Updated Management of STEMI

Updated Management of STEMI
ICU presentation 28/08/2009 Chairperson: Dr KC Chan Presenter: Dr KL Wu Updated Management of STEMI

Hospitalizations in the U.S. Due to Acute Coronary Syndromes (ACS)
1.57 Million Hospital Admissions - ACS UA/NSTEMI† STEMI 1.24 million Admissions per year .33 million Admissions per year Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115: *Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA. Updated Management of STEMI

M/60, Admitted for chest pain, ECG showed new onset LBBB, SK given. He c/o dizziness in the midnight. Pulse 55bpm. Pace or not? Updated Management of STEMI

IV Beta-Blockers Updated Management of STEMI

COMMIT: Study design TREATMENT: Metoprolol 15 mg iv over 15 mins, then 200 mg oral daily vs matching placebo INCLUSION: Suspected acute MI (ST change or LBBB) within 24 h of symptom onset EXCLUSION: Shock, systolic BP <100 mmHg, heart rate <50/min or II/III AV block 1 OUTCOMES: Death & death, re-MI or VF/arrest up to 4 weeks in hospital (or prior discharge) Mean treatment and follow-up: 16 days Updated Management of STEMI

ClOpidogrel and Metoprolol in Myocardial Infarction Trial (COMMIT)
45,852 patients within 24 h acute MI ― 93% STEMI or LBBB Up to 15 mg IV → 500 mg po metoprolol daily vs placebo Co-primary outcomes ― death, reinfarction, or cardiac arrest ― death from any cause to discharge or up to 4 wk in hospital Neither co-primary outcome ↓ by metoprolol ― 5 fewer reinfarctions, 5 fewer VF ― 11 more/1000 → cardiogenic shock  Risk cardiogenic shock especially with initial hemodynamic instability ― moderate late benefit with relative stability Recommend: start -blocker po when hemodynamically stable Chen ZM, et al. Lancet 2005;366:1622–32. Updated Management of STEMI

Beta-Blockers Oral beta-blocker therapy should be initiated in the first 24 hours for patients who do not have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart block, active asthma, or reactive airway disease). It is reasonable to administer an IV beta blocker at the time of presentation to STEMI patients who are hypertensive and who do not have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart block, active asthma, or reactive airway disease). I IIa IIb III B I IIa IIb III B *Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the risk of developing cardiogenic shock): age > 70 years, systolic blood pressure < 120 mmHg, sinus tachycardia > 110 or heart rate < 60, increased time since onset of symptoms of STEMI. Updated Management of STEMI

Beta-Blockers IV beta blockers should not be administered to STEMI patients who have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart block, active asthma, or reactive airway disease). I IIa IIb III A *Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the risk of developing cardiogenic shock): age > 70 years, systolic blood pressure < 120 mmHg, sinus tachycardia > 110 or heart rate < 60, increased time since onset of symptoms of STEMI. Updated Management of STEMI

Primary PCI Updated Management of STEMI

Primary PCI I IIa IIb III A STEMI patients presenting to a hospital with PCI capability should be treated with primary PCI within 90 min of first medical contact as a systems goal. STEMI patients presenting to a hospital without PCI capability, and who cannot be transferred to a PCI center and undergo PCI within 90 min of first medical contact, should be treated with fibrinolytic therapy within 30 min of hospital presentation as a systems goal, unless fibrinolytic therapy is contraindicated. I IIa IIb III B Note “medical contact” is defined as the “time of EMS arrival on scene” after the patient calls EMS/9-1-1 or the “time of arrival at the emergency department door” (whether PCI-capable or non–PCI-capable hospital) when the patient self-transports. Updated Management of STEMI

Facilitated PCI Updated Management of STEMI

Facilitated PCI I IIa IIb III B A planned reperfusion strategy using full-dose fibrinolytic therapy followed by immediate PCI is not recommended and may be harmful. Facilitated PCI using regimens other than full-dose fibrinolytic therapy might be considered as a reperfusion strategy when all of the following are present: a. Patients are at high risk, b. PCI is not immediately available within 90 minutes, and c. Bleeding risk is low (younger age, absence of poorly controlled hypertension, normal body weight). I IIa IIb III C Updated Management of STEMI

