Presentation on theme: "ST Elevation Myocardial Infarction (STEMI)"— Presentation transcript:
1 ST Elevation Myocardial Infarction (STEMI) William J. Mosley II, MDCardiovascular Disease Fellow(Updated from John Rapp with 2007 guidelines)
2 ACUTE CORONARY SYNDROMES ACS-STEMINo ST elevationST elevationStableanginaUnstableanginaNSTEMISTEMIACUTE CORONARY SYNDROMES
3 Outline Class/Evidence General Therapy Beta-blockers Reperfusion Facilitated PCIComplications
4 Applying Classification of Recommendations and Level of Evidence Class I Benefit >>> RiskProcedure/ Treatment SHOULD be performed/ administeredClass IIa Benefit >> Risk Additional studies with focused objectives neededIT IS REASONABLE to perform procedure/administer treatmentClass IIb Benefit ≥ Risk Additional studies with broad objectives needed; Additional registry data would be helpfulProcedure/TreatmentMAY BE CONSIDEREDClass IIIRisk ≥ Benefit No additional studies neededProcedure/Treatment should NOT be performed/administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFULLevel A: Recommendation based on evidence from multiple randomized trials or meta-analyses Multiple (3-5) population risk strata evaluated; General consistency of direction and magnitude of effectLevel B: Recommendation based on evidence from a single randomized trial or non-randomized studies Limited (2-3) population risk strata evaluatedLevel C: Recommendation based on expert opinion, case studies, or standard-of-care Very limited (1-2) population risk strata evaluated
5 Hospitalizations in the U.S. Due to Acute Coronary Syndromes (ACS) 1.57 Million Hospital Admissions - ACSUA/NSTEMI†STEMI1.24 million Admissions per year.33 million Admissions per yearHeart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115: *Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA.
7 General Therapy MONA Morphine (q 5-15 min CLASS I) Oxygen (pulse ox>90% CLASS I)Nitroglycerin (0.4 mg SL NTG x 3 for ischemic pain CLASS I)Aspirin
8 AspirinAspirin should be chewed by patients who have not taken aspirin before presentation with STEMI. The initial dose should be 162 mg (Level of Evidence: A) to 325 mg (Level of Evidence: C). Class IIn a dose of 162 mg or more, aspirin produces a rapid clinical antithrombotic effect caused by immediate and near-total inhibition of thromboxane A2 production. (ISIS-2-->ASA led to 23% reduction in mortality):1. Antithrombotic Trialists’ Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ. 2002; 324: 71–86.2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among cases of suspected acute myocardial infarction. Lancet 1988;ii:
10 COMMIT: Study designINCLUSION: >45,000 patients with suspected acute MI (ST change or LBBB) within 24 h of symptom onsetTREATMENT: Metoprolol 15 mg iv over 15 mins, then 200 mg oral daily vs matching placeboEXCLUSION: Shock, systolic BP <100 mmHg, heart rate <50/min or II/III AV block1 OUTCOMES: Death & death, re-MI or VF/arrest up to 4 weeks in hospital (or prior discharge)Mean treatment and follow-up: 16 days
11 30% relative increase in *cardiogenic shock Effects of MetoprololCOMMIT (N = 45,852)Totality of Evidence (N = 52,411)Death 13% P=0.0006ReMI 22% P=0.000230% relative increase in *cardiogenic shockISIS-1 Between mid-1981 and Jan 1, 1985, patients entering 245 coronary care units at a mean of 5.0 h after the onset of suspected acute myocardial infarction were randomised either to a control group or to a group receiving atenolol (5-10 mg iv immediately, followed by 100 mg/day orally for 7 days).MIAMI - The MIAMI trial randomized 5778 patients to blind treatment with iv metoprolol or placebo Treatment with intravenous metoprolol (15 mg) or placebo was started shortly after the patient's arrival in hospital within 24 h of the onset of symptoms, and then oral treatment (200 mg daily) was continued for the study period (15 days)VF 15% P=0.002Lancet. 2005;366:1622.*Risk factors for cardiogenic shock :heart failure, age > 70 , systolic blood pressure < 120, sinus tachycardia > 110 or heart rate < 60, increased time since onset of STEMI symptoms
12 Beta-Blockers Recommendations - Class Ia (B) ORAL beta-blocker therapy SHOULD BE initiated in the first 24 hours for patients who DO NOT have any of the following:signs of heart failure,evidence of a low output state,increased risk for cardiogenic shock, orrelative contraindications to beta blockade1AVB > 0.24 sec,2nd- or 3rd-degree heart blockreactive airway disease** There is no study evaluating oral beta blockers alone*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.*Risk factors for cardiogenic shock :heart failure, age > 70 , systolic blood pressure < 120, sinus tachycardia > 110 or heart rate < 60, increased time since onset of STEMI symptoms
