diabetics have 60 or more minute longer delays (Ting HH et al).
Without reperfusion treatment, patients presenting early have the highest mortality, but with optimal reperfusion treatment, they may attain the same mortality as those presenting late (Terkelsen CJ).
Primary PCI has replaced fibrinolytic therapy as a preferred treatment despite delays inherent in requiring cardiac catheterization and then performing the procedure.
The benefit of PCI is more pronounced it in the early hours after symptom onset and indicates that the reduction in mortality achieved by earlier perfusion is under estimated when evaluated from observational data (Terkelsen CJ).
In patients treated with thrombolytic therapy the risk of hemorrhagic stroke is approximately 1%.
30% of patients 75 years or older.
35-51 percent of patients have non–infarct related artery disease.
There is no difference in infarct size in patients with or without non-infarct related artery disease, they have similar rates of recurrent MI.
If there is a high suspicion for a STEMI in the setting of a nondiagnostic initial ECG, serial ECGs at 5-10 minute intervals or continuous 12 lead ST segment monitoring are recommended.
Patients who survive STEMI are at risk for developing infarct expansion and left ventricular remodeling, and both are associated with heart failure and death.
Risk factors for infarct expansion and left ventricular remodeling include the size of the infarct, extent of apoptosis, an anterior location of the infarction, severe microvascular obstruction and advanced age.
It is recommended by American College of Cardiology and American Heart Association that a decision regarding reperfusion therapy be made within 10 minutes of interpreting the diagnostic electrocardiogram.
Goal of treatment is effective and rapid reperfusion and percutaneous coronary intervention is preferred over fibrinolytic therapy with superior outcomes.
Door to balloon time is recommended to be 90 minutes or less.
The door to balloon time has decreased to 64 minutes while the median door in to door out time decreased from 76 to 62 minutes.
The reduction in door to balloon time for STEMI patient shows a strong association between shorter reperfusion time and lower mortality.
This reduction in door to balloon time for STEMI patients is one of the most impactful accomplishments in cardiovascular care.
Fibrinolytic therapy outcomes nonlinear with best chance of survival when the drug administered within 2-3 hours after onset of symptoms.
Little gain after 12 hours due to loss of myocardial salvage and restoration of blood flow as the thrombus organizes with time in the coronary artery.
Approximately one third of STEMI patients do not receive early reperfusion.
Criteria for emergent reperfusion with acute myocardial infarction include at least 0.1 mV of ST segment elevation in 2 or more contiguous leads and symptoms of 12 hours or less duration.
PCI within 90 minutes associated with a 3% mortality rate while a 7.4% rate associated with those treated after 150 minutes (McNamara).
While median door-to balloon time has dramatically decreased in-house mortality has been unchanged (Flynn A et al).
Clinical approach of patients with occluded infarct related artery late after myocardial infarction is controversial.
Primary percutaneous coronary intervention is the preferred reperfusion strategy for older patients given a greater baseline isschemic and hemorrhagic risk, presentation delay, and grated relative contraindication to pharmacologic based reperfusion.
Despite optimal reperfusion treatment, morbidity and mortality remain significant with about 5-6% of patients having a subsequent cardiovascular event by 30 days.
Late percutaneous coronary intervention of an occluded infarct related artery may be improvement in outcomes from reduction in left ventricular remodeling, preservation of left ventricular function, increased electrical stability and the addition of collateral blood vessels for protection of future cardiovascular events.
Late percutaneous coronary intervention may be harmful by causing distal embolization of atheromatous debris and cause myocardial damage, and loss of collateral flow to other coronary areas.
OASIS-5 (Organization to Assess Strategies for Ischemic Syndromes) trial compared fondaparinux with enoxaparin.
OASIS-6 (Organization to Assess Strategies for Ischemic Syndromes) trial utilized fondaparinux indicating that it is superior to the usual care for reducing 30 day risk of death or recurrent myocardial infarction.
OASIS-6 (Organization to Assess Strategies for Ischemic Syndromes) trial compared fondaparinux, no anticoagulation or unfractionated heparin.
OASIS-5 and 6 (Organization to Assess Strategies for Ischemic Syndromes) trials revealed reduction in bleeding with the use of fondaparinux.
ASSENT-4PCI, Assessment of the Safety and Efficacy of a New Treatment Strategy with Percutaneous Coronary Intervention trial found fibrinolytic therapy alone to be harmful possibly due to deleterious effects of early activation of platelets by the fibrinolytic agents without effective antiplatelet treatment or plaque hemorrhage at the time of PCI.
In a study of 2166 stable patients with total occlusion of the infarct related artery 3-28 days after myocardial infarction randomized to medical care vs percutaneous coronary intervention the occurrence of death, reinfarction, and congestive heart failure were the same.
In a Quebec study reperfusion of patients with STEMI delivered outside of guideline recommended treatment delays was associated with significantly increased 30 day mortality, a non significant increase in 1 year mortality , and significantly increased risk of the composite outcome of mortality or readmission for acute myocardial infarction or heat failure.
Facilitated Intervention with Enhanced Reperfusion Speed to Stop Events (FINESSE) study of 2452 patients with early ST-segment elevation myocardial infarction randomly assigned to combination facilitated PCI, abciximab-facilitated PCI, or primary PCI: all patients received unfractionated heparin or enoxaparin before PCI and a 12 hour infusion of abciximab after PCI-neither facilitation of PCI with reteplase plus abciximab nor facilitation with abciximab alone significantly improved the clinical outcomes, as compared with abciximab given at the time of PCI.
PRAMI study demonstrated that in patients with STEMI and multivessel coronary artery disease undergoing infarction artery PCI, preventive PCI in non infarct coronary arteries with major stenoses reduces the risk of adverse cardiovascular events, as compared with PCI limited to the infarct artery alone (Wald DS et al).
Patients with STEMI often have multivessel coronary artery disease separate from the culprit lesion that caused the acute event.
COMPLETE Study show that among patients with STEMI and multivessel coronary disease, a strategy of routine non-culprit lesion PCI with completing revascularization was associated with improved risk of death from cardiovascular or new myocardial infarction vs. treating the culprit lesion alone.
In a three-year follow-up study death from cardiovascular causes or new MI occurred in 7.8% of patients with complete revascularization versus 10.5% of patients in the group which had only the culprit lesion treated.
The exact optimal timing of revaculization of non-culprit coronary artery lesions is uncertain and is determined based on patient characteristics such as coronary anatomy and kidney function.
When cardiogenic shock is present during the initial event, only the occluded artery responsible for the STEMI should be treated.
Up to half of patients with acute ST-segment elevation myocardial infarction have multivessel coronary artery disease.
In patients with STEMI treated with successful reperfusion with primary or rescue PCI, EPO bolus treatment within 4 hours of PCI does not reduce infarct size and is associated with higher rates of adverse cardiovascular events (Najjar SS et al).
Erythropoietin may increase infarct size in patients with STEMI in patients older than 70 years (Najjar SS et al).
With STEMI early studies suggested early PCI of non-culprit lesions was associated with a lower risk of major adverse cardiac events than culprit lesion only PCI, driven by approximately 50% lower risk of urgent revascularization.
Studies show the edition of fractional flow reserve studies does not improve results in evaluating non-culprit lesions.
Up to 10% of patients who undergo cardiac cardiac catheterization for presumed STEMI, etiologies of ST segment elevation of the coronary artery occlusion, such as pericarditis are ultimately diagnosed.
In approximately 1% of patients cardiac surgery is required because of the mechanical complication of STEMI such as mitral regurgitation, ventricular septal defect or myocardial free wall rupture.