Rescue and Late PCI Updated Management of STEMI

Meta-analysis: Rescue PCI vs Conservative Tx
Outcome Rescue PCI Conservative Treatment RR (95% CI) P Mortality, % (n) 7.3 (454) 10.4 (457) 0.69 (0.46–1.05) .09 HF, % (n) 12.7 (424) 17.8 (427) 0.73 (0.54–1.00) .05 Reinfarction, % (n) 6.1 (346) 10.7 (354) 0.58 (0.35–0.97) .04 Stroke, % (n) 3.4 (297) 0.7 (295) 4.98 (1.10–22.48) Minor bleeding, % (n) 16.6 (313) 3.6 (307) 4.58 (2.46–8.55) <.001 Wijeysundera and colleagues performed a meta-analysis of 8 randomized trials enrolling 1177 patients to estimate the benefits and risks associated with rescue PCI and repeat fibrinolytic therapy compared with conservative management in patients with failed fibrinolytic therapy for STEMI. As shown on the slide, rescue PCI was associated with no significant reduction in all-cause mortality (relative risk [RR] 0.69; 95% CI, ), but was associated with significant risk reductions in heart failure (RR 0.73; 95% CI, ) and reinfarction (RR 0.58; 95% CI, ) compared with conservative treatment. Rescue PCI also was associated with an increased risk of stroke (RR 4.98; 95% CI, ) and minor bleeding (RR 4.58; 95% CI, ). In 3 trials enrolling 700 patients that reported the composite end point of all-cause mortality, reinfarction, and heart failure, rescue PCI was associated with a significant relative risk reduction of 28% (RR 0.72, 95% CI, ; P=.001). Further, there was an 11% absolute risk reduction (95% CI, 5%-18%; P<.001) in this composite end point with an incidence of 29.2% in the PCI arm and 41.0% in the conservative arm, leading to a number needed to treat of 9. Repeat fibrinolytic therapy was not associated with significant improvements in all-cause mortality (RR 0.68; 95% CI, ) or reinfarction (RR 1.79; 95% CI, ), but was associated with an increased risk for minor bleeding (RR 1.84; 95% CI, ). Thus, the investigators concluded that rescue PCI is associated with improved clinical outcomes for STEMI patients after failed fibrinolytic therapy, but these benefits must be interpreted in the context of potential risks. On the other hand, repeat fibrinolytic therapy is not associated with significant clinical improvement and may be associated with increased harm. In 3 trials, enrolling 700 patients that reported the composite end point of all-cause mortality, reinfarction, and HF, rescue PCI was associated with a significant RR reduction of 28% (RR 0.72; 95% CI, ; P=.001) Wijeysundera HC, et al. J Am Coll Cardiol. 2007;49: Updated Management of STEMI Wijeysundera HC, Vijayaraghavan R, Nallamothu BK, et al. Rescue angioplasty or repeat fibrinolysis after failed fibrinolytic therapy for ST-segment myocardial infarction: a meta-analysis of randomized trials. J Am Coll Cardiol. 2007;49:

Rescue PCI A strategy of coronary angiography with intent to perform PCI (or emergency CABG) is recommended in patients who have received fibrinolytic therapy and have: Cardiogenic shock in patients < 75 years who are suitable candidates for revascularization b. Severe congestive heart failure and/or pulmonary edema (Killip class III) c. Hemodynamically compromising ventricular arrhythmias. I IIa IIb III B I IIa IIb III B I IIa IIb III c Updated Management of STEMI

Rescue PCI A strategy of coronary angiography with intent to perform PCI (or emergency CABG) is reasonable in patients ≥ 75 years who have received fibrinolytic therapy, and are in cardiogenic shock, provided they are suitable candidates for revascularization. Updated Management of STEMI

Rescue PCI A strategy of coronary angiography with intent to perform rescue PCI is reasonable for patients in whom fibrinolytic therapy has failed (ST-segment elevation < 50% resolved after 90 min following initiation of fibrinolytic therapy in the lead showing the worst initial elevation) and a moderate or large area of myocardium at risk [anterior MI, inferior MI with right ventricular involvement or precordial ST-segment depression]. I IIa IIb III B Updated Management of STEMI