13 Beta-Blockers Recommendations - Class IIa (B) 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:signs of heart failure,evidence of a low output state,increased risk for cardiogenic shock, orrelative contraindications to beta blockade1AVB > 0.24 sec,2nd- or 3rd-degree heart blockreactive airway disease*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.*Risk factors for cardiogenic shock :heart failure, age > 70 , systolic blood pressure < 120, sinus tachycardia > 110 or heart rate < 60, increased time since onset of STEMI symptoms
14 Beta-Blockers Recommendations - Class III (A) IV beta blockers SHOULD NOT be administered to STEMI patients who have any of the following:signs of heart failureevidence of a low output stateincreased risk* for cardiogenic shockrelative contraindications to beta blockade1AVB > 0.24 sec,2nd- or 3rd-degree heart blockreactive airway disease*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.*Risk factors for cardiogenic shock :heart failure, age > 70 , systolic blood pressure < 120, sinus tachycardia > 110 or heart rate < 60, increased time since onset of STEMI symptoms
17 ReperfusionSTEMI 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. Class IaSTEMI 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. Class IbNote “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.
18 PCI vs Fibrinolysis for STEMI: Short-Term Clinical OutcomesPCIN=7739FibrinolysisP<.0001Frequency (%)P<.0001P=.0002P=.0003P<.0001P=.032Metaanalysis of 23 trials, which together randomly assigned 7739 thrombolytic-eligible patients with ST-segment elevation AMI to primary PTCA (n=3872) or thrombolytic therapy (n=3867). Streptokinase was used in eight trials (n=1837), and fibrin-specific agents in 15 (n=5902). Most patients who received thrombolytic therapy (76%, n=2939) received a fibrin-specific agent.P=.0004P<.0001DeathDeath, no shock dataReMIRec. IschemiaTotal StrokeHem. StrokeMajor BleedDeath MI CVAKeeley E, et al. Lancet ;361:13-20.
19 Brief Review of Thrombolytic Trials GISSI-1: Streptokinase 18% reduction in mortality at 21 dGUSTO-1: tPA. 15% reduction in 30-day mortality compared to StreptokinaseGUSTO-3: Reteplase had no benefit over tPA but is easier to use (double bolus)ASSENT: TNKase is similar to tPA but with less non-cerebral bleeding and better mortality with symptoms>4 hrs: Single bolus, fibrin selective, resistance to PAI-1*Overall risk of ICH is 0.7%; Strokes occurred in 1.4%
20 AnticoagulantsPatients undergoing reperfusion with fibrinolytics should receive anticoagulant therapy for a minimum of 48 hours (unfractionated heparin) or up to 8 daysAnticoagulant regimens with established efficacy include:♥ UFH (LOE: C)♥ Enoxaparin (LOE:A)♥ Fondaparinux (LOE:B)Reduction in Mortality
21 Summary of Observations from Trials of Anticoagulants for STEMI Efficacy (through 30 d)SafetyUse During PCIReviparinFibrinolysis: probably superiorto placebo.*No reperfusion: probably superior to placebo.*↑ risk of serious bleeds†No data on reviparin alone during PCI. Additional anticoagulant with anti-IIa activity, such as UFH or bivalirudin, recommended.FondaparinuxFibrinolysis: appears superior to control rx (placebo/UFH). Relative benefit vs placebo and UFH separately cannot be reliably determined from available data.*Primary PCI: when used alone, no advantage over UFH and trend toward worse outcome.No reperfusion: appears superior to control therapy (placebo/UFH). Relative benefit versus placebo and UFH separately cannot be reliably determined from available data.*Trend toward ↓ risk of serious bleeds†↑ risk of catheter thrombosis when fondaparinux used alone. Additional anticoagulant with anti-IIa activity, such as UFH or bivalirudin, recommended.EnoxaparinFibrinolysis: appears superior to UFHEnoxaparin can be used to support PCI after fibrinolysis. No additional anticoagulant needed.* See 2007 STEMI Focused Update for further discussion and subgroup analysis (Antman EM, et al. J Am Coll Cardiol Published ahead of print on December 10, Available at† Definitions of significant bleeds varied among the trials. The original references should be consulted for details.Antman EM, et al. J Am Coll Cardiol Published ahead of print on December 10, Available at Table 10.
