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STEMI MANAGEMENT

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ACC/AHA Guidelines STEMI. DR RAJESH K F. Applying Classification of Recommendations and Level of Evidence. Applying Classification of Recommendations and Level of Evidence. Evolution of Guidelines for STEMI. 1990 ACC/AHA MI R Gunnar - PowerPoint PPT Presentation

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Page 1: ACC/AHA Guidelines  STEMI

STEMIMANAGEMENT

Page 2: ACC/AHA Guidelines  STEMI

• DefinitionCriteria.. e/o myocardial necrosis in a clinical setting consistent with

myocardial ischaemia. Detection of rise &/or fall of cardiac biomarkers (preferably troponin)

with at least one value >99th percentile of the URL together with e/o myocardial ischaemia with at least one of the following:

• Symptoms of ischaemia;• ECG changes indicative of new ischaemia(new STE or new LBBB)• Dvpt of pathological Q waves in the ECG;• Imaging e/o new loss of viable myocardium or new RWMA

• For PCI/ CABG with normal baseline troponin values, elevations

>99th percentile URL are s/o peri-procedural myocardial necrosis. By convention, increases of biomarkers >3 x 99th percentile URL have been designated as defining PCI-related MI. •Increases of biomarkers >5 x 99th percentile URL plus either new pathological Q waves or new LBBB, or angiographically documented new graft or native coronary artery occlusion, or imaging evidence of

new loss of viable myocardium ……….CABG-related MI. Pathological findings of an acute myocardial infarction.

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Chronology of the interface between the patient and the clinician through the progression of plaque formation and the onset of complications of STEMI.

Ischemic Discomfort

Acute Coronary Syndrome

No ST Elevation ST Elevation

Page 4: ACC/AHA Guidelines  STEMI

• Prehospital Chest Pain Evaluation and TreatmentPrehospital Chest Pain Evaluation and Treatment

• Prehospital EMS providers …162 to 325 mg of aspirin (chewed) to chest pain patients suspected of having STEMI unless contraindicated or already taken by the patient…non–enteric-coated formulations.

• Previously on NTG take I tab S/L Not improving after 5 mts Seek medical help

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III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

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Prehospital IssuesPrehospital Issues

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Prehospital 12-lead ECG by ACLS….Class IIa (B)Prehospital fibrinolysis….Class IIa (B)

Prehospital destination protocols

•Patients with STEMI who have cardiogenic shock and are <75 yrs old

should be brought immediately or secondarily transferred to facilities

capable of cardiac catheterization and rapid revascularization within

18 hrs of shock (Class I)

•Patients with STEMI who have contraindications to fibrinolytic

therapy should be brought immediately or secondarily transferred

promptly (primary-receiving hospital door-to-departure time less than

30 min.) to facilities capable of cardiac catheterization and rapid

revascularization

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Fibrinolysis

Primary PCI

Noninvasive Risk Stratification

LateHospital Careand Secondary

Prevention

PCI or CABG

NotPCI Capable

PCI Capable

Rescue Ischemiadriven

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Initial Recognition and Management in the Initial Recognition and Management in the Emergency DepartmentEmergency Department

EExamine• 1. Airway, Breathing, Circulation (ABC)

• 2. Vital signs, general observation

• 3. Presence or absence of jugular venous distension

• 4. Pulmonary auscultation for rales

• 5. Cardiac auscultation for murmurs and gallops

• 6. Presence or absence of stroke

• 7. Presence or absence of pulses

• 8. Presence or absence of systemic hypoperfusion (cool, clammy, pale, ashen)

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• Laboratory examinations should be performed as part of the management of STEMI patients, but should not delay the implementation of reperfusion therapy.