Rescue PCI A strategy of coronary angiography with intent to perform PCI in the absence of any of the above Class I or IIa indications might be reasonable in moderate- or high-risk patients, but its benefits and risks are not well established. The benefits of rescue PCI are greater the earlier it is initiated after the onset of ischemic discomfort. I IIa IIb III C Updated Management of STEMI

Rescue PCI A strategy of coronary angiography with intent to perform PCI (or emergency CABG) is not recommended in patients who have received fibrinolytic therapy if further invasive management is contraindicated or the patient or designee do not wish further invasive care. I IIa IIb III c Updated Management of STEMI

Occluded Artery Trial (OAT)
Eligibility: Confirmed Index MI Total IRA occlusion 3-28 days (>24 hours) Exclusion criteria: Significant left main or 3 vessel CAD Hemodynamic or electrical instability Rest or low-threshold angina NYHA Class III-IV HF or shock RESULTS 2166 randomized 1082 PCI + optimal medical therapy 1084 Optimal medical therapy (MED) Death, MI, CHF Class IV 4 year event rate: 17.2% PCI vs 15.6% MED Hazard Ratio: PCI vs MED=1.16; 95% Cl (0.92, 1.45); p=0.20 Fatal and Non fatal MI 7.0% PCI vs 5.3% MED Hazard Ratio: PCI vs MED=1.36; 95% Cl (0.92, 2.00); p=0.13 Hochman JS, et al. Am Heart J 2005;150:627-42; Hochman JS, et al. N Engl J Med 2006;355: Updated Management of STEMI

Late PCI after Fibrinolysis or for Patients Not Undergoing Primary Reperfusion I IIa IIb III B PCI of a hemodynamically significant stenosis in a patent infarct artery > 24 hours after STEMI may be considered as part of a invasive strategy. PCI of a totally occluded infarct artery > 24 hours after STEMI is not recommended in asymptomatic patients with 1- or 2-vessel disease if they are hemodynamically and electrically stable and do not have evidence of severe ischemia. I IIa IIb III B Updated Management of STEMI

Anticoagulants Updated Management of STEMI

Anticoagulants Patients undergoing reperfusion with fibrinolytics should receive anticoagulant therapy for a minimum of 48 hours (Level of Evidence: C) and preferably for the duration of the index hospitalization, up to 8 days (regimens other than unfractionated heparin [UFH] are recommended if anticoagulant therapy is given for more than 48 hours because of the risk of heparin-induced thrombocytopenia with prolonged UFH treatment). (Level of Evidence: A) Anticoagulant regimens with established efficacy include: ♥ UFH (LOE: C) ♥ Enoxaparin (LOE:A) ♥ Fondaparinux (LOE:B) I IIa IIb III C I IIa IIb III A Dosing regimens for UFH, enoxaparin and fondaparinux in patients undergoing reperfusion with fibrinolytics or PCI can be found in the 2007 STEMI Focused Update (Antman EM, et al. J Am Coll Cardiol Published ahead of print on December 10, Available at Updated Management of STEMI

Unfractionated Heparin
Advantages Disadvantages Immediate anticoagulation Multiple sites of action in coagulation cascade Long history of successful clinical use Readily monitored by aPTT and ACT Indirect thrombin inhibitor so does not inhibit clot-bound thrombin Nonspecific binding to: Serine proteases Endothelial cells (can lead to variability in level of anticoagulation) Reduced effect in ACS Inhibited by PF-4 Causes platelet aggregation Nonlinear pharmacokinetics Risk of HIT Some of the advantages of unfractionated heparin include immediate anticoagulation with a bolus, multiple sites of action in the clotting cascade, and a long history of successful clinical use. UFH can be readily monitored by either activated partial thromboplastin time (aPTT) or by activated coagulation time (ACT). Some of the disadvantages of UFH include that it is an indirect thrombin inhibitor and thus, does not have the ability to inhibit clot-bound thrombin. It is characterized by areas of nonspecific binding, which can lead to variability in the level of anticoagulation. The inhibition of platelet factor 4 (PF-4) also contributes to variability in anticoagulation. Paradoxically, the long chains on UFH can actually cause platelet aggregation. Other disadvantages include nonlinear pharmacokinetics, which make the anticoagulant response to UFH nonlinear at therapeutic doses, with both the intensity and duration of effect rising disproportionately with increasing dose. Moreover, the possibility of heparin-induced thrombocytopenia (HIT) exists with UFH administration. HIT is an antibody-mediated adverse reaction to heparin that can result in venous or arterial thrombosis. Hirsh J, et al. Circulation. 2001;103: aPTT = activated partial thromboplastin time; ACT = activated coagulation time; PF-4 = platelet factor 4; HIT = heparin-induced thrombocytopenia. Updated Management of STEMI Hirsh J, Anand SS, Halperin JL, Fuster V. Guide to anticoagulant therapy: Heparin: A statement for healthcare professionals from the American Heart Association. Circulation. 2001;103:

ExTRACT-TIMI 25: Primary End Point (ITT) Death or Nonfatal MI
UFH 12.0% 17% RRR 9.9% Enoxaparin Primary End Point (%) Relative Risk 0.83 (95% CI, 0.77 to 0.90) P<.001 This slide shows the primary endpoint with a highly significant (P<.001) 17% reduction in the relative risk of death or nonfatal MI in an intention-to-treat analysis. As shown, the curves begin to separate early and then separate more widely beginning after the first 48 hours. There is, however, a reduction of events in the enoxaparin group even during the first 48 hours. Lost to follow-up = 3 Days after Randomization Updated Management of STEMI Adapted with permission from Antman EM, et al. N Engl J Med. 2006;354: Antman EM, Morrow DA, McCabe CH, Murphy SA, Ruda M, Sadowski Z, Budaj A, Lopez-Sendon JL, Guneri S, Jiang F, White HD, Fox KA, Braunwald E, for the ExTRACT-TIMI 25 Investigators. Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction. N Engl J Med. 2006;354:

Low-Molecular-Weight Heparin
Advantages Disadvantages Increased anti-Xa to anti-IIa activity  inhibits thrombin generation more effectively Induces ↑ release of TFPI vs UFH Not neutralized by platelet factor 4 Less binding to plasma proteins (eg, acute-phase reactant proteins)  more consistent anticoagulation Lower rate of HIT vs UFH Lower fibrinogen levels Easy to administer (SC administration) Long history of clinical studies and experience, FDA-approved indications Monitoring typically unnecessary Indirect thrombin inhibitor Less reversible Difficult to monitor (no aPTT or ACT) Renally cleared Long half-life Risk of HIT This slide shows some of the advantages and disadvantages of low-molecular weight heparin. Compared with UFH, the increased anti-Xa to anti-2A activity will inhibit thrombin generation to a greater degree. LMWH also induces tissue factor pathway inhibitor release as compared with UFH and other anticoagulants, thereby enhancing anti-clotting effects. It's not neutralized by platelet factor 4, and has less binding to all the proteins resulting in more consistent anticoagulation. With fewer long chains, there is a lower rate of heparin-induced thrombocytopenia, and there are lower fibrinogen levels. LMWH is also easier to administer because of its subcutaneous administration, and has a long history of use in clinical trials and is FDA-approved for multiple different indications. Some of the disadvantages include that it has an indirect action and therefore does not bind to clot-bound thrombin. It is less reversible because of its subcutaneous administration, which makes reversal with protamine more difficult, albeit it possible. LMWH is difficult to monitor, but monitoring is typically unnecessary. It is renally cleared which necessitates does adjustments for renal dysfunction. Hirsh J, et al. Circulation. 2001;103: TFPI = tissue factor pathway inhibitor; UFH = unfractionated heparin; SC = subcutaneous; aPTT = activated partial thromboplastin time; ACT = activated coagulation time. Updated Management of STEMI Hirsh J, Anand SS, Halperin JL, Fuster V. Guide to anticoagulant therapy: Heparin: A statement for healthcare professionals from the American Heart Association. Circulation. 2001;103:

OASIS-6 Trial: Results Reduction in Death/MI at 30 days: Stratum 1 (No UFH indicated) P<.05 14% 14% Primary End Point: Death/Reinfarction (%) 12% 11.2% 10% 14.8% 15% 8% 13.4% 6% 12% 11.2% 9.7% 4% 8.9% 9% 2% 7.4% Frequency 0% 6% Fondaparinux Placebo Reduction in Death/MI: Stratum 2 (UFH Indicated) P=NS 3% 14% The overall results are shown on the left of this slide. The primary endpoint was reduced from 11.2% for control (either placebo or unfractionated heparin) to 9.7% with fondaparinux, a highly significant P value of This was also seen at the earlier time point of 9 days and at the later follow-up of three to six months. There were some differences at the 30 day time period in the results by strata. A significant difference in stratum one (fondaparinux vs placebo) was seen with an absolute 3% reduction in death or MI, whereas in patients who had unfractionated heparin in the control group, there was a nonsignificant difference that went from 8.7% for unfractionated heparin down to 8.3% for fondaparinux. P=.008 P=.003 P=.008 12% 0% 10% 8.3% 8.7% 30 days 9 days 3-6 months 8% p=0.97 Fondaparinux (n=6036) Control (n=6056) 6% 4% 2% 0% Yusuf S, et al. JAMA. 2006;295: Adapted with permission from Fondaparinux UFH Updated Management of STEMI Yusuf S, Mehta SR, Chrolavicius S, et al. for the OASIS-6 Trial Group. Effects of fondaparinux on mortality and reinfarction in patients with acute ST-segment elevation myocardial infarction: the OASIS-6 randomized trial. JAMA. 2006;295:

Fondaparinux Advantages Disadvantages SC administration Potential exists for outpatient management Once-daily administration Predictable anticoagulant response Fixed dose No antigenicity Potentially no need for serologic parameters Does not cross the placenta HIT antibodies do not cross-react Decreased bleeding complications vs UFH or LMWH Difficult to monitor (no aPTT or ACT) Long half-life Catheter thrombosis during PCI The advantages of fondaparinux include that it is administered subcutaneously, which facilitates possible outpatient management with once-daily administration. It has a predictable anticoagulant response and is administered using a fixed dose (uses a milligram dose as opposed to a milligram per kilogram dose). It has no antigenicity, and thus, no need for serologic parameters. It does not cross the placenta and does not cross react with HIT antibodies. It has been shown to have decreased bleeding complications as compared with either unfractionated heparin or low molecular weight heparin. Some of the disadvantages are that it is difficult to monitor. It has a long half life (15 hours), and thrombosis on catheters has been noted when using only fondaparinux in the cath lab. Simoons ML, et al. J Am Coll Cardiol. 2004;43: Yusuf S, et al. N Engl J Med. 2066;354: Updated Management of STEMI Simoons ML, Bobbink IWG, Boland J, et al. A dose-finding study of fondaparinux in patients with non-ST-segment elevation acute coronary syndromes. The Pentasaccharide in Unstable Angina (PENTUA) Study. J Am Coll Cardiol. 2004;43: Yusuf S, Mehta SR, Chrolavicius S, et al. for the Fifth Organization to Assess Strategies in Acute Ischemic Syndromes Investigators. N Engl J Med. 2006;354:

M/71, case of inferior STEMI, which one is the infarct related artery
M/71, case of inferior STEMI, which one is the infarct related artery? RCA ? LCx?

Greater ST elevation in lead III than in lead II has been shown to indicate RCA-related infarction ST elevation in V3R, V4R: Reported to be seen in proximal RCA infarct ST elevation in V4-6: Reported to be more common in LCx infarct ST depression in V1-3: Reported to be more common in LCx infarct Updated Management of STEMI

AMI due to RCA infarct

ECG of a 70yrs old gentlemen after giving TNK

Thienopyridines Updated Management of STEMI

CLARITY-TIMI 28 Primary Endpoint: Occluded Artery (or D/MI thru Angio/HD) Odds Ratio 0.64 (95% CI ) 36% Odds Reduction 21.7 25 20 P= 15.0 Occluded Artery or Death/MI (%) 15 10 5 0.4 0.6 0.8 1.0 1.2 1.6 n=1752 n=1739 Clopidogrel better Placebo better Clopidogrel LD 300 mg MD 75 mg Placebo Sabatine N Eng J Med 2005;352:1179. STEMI, Age 18-75 Updated Management of STEMI

