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    ECG is the most important diagnostic test to detect STEMI as clinical features, physical examination, and CAD risk factor profile only have modest sensitivity and specificity in diagnosing STEMI. Current guidelines define ST elevation at the J point in at least two continuous leads of 2 mm or greater in men or 1.5 mm or greater in women in leads V2 to V3 and/or 1 mm or greater in other contiguous chest leads or the limb leads in the absence of left ventricular hypertrophy or left bundle branch block (LBBB). Other ECG abnormalities such as paced rhythm, drug or electrolyte (hyperkalemia) effects, or Brugada syndrome also reduce the sensitivity and specificity of STEMI ECG interpretation.

    Some patients present with ECG changes though not with typical ST elevation, indicating equivalent clinical risk to STEMI, and should be treated as having a true STEMI. These STEMI-equivalent ECG patterns include (1) isolated ST depression in two or more precordial leads (V1 to V4), indicating true posterior wall MI; (2) ST depression in multiple leads with ST elevation in aVR, indicating left main or triple-vessel CAD; (3) Wellen sign with symmetrical deep T-wave inversions in anterior precordial leads; (4) hyperacute T wave; and (5) de Winter sign showing ST depression and peaked T waves in the precordial leads. Occasionally patients with left circumflex artery occlusion can present with a normal or near-normal ECG.

    Serum Biomarkers

    Serum biomarkers of myocardial necrosis such as cardiac-specific troponins T and I are complementary to diagnosing STEMI. In clinical practice, STEMI is often diagnosed with ECG alone while the laboratory result of biomarkers is not yet available. The troponin level typically rises 4 to 6 hours after the onset of symptoms and peaks within 12 to 24 hours if reperfusion therapy succeeds in reperfusing the occluded coronary artery and patients present early in the course of STEMI; its level tends to peak after 24 hours if reperfusion therapy fails or in patients who receive no reperfusion therapy. After STEMI, successfully reperfused or not, the troponin level remains elevated for 7 to 10 days. For patients suspected of having recurrent ACS within a week after the index STEMI, given the troponin level remaining elevated, creatine kinase (CK) and the MB isoform of CK (CK-MB) levels can be used as biomarkers to establish additional myocardial necrosis from a recurrent event since CK and CK-MB levels usually return to normal 48 to 72 hours after the initial index event.


    STEMI is commonly accompanied with wall motion abnormalities on echocardiogram, but echocardiogram is not essential to diagnose STEMI. Echocardiogram is extremely useful in managing patients with STEMI, especially when they present with acute complications from STEMI such as acute heart failure, acute mitral regurgitation, free wall or ventricular septal rupture, pericardial effusion, cardiogenic shock, or left ventricular thrombus.

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    Management of STEMI

    The principal concept of managing STEMI is “time is muscle”; hence it is important for patients to recognize symptoms for early presentation and for the medical community to administer suitable reperfusion therapy in a timely manner.

    Prehospital Phase

    Current guidelines recommend that patients with STEMI receive reperfusion therapy as soon as possible but within 12 hours of symptom onset to achieve optimal myocardial salvage to reduce mortality and morbidity. In daily clinical practice, a substantial number of patients still present late and miss the golden window of reperfusion. Common reasons for late presentation include (1) patients’ lack of knowledge to recognize symptoms, (2) patients’ inertia to seek medical care, (3) patients’ lack of access to medical care, and (4) atypical symptoms that mislead patients or medical care providers to consider noncardiac problems.

    Patients with suspicious myocardial ischemic symptoms are encouraged to call emergency medical services (EMS) immediately for help; this has the following benefits: (1) patients can receive early treatment, (2) patients can receive immediate resuscitation should STEMI complications such as cardiac arrest occur en route to the hospital, and (3) an early prehospital ECG and communication with a hospital capable of percutaneous intervention (PCI) by EMS significantly reduce reperfusion time and improve outcome. However currently only a fraction of such patients are transported by EMS. Improving this requires public education to enhance recognition of symptoms, implementation of an efficient EMS system, and infrastructures with standardized treatment algorithms for STEMI.