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Serum biomarkers for cardiac damage Complete blood count (CBC) with platelets International normalized ratio (INR) Activated partial thromboplastin time (aPTT) Electrolytes and magnesium Blood urea nitrogen (BUN) Creatinine Glucose Complete Lipid Profile

Page 9: ACC/AHA Guidelines  STEMI

Supplemental oxygen should be administered to patients with arterial oxygen desaturation (SaO2 < 90%)…Class I (B)

• It is reasonable to administer supplemental oxygen to all patients with uncomplicated STEMI during the first 6 hours…Class II a

NTG : Patients with ongoing ischemic discomfort should receive sublingual NTG (0.4 mg) every 5 minutes for a total of 3 doses, after which an assessment should be made about the need for intravenous NTG. Class I (C)

IV NTG is indicated for relief of ongoing ischemic discomfort that

responds to nitrate therapy, control of hypertension, or management of pulmonary congestion. Class I

Class III• systolic pressure < 90 mm Hg or ≥ to 30 mm Hg below baseline• severe bradycardia (< 50 bpm)• tachycardia (> 100 bpm) or• suspected RV infarction.• who have received a phosphodiesterase inhibitor for erectile

dysfunction within the last 24 hours (48 hours for tadalafil).9

Page 10: ACC/AHA Guidelines  STEMI

• Analgesia Analgesia • Morphine sulfate (2 to 4 mg intravenously with increments of 2 to

8 mg intravenously repeated at 5 to 15 minute intervals) is the analgesic of choice for management of pain associated with STEMI. [Class I]

• NSAIDS should be discontinued immediately at the time of

STEMI ..d/t Increased risk of cardiovascular events [A substudy analysis from the ExTRACT TIMI-25 trial ….increased risk of death, reinfarction, heart failure, or shock among patients on NSAIDs

within 7 days of enrollment].

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• Aspirin Aspirin • Aspirin 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).. maintenance dose of 75 to 162 mg) should be given indefinitely after STEMI to all patients without a true aspirin allergy.

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III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

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• ThienopyridinesThienopyridinesIn patients for whom PCI is planned, clopidogrel should be started and continued:

• ≥ 1 month after bare-metal stent

• ≥ 3 months after sirolimus-eluting stent

• ≥ 6 months after paclitaxel-eluting stent

• Up to 12 months in absence of high risk for bleeding.

• CABG planned ?... the drug should be withheld for at least 5 days, and preferably for 7 days, unless the urgency for revascularization outweighs the risk of excessive bleeding.

• Probably indicated in patients receiving fibrinolytic therapy who are unable to take aspirin because of hypersensitivity or GI intolerance. 12

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

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• Beta Blockers

• Oral β blockers should be given promptly to those pts without a C/I, irrespective of concomitant fibrinolytic therapy or PCI..Class 1 (A)

• It is reasonable to administer IV β -blockers promptly to STEMI patients without C/I, esp if a tachyarrhythmia or SHT is present Class IIa (B) …. [COMMIT/CCS-2……. end points were not significantly reduced by metoprolol. For every 1000 pts treated…5 fewer episodes of reinfarction & VF, but 11 more episodes of cardiogenic shock. The excess of CS was seen chiefly from Days 0 to 1 after hospitalization, whereas the reductions in reinfarction and VF appeared from Day 2 onward ..

• avg relative increase in CS..30%, with higher rates for those >70 yrs, or SBP <120 mm Hg, or presenting HR >110 bpm, or with Killip class >1.

• Pts with sinus tachycardia or AF should have LV function rapidly evaluated before IV BBs. From Day 2 onward, when beneficial effects on reinfarction and VF are seen, administration of 200 CR oral metoprolol

daily appears to be safe in stable patients. It is prudent to initiate with 50 mg orally every 6 hours, transitioning to a dose equivalent to 200 mg /d orally or the maximum tolerated dose.]

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• GlycoproteinGlycoprotein IIb/IIIa InhibitorsIIb/IIIa Inhibitors• It is reasonable to start abciximab as early as possible before primary PCI (with or without stenting) in patients with STEMI.

• Tirofiban or eptifibatide may be considered before primary PCI

(with or without stenting) in patients with STEMI.

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III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

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ReperfusionReperfusion• Most imp… minimize total ischemic time [time from onset of

symptoms to initiation of reperfusion therapy]….[timely use of some reperfusion therapy is likely more important than the choice of therapy].