23 Meta-analysis: Facilitated PCI vs Primary PCI MortalityReinfarctionMajor BleedingLytic aloneN=2953IIb/IIIa aloneN=1148Lytic +IIb/IIIaN=399All (N=4500)1.43( )( )1.03( )( )3.07( )1.03( )Facilitated PCI (PCI with additional therapy) with fibrinolytics shows clear increase mortality. Primary PCI vs Facilitated with GPIIb/IIIa shows no difference.1.38 ( )1.71 ( )1.51 ( )0.11100.11100.1110Fac. PCI BetterPPCI BetterFac. PCI BetterPPCI BetterFac. PCI BetterPPCI BetterKeeley E, et al. Lancet 2006;367:579.
24 Rescue PCI If evidence of cardiogenic shock, severe heart failure hemodynamically compromising ventricular arrhythmias.If fibriolysis has failedEvaluate 90 minutes for a <50% ST resolution in lead with greatest elevation
25 Summary of Acute STEMI Treatment Stabilize, MONA/BBASA if MI is even considered.The artery is CLOSED; time is musclePCI is preferred method of reperfusionCath lab (regardless of method of reperfusion) ifHemodynamic or electrical instabilityFailed Fibrinolysis
26 Case Presentation51 y.o. man with increasing shortness of breath and chest pain x 60minCame to ED because she can no longer walk up a flight of stairs or lay down flat.No N/V/Diaphoresis. No LH or dizzinessNo known history of cardiac or pulmonary disease.
27 Physical Exam Vital Signs: HR 120; BP 90/60; RR 28. General: Alert and oriented x 3. Mild respiratory distress.HEENT: NC, no trauma.Neck: Supple, no lymphadenopathy.Heart: Regular S1 and S2. 2/6 early SEM along L sternal border (no significant radiation). No carotid bruits. ? JVD.Lungs: Tachypnic. Rales 1/3 up the back bilaterally. Otherwise clear.Abdomen: Obese. BenignExtremities: Warm. No C/C. Trace edema.
32 Ventricular Arrhythmias BPM; Up to 20% STEMI patients have thisUsually a result of reperfusion; no specific therapy needed if HD stable. Otherwise, atropine or even atrial pacing may increase sinus rate to overdrive pace the AIVRRoutine post-MI management with B-blockers, ACE, etc.
33 PVC’s Extremely common, along with short runs of NSVT Amiodarone won’t increase mortality, other antiarrhythmics (other than B-blockers) do.B-blockers, electrolytesBest if no antiarrhythmics are used
34 Not So Benign RhythmIschemic VT is often polymorphic; HR> BPMHigher risk with more LV damage and in first 2 days after MITreat: DCCV, cath lab (if needed), electrolyte correction, amiodarone, lidocaine, B-Blockers
35 If That Didn’t Make You Nervous… Primary VF: Sudden event with no warning--10% STEMI patients before lytics. MUCH MUCH less nowSecondary VF: Occurring in setting HF or shockLate VF: >48 hrs after MI-->Increased risk with IVCD, anterior wall MI, persistent SVT early in course, and RV infarction requiring pacing***Have to worry about structural complication (free wall rupture)/ischemiaTreat: Non-synced DCCV, electrolyte correction
36 Why get worked up about electrolytes? NOTE: Pre-lytic studyNordrehaug JE, van der Lippe G: Hypokalemia and ventricular fibrillation in acute myocardial infarction. Br Heart J 50:525, 1983.