    Initial management by EMS usually includes pain relief by morphine, administration of nitroglycerin,1 oxygen, and non-enteric- coated aspirin (162 to 325 mg)1 unless contraindicated. The role of routine oxygen supplementation to patients with STEMI has recently been questioned. A recent randomized clinical trial (Air Versus Oxygen in Myocardial Infarction [AVOID] trial) suggests that supplemental oxygen therapy (8 L/min via face mask) in patients with STEMI without hypoxia (oxygen saturation > 94%) may increase early myocardial injury and is associated with larger myocardial infarction size at 6 months.

    Once STEMI is identified by a prehospital ECG performed by EMS, an assessment of candidacy for and availability of reperfusion therapy is an important next step of management to ensure immediate reperfusion and administration of its adjunctive therapy to maintain culprit coronary artery patency, limit infarct size and adverse left ventricular (LV) remodeling, and improve outcome. To achieve the best outcome from reperfusion therapy, patients with STEMI should receive suitable reperfusion therapy within 12 hours of symptom onset—the earlier the better. Current reperfusion therapy options for STEMI include primary percutaneous coronary intervention (PPCI) or fibrinolysis. PPCI is the treatment of choice for STEMI because it confers a beneficial reduction in mortality and recurrent ischemia when compared with fibrinolysis. Hence current guidelines recommend EMS to transport patients to a PCI-capable hospital and PPCI as the preferred method of reperfusion therapy with a system goal of less than 90 minutes from first medical contact (FMC) to device time.

    Not every hospital is PCI capable. Based on the Nationwide Inpatient Sample database, only 33.7% of hospitals in the United States provided STEMI-related PCI in 2011. If a patient is sent to or arrives at a non-PCI-capable hospital, guidelines recommend transferring that patient to a PCI-capable hospital for PPCI with a system goal of less than 120 minutes from FMC to device time. If there is an anticipated delay of FMC to device time of 120 minutes or more, a fibrinolytic agent can be given within 30 minutes of hospital arrival if the patient has no contraindications for fibrinolysis (Table 1).

    Prehospital fibrinolysis, administered by EMS with physician supervision, has been shown to be feasible and safe, with a shortened reperfusion time and reduced mortality. Such strategy, however, is not used in the United States.

    Table 1

    Contraindications for Intravenous Fibrinolysis

    Modified from 2013 ACCF/AHA STEMI  guideline.

    Abbreviations: DBP = diastolic blood pressure; SBP = systolic blood  pressure.

    In clinical practice sometimes it is not possible to achieve strict time goals because of uncertainty of the initial diagnosis, necessity to treat concomitant comorbidities or complications, patient preference or consent issues, and local factors delaying transport. Therefore emphasis should be to deliver reperfusion therapy to eligible patients as rapidly as possible.

    In-Hospital Reperfusion Strategy

    Primary Percutaneous Coronary Intervention

    PPCI performed in a high-volume hospital by experienced operators achieves a higher patency rate of infarct-related artery (IRA) and lower rate of recurrent ischemia, reinfarction, hemorrhagic stroke, and death when compared to fibrinolysis. In particular, PPCI has the greatest benefit in high-risk patients such as those with cardiogenic shock. Hence PPCI is the preferred method of reperfusion whenever possible with the system goal of 90 to 120 minutes.

    The reperfusion technique used in PPCI has evolved greatly in the past few decades, from balloon angioplasty, bare-metal stent (BMS), and drug-eluting stent (DES) to bioresorbable vascular scaffolds (BVSs). Compared to balloon angioplasty, BMS used in PPCI confers reduced risk for subsequent target-vessel revascularization but does not reduce the mortality rate. Compared to BMS, DES used in PPCI decreases the restenosis rate and need for reintervention without reduction in reinfarction and death. BVS is a new stent technology, but its role in PPCI has not been well established because data concerning using BVSs in STEMI are insufficient and because of its association with a higher rate of stent thrombosis, especially in the first 30 days after implantation, and late lumen loss when compared to DES.