• TIME IS MYOCARDIUM…time - dependent “ wave - front ” of myocardial necrosis beginning at the subendocardium and moving towards the epicardial surface.

• goal ..rapid Rx… keep total ischemic time within 120 minutes (ideally within 60 minutes) … door-to- needle within 30 mts or that door-to-balloon within 90 mts.

• Fibrinolytics VS PCI

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• Fibrinolytics…plasminogen activators, • directly or indirectly converts the

proenzyme plasminogen to plasmin [cleaving the arginine 560 - valine 561 bond].

• Plasmin degrades several proteins, including fibrin, fibrinogen, prothrombin, and factors V and VII.

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• tPA…recomb DNA tech .. five domains: finger, epidermal growth factor, kringle 1 and kringle 2, and serum protease[resp for enzymatic activity] .. inhibited by circulating PAI - I, so rapidly cleared (half - life about 5 minutes). So needs bolus/infusion regimens (over 1 – 3 hours).. The accelerated dose regimen over 90 minutes produces more rapid thrombolysis than the standard 3-hour infusion of t-PA.

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rPA…non - glycosylated, single chain deletion variant consisting only of the kringle 2 and proteinase (plasmin cleavage site) domains of human tPA. TNK – tPA…mutant of t-PA with specific amino acid substitutions in the kringle 1 domain and protease domain ...decrease plasma clearance, increase fibrin specificity, and reduce sensitivity to PAI-1.

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Effects on coronary arterial patency• Granger et al…14124 angiographic observations from 58 studies. Without fibrinolytic therapy, spontaneous perfusion …15% and 21%

at 60 and 90 minutes after study entry, respectively, remains unchanged at 1 day, then gradually increases to about 60% by 3 weeks.

All fibrinolytic regimens improve early patency rates.• patency rates at > 3 hours were similar for all regimens, and

reocclusion rates were higher after tPA than non - fibrin specific (systemically active) agents (13% vs 8%) (P =0.002).

• The GUSTO angiographic study …. early but not late patency rates accurately predict mortality differences among AMI therapies.

• Studies showing mortality benefit with FT• GISSI…1st definitive mortality trial..11806 pts….SK vs standard

rx.Aspirin not given.Inhosp mortality [10.7 vs 13%...P 0.0002]…also showed time dependant benefit

• ISIS-2…17187 pts … SK vs Asp vs both vs placebo…35 d mort reduced by 23% by asp .. 25 % by SK42 % by both..all P <0.00001

• ASSET study…tPA vs heparin..30 d mort 7.2 vs 9.8 % P 0.001122

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• Fibrinolytic Therapy Trialists Collaborative Group …. database from nine controlled trials…58600 pts of whom 6177 (10.7%) died, 564 (1.0%) had strokes, and 436 had major non - cerebral bleeds.

The 45000 patients who presented with STE or BBB had an absolute mortality reduction of 30 per 1000 for Rx within the first 6 hours, 20/1000 for hrs 7 – 12, and a statistically uncertain reduction of 13 per 1000 beyond 12 hours.

• These data led to the national guidelines ( Class I, Level A ) that all STEMI patients should undergo rapid evaluation for reperfusion therapy and have a reperfusion strategy implemented promptly after contact with the medical system.

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• Those with BBB & Ant STE benefit the most with FT.

• Those with normal ECGs or with ST depression alone showed no benefit and adverse trends (7 and 14 more deaths per 1000, respectively).

• The magnitude of mortality reductions in FTT was dependent on time to therapy from symptom onset.