37 Sinus Bradycardia/Junctional Escape Rhythm 4-5% of STEMI patients have a bradyarrhythmiaSinus node ischemia--Blood supply to SA node is: 65% RCA, 25% LCX, 10% dual supply.Most commonly seen in Inferior/posterior MI’s.Often induced by vagal reaction that may be protective
38 Atrioventricular Block First-Degree: Usually the RCA and does not require treatment. Hold the B-blocker for PR>240 msSecond-Degree: Usually RCA disease and does not require treatment unless HR less than 50 and arrhythmia or symptoms. Otherwise, atropine or paceThird-Degree: Can be from any location of infarct. Can be preceded by Mobitz II BlockPace for symptoms and for hemodynamic support. Usually not needed in inferior MI’s as block is transient (pace for HR<40-50)
39 Post-MI VSD ~2% of acute MI’s prior to reperfusion era ~0.2% in GUSTO-I streptokinase trialWithout reperfusion, usually occurs within first weekDay 1--Large intramural hematomas that dissectDay 3-5--Coagulation necrosis24 hr or less if receive lysis--Lytics reduce infarct size but may promote hemorrhagic dissection of myocardium
40 Symptoms, Exam, and Diagnosis Chest pain, dyspneaPE: Harsh, holosystolic murmur along sternal border radiating to base/apex/R parasternum; thrill in 1/2 patients; S3; Loud P2; TR.Compared to acute MR, murmur is loud. Up to 20% of patients may have MR as well though
41 CCU Management IABP Ventilation Diuresis/HF Management Inotropes (can increase shunt)Nitroprusside if tolerated (can cause hypotension)Mortality with conservative management is HIGH (24%, 46%, 67-82% at 24 hrs, 1 wk, and 2 months, respectively)Ultimately, mechanical closure needed (surgery vs. percutaneous)-TIMING is questionable but clinical status should not preclude this
42 Acute Mitral Regurgitation Caused by papillary muscle ischemia or rupture (less likely). Rupture is usually partial since total is essentially incompatible with lifeUsually in setting of inferior MI involving the posteromedial papillary muscle (single PDA blood supply as opposed to anterolateral)Rupture usually occurs 3-5 days post-MI and in 1% of MI’s and requires emergent operative repair (50% mortality in 24 hrs)Accounts for 7% of cardiogenic shock and 5% of mortality associated with acute MIArea of infarction does NOT have to be large
43 Symptoms, Exam, Diagnosis Symptoms: Those of heart failurePE: May or may not hear loud systolic murmur (need a gradient)
44 CCU Management Mechanical ventilation if needed IABP--especially for hypotensionPCI if papillary m. ischemia (not rupture)Afterload reduction (nitroprusside if possible) to MAP of mm HgSince mortality is 90% with medical therapy alone, surgery is the major therapy of choicePerioperative mortality 20-25%Overall surgical mortality is even higher
45 Free Wall Rupture ~10% of patients who die in hospital from STEMI Most commonly between 1 and 4 days (up to 3 weeks)Caused by tear or dissecting hematomaMore common with fibrinolysis compared to PCIMore common in patients without previous infarction
46 Symptoms, Exam, Diagnosis Acute symptoms include sudden chest pain (esp with cough, strain) and sudden deathSubacute symptoms: Pericarditis-like symptoms (chest pain, nausea, vomiting)Exam (think HF and tamponade): JVD, pulsus, diminished heart sounds, rub, possibly a new murmur
47 Treatment Pericardiocentesis if time Surgical repair is the only treatmentMortality is reasonable ifpatient gets to the ORin time90% mortality withoutsurgery
48 Summary of Acute STEMI Complications Much more rare in the reperfusion eraLook for them especially in delayed presentationArrhythmias are most common complication and may require emergent treatmentVSD’s, papillary muscle rupture, and free wall ruptures carry a VERY high mortality and require emergent surgical consultationSupport mechanically until patient receives operation
49 Other ReferencesCrawford PA, ed. The Washington Manual Subspecialty Consult Series: Cardiology Subspecialty Consult. Philadelphia: Lippincott Williams and Wilkins, 2004.Griffin BP, Topol EJ, eds. Manual of Cardiovascular Medicine, 2nd ed. Philadelphia: Lippincott Williams and Wilkins, 2004Zipes, Libby, Bonow, Braunwald, eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 7th ed. Philadelphia: Elsevier Saunders, 2005