    The currently available intravenous fibrinolytic agents are tenecteplase (TNKase), reteplase (Retavase), and alteplase (Activase) (Table 2). A fibrinolytic agent should be administered to eligible patients without contraindication within 30 minutes of arrival at the emergency department. It is important to evaluate the risk/benefit ratio for each individual patient before administering fibrinolytic therapy as it carries a small but fatal risk of hemorrhage stroke (about 1%). The ideal patient to receive a fibrinolytic agent would be with symptom onset within 1 to 2 hours, low bleeding risk, and age younger than 65 years.

    Table 2

    Comparison of Fibrinolytic Agents

    Modified from 2013 ACCF/AHA STEMI  guideline.

    Although fibrinolysis achieves a reasonable patency rate of IRA (Table 2), a substantial portion of patients fail to achieve successful reperfusion as defined by the following clinical criteria: (1) resolution of chest pain, (2) reduction of greater than 50% of the initial ST- segment elevation pattern on follow-up ECG 60 to 90 minutes after initiation of fibrinolysis, and (3) occurrence of reperfusion arrhythmia (accelerated idioventricular rhythm [AIVR]). If fibrinolysis does not achieve resolution of ST elevation by at least 50% in the worst lead at 60 to 90 minutes, rescue PCI (transfer to PCI-capable hospital if necessary) should be strongly considered.

    Percutaneous Intervention After Fibrinolysis

    Approximately 40% of STEMI patients who receive fibrinolysis fail to achieve successful reperfusion and require emergent rescue PCI. Other indications for rescue PCI include severe heart failure, cardiogenic shock, persistent chest pain or electrical instability. Hence these patients should be transferred to a PCI-capable hospital immediately if fibrinolysis has been administered in a non-PCI capable hospital.

    Otherwise, stable patients after successful fibrinolysis can undergo coronary angiography with an intent to revascularize as soon as logistically feasible, ideally between 3 and 24 hours after fibrinolysis (so-called pharmaco-invasive strategy). In patients older than 75 years, if a pharmaco-invasive strategy is chosen as the reperfusion strategy, a fibrinolytic agent at half dose (such as the half dose of tenecteplase used in the STREAM trial) should be used to reduce bleeding risks since patients will receive concomitant antiplatelets and anticoagulants for PCI. Very early PCI after successful fibrinolysis (< 2 to 3 hours) is not recommended.

    Facilitated Percutaneous Intervention

    This strategy refers to a full dose or partial dose of fibrinolysis plus a glycoprotein IIb/IIIa antagonist or antithrombotic followed by immediate PCI if there is no evidence of reperfusion failure. Current guidelines do not recommend this strategy owing to potential harms such as an increase in ischemic events, bleeding, and mortality.

    Patients with STEMI and Multivessel Coronary Artery Disease

    About 40% to 65% of patients with STEMI undergoing PPCI for culprit IRA have multivessel CAD. Significant multivessel CAD, if left unrevascularized, is associated with a worse clinical prognosis. For patients with STEMI with cardiogenic shock or severe heart failure, it is reasonable to perform multivessel PPCI (or emergent coronary artery bypass grafting [CABG] in selected patients) to achieve as complete a revascularization as possible. For stable patients, the 2013 American Heart Association (AHA) STEMI guidelines recommend staged PCI to the nonculprit coronary artery before hospital discharge in patients with spontaneous symptoms of myocardial ischemia or with intermediate- or high-risk features on noninvasive testing.

    Newer randomized clinical trials have demonstrated the feasibility of performing multivessel PPCI in acute settings. This approach has the following advantages: complete revascularization leading to improved left ventricular function and prognosis, decreased vascular complications from repeated procedures, and reduced length of stay and medical costs. However, the procedure will be longer with potentially higher radiation exposure, higher risk for contrast nephropathy owing to a higher contrast load, risk of compromising viable myocardium supplied by the nonculprit coronary artery owing to procedure complications, and unnecessary stenting to the nonculprit artery without objective evidence of ischemia. The 2015 American College of Cariology (ACC)/AHA/Society for Cardiovascular Angiography and Interventions (SCAI) focused update on PPCI for patients with STEMI supports multivessel PCI, either at the time of PCI to the STEMI culprit vessel or as a staged procedure in selected hemodynamically stable patients. Interventional cardiologists should integrate clinical data, characteristics of lesions and procedures, clinical risks, and complications from procedures to determine the best timing and strategy to achieve the optimal benefit. The guideline does not endorse routine multivessel PPCI in patients with STEMI and multivessel CAD.