• For those with STE or BBB, the absolute benefit was 39 (0 –1 h), 30( >1–3 h), 27( >3-6 h), 21(>6–12 h) & 7 (>12–24h) lives saved /1000 treated 24

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mortality in each subgroup of fibrinolytic treated (black bars) versus placebo - treated

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Very early therapy can even abort a myocardial infarction. Role of fibrinolytic therapy in the prehospital setting. So the ACC/AHA guidelines have given a indication ( Class IIa, Level A) for the establishment of a prehospital fibrinolysis protocol in (1)settings in which physicians are present in the ambulance or (2) well - organized EMS systems with full - time paramedics who have 12 - lead ECGs in the field with transmission capability, paramedic initial and ongoing training in ECG interpretation and STEMI treatment, on - line medical command, a medical director with training/experience in STEMI management, and an ongoing continuous quality improvement program.

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The benefit of fibrinolysis after 6 hours is less certain • LATE study….5711 pts …MI 6 - 24 hours …tPA (100 mg over 3h)

or placebo. A 26% relative mortality reduction (8.9% vs 11.9%, P= 0.02) was observed for those treated within 12 hours. The 12 – 24 hour subgroup showed a non - significant trend to benefit (8.7% vs 9.2% mortality rate).

• The South American EMERAS collaborative group ….4534 pts with IV SK or placebo within 24 hours after suspected AMI and found a non - significant trend towards a mortality benefit b/n 7 &12 hrs (SK 11.7%, placebo 13.2%).

This provides the rationale for recommending FT 7-12 hrs group with persistent symptoms and ECG changes.

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CONTRAINDICATIONS for FT

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• Risks of FTICH is the most imp risk, occurring in about 0.5 – 1.0% ….risk of

fatality (44 – 75%). MC with fibrin selective agents 7 predictors of ICH [GUSTO-1 group]….advanced age, lower

weight, h/o cerebrovascular disease, h/o hypertension, higher SBP/DBP on presentation, and randomization to tPA (vs SK). In contrast, the incidence of non cerebral bleeding is higher with SK.

Allergy, hypotension, and fever Anaphylaxis or bronchoconstriction is rare ( < 0.2 – 0.5%). SK may acutely release bradykinin, a vasodilator. The incidence of clinical hypotension after SK (11.8%) was greater

than after tPA (7.1 %); Repeat thrombosis and its associated reinfarction is a known,

potentially devastating risk after fibrinolytic therapy.

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• Comparative fibrinolytic trials :• ASSENT – 2………compared weight - adjusted TNK (as a 30 – 50

mg bolus over 5 – 10 seconds) and accelerated rt - PA. All patients received aspirin and heparin. 30 day mortality rates were virtually identical [6%]..

A lower mortality rate with TNK - tPA was observed among patients presenting 4 hours after symptom onset (7.0% vs 9.2%), which may be due to either greater activity of the more fibrin - specific TNK - tPA against older, fibrin - rich clots or chance.

• GISSI-2…..ISIS-3…..tPA vs SK….mortality rates at 35 days were similar

• GUSTO…. The primary endpoint, 30 - day mortality, was lowest with accelerated tPA with IV heparin compared to SK with IV/SC heparin

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• FT in elderly : Analyses restricted to elderly patients with clear indications for

fibrinolytic therapy suggested similar or greater absolute benefit vs younger patients.

? Safety concerns……..SK, which carries a lower risk of ICH, or PCI should be considered as preferred reperfusion strategies in the elderly.

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• FibrinolysisFibrinolysis• CLASS ICLASS I • symptom onset within the prior 12 hours. [AA]• symptom onset within the prior 12 hours and new or presumably

new left bundle branch block (LBBB). [AA]

• CLASS II a CLASS II a • symptom onset within the prior 12 hours and 12-lead ECG findings

consistent with a true posterior MI. [C]• symptoms of STEMI beginning in the prior 12 to 24 hours who have

continuing ischemic symptoms and ST elevation > 0.1 mV in ≥ 2 contiguous precordial leads or ≥ 2 adjacent limb leads. [B]

• CLASS IIICLASS III• initial symptoms of STEMI began more than 24 hours earlier• 12-lead ECG shows only ST-segment depression, except if a true

posterior MI is suspected.

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Assessment of Reperfusion after fibrinolysisAssessment of Reperfusion after fibrinolysisIt is reasonable [Class IIa ] to monitor• the pattern of ST elevation,cardiac rhythm and clinical symptoms

over the 60 to 180 mts after initiation of fibrinolytic therapy.