COMMIT: Effect of CLOPIDOGREL on Death In Hospital
Placebo + ASA: 1,846 deaths (8.1%) Clopidogrel + ASA: 1,728 deaths (7.5%) 0.6% ARD 7% RRR P = 0.03 Dead (%) N = 45,852 No Age limit ; 26% > 70 y Lytic Rx 50% No LD given Chen ZM, et al. Lancet. 2005;366:1607. Days Since Randomization (up to 28 days) Updated Management of STEMI

Thienopyridines Clopidogrel 75 mg per day orally should be added to aspirin in patients with STEMI regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy. Treatment with clopidogrel should continue for at least 14 days. I IIa IIb III A I IIa IIb III B Updated Management of STEMI

Thienopyridines In patients < 75 years who receive fibrinolytic therapy or who do not receive reperfusion therapy, it is reasonable to administer an oral clopidogrel loading dose of 300 mg. (No data are available to guide decision making regarding an oral loading dose in patients ≥ 75 years of age.) Long-term maintenance therapy (e.g., 1 year) with clopidogrel (75 mg per day orally) can be useful in STEMI patients regardless of whether they undergo reperfusion with fibrinolytic therapy or do not receive reperfusion therapy. I IIa IIb III C I IIa IIb III C Updated Management of STEMI

A very lethal disease

Variables Used in the TIMI Risk Score
Age ≥ 65 years At least 3 risk factors for CAD Prior coronary stenosis of ≥ 50% ST-segment deviation on ECG presentation At least 2 anginal events in prior 24 hours Use of aspirin in prior 7 days Elevated serum cardiac biomarkers The TIMI risk score is determined by the sum of the presence of the above 7 variables at admission. 1 point is given for each variable. Primary coronary stenosis of 50% or more remained relatively insensitive to missing information and remained a significant predictor of events. Antman EM, et al. JAMA 2000;284:835–42. TIMI = Thrombolysis in Myocardial Infarction. Updated Management of STEMI

TIMI Risk Score TIMI Risk Score All-Cause Mortality, New or Recurrent MI, or Severe Recurrent Ischemia Requiring Urgent Revascularization Through 14 Days After Randomization % 0-1 4.7 2 8.3 3 13.2 4 19.9 5 26.2 6-7 40.9 Reprinted with permission from Antman EM, et al. JAMA 2000;284:835–42. Copyright © 2000, American Medical Association. All Rights reserved. The TIMI risk calculator is available at Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Table 8. TIMI = Thrombolysis in Myocardial Infarction. Updated Management of STEMI

GRACE Risk Score Variable Odds ratio Older age 1.7 per 10 y Killip class 2.0 per class Systolic BP 1.4 per 20 mm Hg ↑ ST-segment deviation 2.4 Cardiac arrest during presentation 4.3 Serum creatinine level 1.2 per 1-mg/dL ↑ Positive initial cardiac biomarkers 1.6 Heart rate 1.3 per 30-beat/min ↑ The sum of scores is applied to a reference monogram to determine the corresponding all-cause mortality from hospital discharge to 6 months. Eagle KA, et al. JAMA 2004;291:2727–33. The GRACE clinical application tool can be found at Also see Figure 4 in Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157. GRACE = Global Registry of Acute Coronary Events. Updated Management of STEMI

B-Type Natriuretic Peptide
B-type natriuretic peptide (BNP): new biomarker of considerable interest BNP is a cardiac neurohormone released on ventricular myocyte stretch as proBNP, which is enzymatically cleaved to the N- terminal proBNP (NT-pro-BNP) and, subsequently, to BNP Natriuretic peptides are strong predictors of both short- and long- term mortality in patients with STEMI and UA/NSTEMI Recommend: Measurement of BNP or NT-pro-BNP may be considered to supplement assessment of global risk in patients with suspected ACS (Class IIb, LOE: B) Galvani M, et al. Circulation 2004;110:128–34. LOE = level of evidence. Updated Management of STEMI

Updated Management of STEMI

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