    Patients with STEMI Who Present Later Than 12 Hours After Symptom Onset

    Patients with STEMI who present between 12 hours and 2 days after symptom onset without unstable symptoms or signs are no longer eligible for fibrinolysis but are still eligible for PPCI to salvage myocardium, which confers the benefit of reduced infarct size when compared to conventional therapy guided by a predischarge symptom-limited exercise test or unplanned PCI guided by clinical instability as demonstrated in the Beyond 12 Hours Reperfusion Alternative Evaluation (BRAVE-2) trial. For patients with STEMI who present more than 48 hours after symptom onset without clinical instability, a strategy of symptom-limited stress test first or coronary angiography first to delineate high-risk features of coronary anatomy is reasonable with an intent to revascularize high-risk coronary anatomy. If patients are clinically stable without high-risk coronary anatomy noted by angiography and present between 3 and 28 days after symptom onset, PCI to open the occluded IRA does not confer a clinical benefit in reducing mortality, congestive heart failure, or nonfatal myocardial infarction when compared to medical therapy as demonstrated in the Occluded Artery Trial (OAT). Irrespective of time of presentation, patients with STEMI who present with hemodynamic or electrical instability should undergo coronary angiography with an intent to revascularize the jeopardized myocardium as soon as possible.

    Figure 1 summarizes current pathways of managing patients with STEMI based on their time of presentation, their clinical status, and availability of reperfusion therapy.

    FIGURE 1    Pathways of managing ST-elevation myocardial  infarction (STEMI).

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    Adjunct therapy

    Antiplatelet Therapy Aspirin

    Unless contraindicated, 162 to 325 mg of aspirin1 should be administered as a loading dose immediately and continued indefinitely at a dose of at least 81 to 325 mg daily in all patients with STEMI, with 81 mg being the preferred maintenance dose. Patients with a history of aspirin allergy can be given clopidogrel (Plavix) instead.

    P2Y12  Receptor Inhibitors

    Clopidogrel is a second-generation thienopyridine and irreversibly blocks the platelet P2Y12 receptor to inhibit platelet activation and aggregation. Current guidelines support the use of clopidogrel during fibrinolysis or PPCI. For patients undergoing fibrinolytic therapy, a loading dose of 300 mg followed by a maintenance dose of 75 mg daily has been recommended for patients younger than 75 years. For patients older than 75 years, only the maintenance dose of 75 mg should be given. Prasugrel (Effient) and ticagrelor (Brilinta) have not been studied and hence are not recommended in the setting of fibrinolysis as reperfusion therapy. For patients undergoing PPCI, depending on whether they are receiving a fibrinolytic agent and the timing of subsequent PCI, a different dosing regimen of clopidogrel may be recommended (Figure 2).

    FIGURE 2    Oral regimen of different P2Y12 receptor inhibitors  based on reperfusion strategies. Modified from 2013 ACCF/AHA STEMI guideline.

    Prasugrel is a third-generation thienopyridine P2Y12 receptor inhibitor. It is metabolized to its active form more quickly than clopidogrel and hence confers a more potent effect. In a subset of patients with STEMI in the TRITON-TIMI 38 trial, prasugrel was more efficacious in preventing composite endpoints of cardiovascular (CV) death, myocardial infarction, and stroke when compared to clopidogrel, but it had a higher major bleeding rate. Prasugrel is also contraindicated in patients older than 75 years, with body weight less than 60 kg, or with prior history of stroke or transient ischemic attack.

    Ticagrelor is a direct reversible P2Y12 receptor inhibitor with a more potent, faster-acting property when compared to clopidogrel or prasugrel. In the pivotal Platelet Inhibition and Patient Outcomes (PLATO) trial ticagrelor lowered composite CV death, myocardial infarction, and stroke when compared to clopidogrel but with an increase in non-procedure-related bleeding.