Noninvasive findings s/o reperfusion include: Relief of symptoms Maintenance and restoration of hemodynamic and/or electrical

instability Reduction of ≥ 50% of the initial STE pattern on follow-up ECG 60

to 90 minutes after initiation of therapy.

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PCI vs Fibrinolysis for STEMI:PCI vs Fibrinolysis for STEMI: early randomized trials tended to favor direct balloon angioplasty

over fi brinolysis in certain settings. [PAMI…395 pts…with in 12 hrs …PCI vs tPA … PCI reduced the composite outcome].

In a meta analysis of 23 randomized STEMI trials comparing primary PCI with FT, significant reductions in short - term (4 – 6 weeks) and long term (6 – 8 months) mortality, non - fatal MI, and stroke were seen. Regardless of whether the fibrinolytic was fibrin specific,primary pci showed similar benefit.

Greatest benefit with pci is seen in high risk settings as in Cardiog shock.. as shown in SHOCK trial…302 pts with CS….emergency revascularsn vs medical stabilisn….Significant mortality reduction is seen @ 6 months 50% vs 63 %... P 0.03.

• As the delay for performing PCI increases, the mortality benefit for primary PCI over fibrinolysis decreases. Compared with a fibrin - specific lytic agent, a PCI strategy may not reduce mortality when a delay > 60 minutes is anticipated vs immediate FT [Nallamothu et al JACC 2003]

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TYPE OF REPERFUSION THERAPY ? STEP 1….. Assess Time and Risk(a)Time Since Symptom Onset(b)Risk of STEMI….TIMI RISK SCORE…Mortality benefit with PCI is high in pts at highest mortality risk.So as the risk decreases the mort benefit also decreases such that mort adv vs FT wont be seen in pts with estimated 30 d mort rate b/w 2-3%.

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(c)Risk of fibrinolysis…(Risk factors for ICH ….increased age, low body weight, and hypertension on admission)….when no PCI is available, FT should still be favored over no reperfusion until the risk of a life-threatening bleed exceeds 4 %.

(d)Time to reach a skilled PCI lab• If presentation is < 3 hours and there is no delay to an invasive

strategy, there is no preference for either strategy.

• Fibrinolysis generally preferred 1. Early presentation ( ≤ 3 hours from symptom onset) and delay to

invasive strategy

2. Invasive strategy not an option Cath lab occupied or not available Vascular access difficulties

No access to skilled PCI lab

3. Delay to invasive strategy Prolonged transport

Door-to-balloon more than 90 minutes > 1 hour vs fibrinolysis (fibrin-specific agent) now

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• Invasive strategy generally preferred Skilled PCI lab available with surgical backup [Team experience

greater than a total of 36 Primary PCI cases/yr & Operator experience > a total of 75 primary PCI cases/yr].

Door-to-balloon < 90 minutes (Door-to-Balloon) – (Door-to-Needle) is <1 hour High Risk from STEMI

Cardiogenic shock, Killip class ≥ 3

Contraindications to fibrinolysis, including increased risk of bleeding (ICH)

Late presentation … > 3 hours from symptom onset

Diagnosis of STEMI is in doubt

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Primary PCIPrimary PCI…CLASS I [A]…CLASS I [A]

Patient with STEMI (including posterior MI) or MI with new or presumably new LBBB

PCI of infarct artery within 12 hours of symptom onset

Balloon inflation within 90 minutes of presentation

Skilled personnel available (individual performs > 75 procedures per year)

Appropriate lab environment (lab performs > 200 PCIs/year of which at least 36 are primary PCI for STEMI)

Cardiac surgical backup available

CLASS I [B]CLASS I [B]

Medical contact–to-balloon or door-to-balloon should be within 90 minutes.