    Clopidogrel, prasugrel, and ticagrelor require several hours to achieve maximal platelet inhibition. Additionally, in the setting of STEMI, the bioavailability of these oral agents may be hampered by clinical factors such as nausea, vomiting, and cardiogenic shock, leading to poor GI absorption and leaving patients not adequately protected by platelet inhibition during immediate PPCI. Cangrelor (Kengreal) is a fast-acting, reversible adenosine diphosphate (ADP) receptor inhibitor that is administered intravenously to achieve P2Y12 inhibition within 2 minutes. Its plasma half-life is 3 to 6 minutes, and platelet function returns to normal within 60 minutes after discontinuation of infusion. The US Food and Drug Administration (FDA) has approved cangrelor to be used as an adjunct therapy during PCI to reduce repeat coronary revascularization and stent thrombosis in patients who have not been pretreated with an oral P2Y12 inhibitor and are not receiving a glycoprotein IIb/IIIa receptor antagonist. How to transition from cangrelor to an oral P2Y12 inhibitor after PCI depends on which oral P2Y12 inhibitor a patient is being transitioned to. Based on the CHAMPION PHOENIX trial, to transition to clopidogrel, 600 mg clopidogrel loading is necessary immediately after discontinuation of cangrelor infusion. Based on pharmacodynamic data, prasugrel 60 mg should be administered immediately after stopping cangrelor infusion, whereas ticagrelor 180 mg can be given anytime during cangrelor infusion or immediately after infusion ends.

    The 2016 ACC/AHA focused update on duration of dual antiplatelet therapy (DAPT) in patients with CAD recommends at least 12 months of DAPT in patients with ACS (STEMI or NSTEMI) after BMS or DES implantation. Continuation of DAPT beyond 12 months is reasonable in patients who tolerate DAPT, do not have bleeding complications, and are not at high bleeding risk (prior bleeding on DAPT, coagulopathy, or oral anticoagulant use).

    Glycoprotein IIb/IIIa Receptor Antagonists

    Glycoprotein (GP) IIb/IIIa receptor antagonists include abciximab (ReoPro, a chimeric monoclonal antibody), eptifibatide (Integrilin, a synthetic peptidic inhibitor), and tirofiban (Aggrastat, a nonpeptidic inhibitor). The benefit of intravenous GP IIb/IIIa receptor antagonists in patients with STEMI was largely established before the era of oral DAPT. With current use of DAPT, contemporary trials fail to show benefit with upstream administration of GP IIb/IIIa receptor antagonists before PPCI with either unfractionated heparin1 or bivalirudin (Angiomax). Current US and European guidelines recommend using GP IIb/IIIa receptor antagonists for bailout situations after a large thrombus burden, no reflow or slow flow, or inadequate P2Y12  receptor antagonist loading during PCI.


    Unfractionated heparin (UFH),1 low-molecular-weight heparin with enoxaparin (Lovenox) as prototype, fondaparinux (Arixtra),1 and bivalirudin are widely used in reperfusion therapy to limit thrombus propagation, reduce reocclusion and reinfarction, and improve vessel patency unless contraindicated. The choice of individual agent and its dose and duration of use depends on the choice of reperfusion therapy, concomitant use of other antiplatelet agents, and renal function (Table 3).

    Table 3

    Dosage of Anticoagulants in Reperfusion Therapy for STEMI

    Modified from 2013 ACCF/AHA STEMI  guideline.

    Abbreviations: ACT = activated clotting time; aPTT = activated partial thromboplastin time; CrCl = creatinine clearance; GPI = ; PCI = percutaneous intervention; STEMI = ST-elevation myocardial infarction.

    *  Not FDA approved for this indication.

    Given that PPCI is the preferred method of reperfusion and occurs early after presentation, and given physicians’ familiarity with UFH, intravenous UFH is the preferred anticoagulant agent for PPCI. In patients with high bleeding risk, bivalirudin with DAPT is a reasonable alternative to UFH (whether or not the patient was pretreated with UFH) when avoidance of GP IIb/IIIa receptor antagonists is desired during PPCI.

    For patients with STEMI who receive fibrinolysis as initial reperfusion therapy, UFH, enoxaparin, and fondaparinux all receive a class I recommendation based on ACC/AHA guidelines. UFH is preferred since a pharmaco-invasive strategy is common or for patients who may need rescue PCI. Bivalirudin may be used after fibrinolysis in patients who develop heparin-induced thrombocytopenia and require continued anticoagulation.

    Guideline-Directed Medical Therapy


    Beta-blocker therapy decreases myocardial oxygen demand and improves myocardial remodeling with the benefits of reducing angina, infarct size, and mortality. Current guidelines recommend initiating oral beta-blockers in the first 24 hours in patients with STEMI who are without contraindications such as congestive heart failure, evidence of a low output state, increased risk for cardiogenic shock, heart block, or reactive airway disease. If not given in the first 24 hours owing to contraindications, physicians need to reevaluate patients to determine their subsequent eligibility. Oral beta-blockers should be continued for 3 years after MI as recommended by the ACC/AHA secondary prevention guideline, and longer if there are other indications (such as systolic LV dysfunction). Commonly used beta-blocker regimens are (1) metoprolol tartrate (Lopressor) 25 to 50 mg every 6 to 12 hours orally, transitioned over the next 2 to 3 days to twice-daily dosing of metoprolol tartrate or to daily metoprolol succinate (Toprol XL), and then titrated to a daily dose of 200 mg as tolerated, and (2) carvedilol (Coreg)1 6.25 mg twice daily, titrated to 25 mg twice daily as tolerated.

    Current guidelines recommend intravenous beta-blocker only for patients with refractory hypertension or ongoing ischemia without contraindications. Several small randomized clinical trials have suggested that early use of intravenous metoprolol tartrate in selected patients with STEMI with Killip class I to II and no atrioventricular (AV) block before PPCI may reduce infarct size with a higher LV ejection fraction or reduce the incidence of malignant arrhythmia in the acute phase without an excess of adverse events.

    Angiotensin-Converting Enzyme Inhibitors or Angiotensin II Receptor Blockers

    Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) reduce afterload and decrease myocardial remodeling. Either ACEIs or ARBs should be started within 24 hours if there are no contraindications such as worsening renal function, advanced kidney disease, bilateral renal artery stenosis, hyperkalemia, or hypotension. These agents have the largest benefit in patients with anterior STEMI, congestive heart failure, or LV ejection fraction (LVEF) less than 40%. ACEIs may be given routinely to all patients without contraindication, whereas ARBs are an alternative for patients intolerant to ACEIs. There is no additional benefit, only more harm if ACEIs and ARBs are given concomitantly.

    Commonly used ACEI regimens are (1) captopril 6.25 to 12.5 mg three times per day to start, titrated to 25 to 50 mg three times per day as tolerated; (2) lisinopril (Prinivil) 2.5 to 5 mg/day to start, titrated to 10 mg/day or higher as tolerated; (3) ramipril (Altace) 2.5 mg twice daily to start, titrated to 5 mg twice daily as tolerated; and (4) trandolapril (Mavik) test dose 0.5 mg, titrated up to 4 mg daily as tolerated. A commonly used ARB regimen is valsartan (Diovan) 20 mg twice daily to start, titrated to 160 mg twice daily as tolerated.

    HMG CoA Reductase Inhibitors (Statins)

    Treatment with statins after ACS lowers the risk of CV mortality, recurrent MI, stroke, and the need for coronary revascularization. Without contraindications, all patients should receive high-intensity statins as early as possible to improve compliance. Although current guidelines do not endorse a particular low-density lipoprotein (LDL) level as a treatment goal, it is recommended to obtain a fasting lipid panel within 24 hours of presentation. A commonly used high- intensity statin regimen is atorvastatin (Lipitor)1 80 mg daily as tolerated. Statins need to be used cautiously with drugs metabolized via CYP3A4 and fibrates, with frequent monitoring for myopathy and hepatic toxicity. Statin use needs to be combined with diet and therapeutic lifestyle therapies.