PCI preferred if > 3 hours from symptom onset

Severe CHF and/or pulmonary edema and onset of symptoms within 12 hrs. 38

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• CLASS II a [C]CLASS II a [C]• onset of symptoms within the prior 12 to 24 hours and 1 or more

of the following:

• a. Severe CHF

• b. Hemodynamic or electrical instability

• c. Persistent ischemic symptoms.

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PCI for Cardiogenic PCI for Cardiogenic ShockShock

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• Primary PCI in Cardiogenic shockPrimary PCI in Cardiogenic shock• CLASS I …CLASS I …patients less than 75 years old with ST elevation or

LBBB who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock.

• CLASS II a …CLASS II a … Those >75 years with ST elevation or LBBB who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock.

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PCI After FibrinolysisPCI After FibrinolysisIn patients whose anatomy is suitable, PCI should be performed for

the following: ie CLASS ICLASS I Objective evidence of recurrent MI [C] [C] Moderate or severe spontaneous/provocable myocardial ischemia

during recovery from STEMI [B] [B] Cardiogenic shock or hemodynamic instability [B][B]

CLASS IIa ...CLASS IIa ...routine PCI in patients with left ventricular ejection fraction (LVEF) ≤ 0.40, CHF, or serious ventricular arrhythmias.

CLASS IIa ...CLASS IIa ...documented clinical heart failure during the acute episode, even though subsequent evaluation shows preserved LV function (LVEF > 0.40).

CLASS IIb CLASS IIb Routine PCI might be considered as part of an invasive strategy after fibrinolytic therapy. [B] [B]

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• Direct stenting vs FT…..Schomig et al, Le May et al, Kastrati et al….superior outcome with stenting

• Primary angioplasty vs primary stenting…meta analyses…no diff in mortality or renifarction..but MACE was reduced due to reduction in TVR with stenting

• DES vs BMS…..DES signif reduce restenosis,TVR …• Trials showing the safety of DES …

TYPHOON,PASSION,SESAMY,MULTISTRATEGY trials..

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Facilitated PCI Facilitated PCI using regimens other than full-dose fibrinolytic therapy might be considered as a reperfusion strategy when all of thefollowing 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).

A planned reperfusion strategy using full-dosefibrinolytic therapy followed by immediate PCI is not recommended and may be harmful.

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Intracoronary aspiration/ thrombectomy devicesSignifi cant clot burden may complicate acute STEMI management. Prospective clinical studies have shown that intracoronary thrombectomy and thrombus aspiration may improve TIMI - 3 fl ow, hasten ST segment elevation resolution, and enhance myocardial tissue perfusion and reduce MI. TAPAS trial…pts randomized to initial aspiration thrombectomy vs standard PCI regardless of the presence or absence of angiographically visible thrombus. At 1yr follow - up, cardiac death was 3.6% (19 of 535) vs 6.7% (36 of 536) (P=0.020). One - year cardiac death or non - fatal reinfarction occurred in 5.6% (30 of 535) vs 9.9% (53 of 536) of patients in the conventional PCI group (P=0.009).So when performing primary PCI for STEMI, aspiration thrombectomy prior to balloon inflation should be performed whenever possible.

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Embolization protection devices…. no benefit has been found when applied to native vessels in the setting of STEMI

• DEDICATION Trial….626 patients with STEMI and undergoing primary PCI were randomized to distal protection using the FilterWire or standard therapy. There was no significant difference in the occurrence of the primary endpoint of complete ( = 70%) ST segment resolution (76% vs 72%, P= 0.29), no difference in maximum troponin - T (4.8 µ g/L and 5 µ g/L, P =0.87) or maximum CK- MB (185µ g/L and 184 µg/L, P= 0.99), and no difference in median LV wall motion index (1.70 vs 1.70, P=0.35). The rate of major adverse cardiac and cerebral events 1 month after PCI was 5.4% with distal protection and 3.2% with conventional treatment (P=0.17).

• So when performing primary PCI for STEMI, use of distal protection devices during balloon inflation is not generally recommended ( Class III, Level A).