    Aldosterone Antagonists

    Eplerenone (Inspra) improves myocardial remodeling and may reduce all-cause and CV mortality and rehospitalization. The 2013 ACC/AHA STEMI guideline recommends starting this medication 3 to 14 days after STEMI in eligible patients (creatinine ≤ 2.5 mg/dL in men and ≤ 2.0 mg/dL in women, potassium ≤ 5.0 mEq/L) with heart failure, with LVEF less than 35% to 40%, and already on adequate doses of beta-blockers and ACEIs or ARBs. However, earlier administration (< 7 days) is preferable to achieve mortality and rehospitalization benefits as suggested by a post hoc analysis of the Eplerenone Post– Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) trial.

    Implantable Cardioverter-Defibrillator

    Patients who develop ventricular tachycardia or fibrillation more than 48 hours after STEMI have the highest risk of sudden cardiac death (SCD) and hence are eligible for an implantable cardioverter- defibrillator (ICD) as a secondary prevention measure for SCD. For primary prevention, multiple trials have established the efficacy of prevention of sudden cardiac death by ICD implantation in patients with LVEF less than 35% and New York Heart Association (NYHA) class II or III symptoms (or LVEF < 30% with NYHA class I symptoms) despite optimal medical therapy 40 days after index STEMI and expectation of at least 1-year survival.

    Other Medical Therapy


    Morphine is a time-honored medication used to reduce pain and anxiety, especially in patients with pulmonary edema during acute presentation of STEMI. However, analysis of results from several clinical trials suggests that a morphine/P2Y12 inhibitor interaction exists, which could lead to adverse clinical consequences. Several recent pharmacokinetic studies in healthy volunteers have shown that intravenous morphine administration can reduce the level of active metabolites of clopidogrel and delay the maximal inhibition of platelet aggregation. A similar effect of morphine on ticagrelor was also reported. Given the current trend of using oral P2Y12 receptor inhibitors before PPCI for STEMI, administration of morphine with P2Y12 receptor inhibitors deserves careful consideration. However, routine avoidance of morphine has not been recommended.


    Nitroglycerin reduces LV preload, increases coronary blood flow, and relieves chest pain symptoms. However, it plays no role in decreasing myocardial injury from coronary artery occlusion in STEMI. Its use in STEMI is mostly for congestive heart failure, hypertension, or rare cases of coronary spasm. It is contraindicated in patients with hypotension (systolic blood pressure [SBP] < 90 mm Hg or SBP > 30 mm Hg below baseline), right ventricular infarction from right coronary artery occlusion, or use of 5’phosphodiesterase inhibitors within 24 to 48 hours.

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    Complications of STEMI

    Cardiogenic Shock

    Cardiogenic shock is defined as an SBP less than 90 mm Hg for longer than 1 hour that is (1) not responsive to fluid administration alone, (2) secondary to cardiac dysfunction, or (3) associated with signs of hypoperfusion or cardiac index less than 2.2 L/min per m2 and pulmonary capillary wedge pressure greater than 18 mm Hg. It occurs in fewer than 10% of STEMI patients (2.4% in 1986 GISSI-1 trial; 6.5% in Germany ALKK-PCI registry as reported in 2013).

    Almost 75% to 80% of cases of cardiogenic shock are due to severe LV systolic dysfunction; right ventricular infarction, mechanical complications from ventricular septal rupture, acute mitral regurgitation, and free wall rupture leading to tamponade account for the rest. Other uncommon causes of shock after STEMI are bleeding, infection, bowel ischemia, or iatrogenic.

    Cardiogenic shock due to mechanical complications after STEMI occurs in a bimodal fashion, with the majority of cases occurring within 24 hours. An early echocardiogram is extremely helpful to delineate the etiology of cardiogenic shock to guide subsequent definitive treatment. Cardiogenic shock carries a high in-hospital mortality, approaching 50%, and is higher in patients older than 75 years. These high-mortality patients require immediate stabilization to prevent end-organ damage followed by emergent coronary angiography and revascularization (Table 4).

    Table 4

    Management Measures for Cardiogenic Shock

    Abbreviations: CABG = coronary artery bypass grafting; IABP = intraaortic balloon pump; LV = left ventricular; PCI = percutaneous intervention; STEMI = ST-elevation myocardial infarction.

    • IABP is more readily available; limited experience with other LV assist devices such as Impella and TandemHeart device.

    Electrical Complications

    Ventricular Arrhythmia

    Lethal ventricular arrhythmia, ventricular tachycardia (VT) or ventricular fibrillation (VF), is the most common cause of out-of- hospital cardiac arrest in STEMI. For hospitalized patients, VT/VF occurs in fewer than 10% of cases in the era of reperfusion therapy, and most cases occur within 48 hours of presentation. VT/VF is often associated with congestive heart failure, cardiogenic shock, or failed reperfusion of an occluded coronary artery. Hence correction of electrolyte and acid-base disturbance, adequate reperfusion to reduce myocardial ischemia, and treatment of heart failure or shock are important preventive measures. Early administration of beta-blockers within 24 hours to patients without contraindications reduces the incidence of VF. If VT/VF occurs, treatment includes immediate defibrillation or cardioversion and an antiarrhythmic agent such as amiodarone (Cordarone). Isolated premature ventricular contractions, nonsustained VT without hemodynamic instability, and AIVR do not generally require specific treatment.

    Supraventricular Arrhythmia

    Common supraventricular arrhythmias after STEMI include atrial fibrillation, atrial flutter, and sinus tachycardia. They are usually the consequence of or triggered by congestive heart failure, atrial infarction, pericarditis, hypoxia, or other underlying systemic problems (such as chronic obstructive pulmonary disease, bleeding, anemia, or infection). Treatment is directed to the underlying causes. For atrial fibrillation/flutter, physicians should pay special attention to anticoagulation use given the frequent concomitant use of DAPT and antithrombotics and the rate versus rhythm control strategy.

    Bradycardia and Heart Block

    Sinus bradycardia may occur after inferior STEMI. Since it is generally mediated through increased vagal tone, close monitoring usually suffices. High-grade AV block (second or third degree) can occur after inferior or anterior STEMI, with a worse prognosis after anterior STEMI owing to a greater degree of myocardial injury. High-grade AV block after inferior STEMI usually is transient and with a narrow complex escape rhythm, which subsides within 2 weeks. Occasionally temporary pacemaker placement may be necessary if bradycardia causes hemodynamic instability. High-grade AV block from anterior STEMI usually requires placement of a prophylactic temporary pacing system as it is commonly associated with hemodynamic instability.

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    Serruys P.W., Chevalier B., Sotomi Y., et al. Comparison of an everolimus-eluting bioresorbable scaffold with an everolimus- eluting metallic stent for the treatment of coronary artery stenosis (ABSORB II): A 3 year, randomised, controlled, single-blind, multicentre clinical trial. Lancet. 2016;388(10059):2479–2491.

    Shah R.U., Henry T.D., Rutten-Ramos S., et al. Increasing percutaneous coronary interventions for ST-segment elevation myocardial infarction in the United States: Progress and opportunity. JACC Cardiovasc Interv. 2015;8:139–146.

    Yadlapati A., Gajjar M., Schimmel D.R., et al. Contemporary management of ST-segment elevation myocardial infarction. Intern Emerg Med. 2016;11(8):1107–1113.

    1 Not FDA approved for this indication.

    1 Not FDA approved for this indication.

    1 Not FDA approved for this indication.

    1 Not FDA approved for this indication.

    1  Not FDA approved for this  indication.

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About Genomic Medicine UK

Genomic Medicine UK is the home of comprehensive genomic testing in London. Our consultant medical doctors work tirelessly to provide the highest standards of medical laboratory testing for personalised medical treatments, genomic risk assessments for common diseases and genomic risk assessment for cancers at an affordable cost for everybody. We use state-of-the-art modern technologies of next-generation sequencing and DNA chip microarray to provide all of our patients and partner doctors with a reliable, evidence-based, thorough and valuable medical service.