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• EMERGENCY CABG•

Class I   a. Failed PCI with persistent pain or hemodynamic instability    b. Persistent or recurrent ischemia refractory to medical therapy ; have a significant area of myocardium at risk, and are not candidates for PCI or fibrinolytic therapy.    c. At the time of surgical repair of postinfarction VSR or MR   d. Cardiogenic shock in pts <75 years old with STE/LBBB/PW MI who develop shock within 36 hrs of STEMI, have severe multivessel or left main disease, and are suitable for revascularization that can be performed within 18 hrs of shock, unless further support is futile because of the patient’s wishes or contraindications/unsuitability for further invasive care.    e. Life-threatening ventricular arrhythmias in the presence of > 50% LMCA stenosis &/or TVD

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Class IIa• Can be useful as primary reperfusion strategy in patients

who have suitable anatomy, who are not candidates for fibrinolysis or PCI, and who are in the early hours (6 to 12 hours) of an evolving STEMI, esp if severe multivessel or LMCA disease is present.

• can be effective in selected pts 75 years or older with STE/LBBB/PW MI who develop shock within 36 hrs of STEMI, have severe multivessel or left main disease, and are suitable for revascularization that can be performed within 18 hrs of shock.

Class III• persistent angina and a small area of risk if they are

hemodynamically stable. • successful epicardial reperfusion but unsuccessful

microvascular reperfusion. 

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• ANCILLARY THERAPY TO REPERFUSION

• Anticoagulants….• more prolonged anticoagulant therapy…..beneficial… (duration of

index hospitalization) in pts receiving fibrinolytics, as seen in the comparisons of reviparin versus placebo (CREATE), fondaparinux versus placebo (OASIS-6), and enoxaparin versus UFH (ExTRACT-TIMI 25).

• The mechanism of benefit from a more prolonged regimen ….includes a longer exposure to anticoagulants to prevent rethrombosis of the infarct artery and prevention of the rebound increase in events seen after abrupt discontinuation of UFH infusions.

• Overall, UFH does not appear to improve early (60 – 90 mt) IRA patency.

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UFH in those on FT : FT release of plasmin..activates platelets ; also triggers thrombin generation via factor V activation.As the free plasmin activity increases (SK),prothrombotic effect will be more marked..

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• UFH in primary PCI :• There are no large - scale data to guide the use of UFH

in PCI and thus it remains relatively empiric. The existing data are from small scale studies from pts undergoing elective procedures.. A meta - analysis of six RCTs suggested optimal benefit with an initial bolus of 70 – 100 U/kg aiming for an ACT of 350–375 s. In patients treated with a Gp IIb/IIIa receptor antagonist, this should be reduced to 50 – 70 U/kg, aiming for an ACT of 200 s.

• LMWH : advantages …more predictable level of anticoagulation & so no need for mandatory laboratory monitoring; a reduction in the incidence of thrombocytopenia, less platelet activation and an easier route of administration.

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• LMWH in pts receiving FT : Trials taken together …. suggest a modest advantage of LMWH over UFH that appears to be d/t enhanced late patency of the infarct - related vessel and an associated reduction in reinfarction rate.

• CREATE Trial… Reviparin vs placebo x 7d.. 15000 STEMI pts…India & China….Primary endpoints of death,MI,stroke was reduced in those treated with reviparin vs placebo at 7 days (9.6 vs 11 %; P=0.0049) and 30 days (11.8% versus 13.6%, P = 0.0014).

ASSENT - 3 trial… 6095 pts were randomized to full - dose TNK + UFH for at least 48 hours, full - dose TNK with enoxaparin x 7d or reduced - dose TNK with abciximab and UFH. The composite of death, reinfarction or refractory ischemia was significantly lower in those treated with enoxaparin than UFH (P=0.0002). This advantage was primarily d/t a reduction in the rate of reinfarction. However, there was an increased incidence of bleeding complications in those treated with enoxaparin compared to UFH

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ExTRACT - TIMI 25 trial :Randomized 20506 pts with STEMI undergoing fibrinolysis to receive

either enoxaparin (30 mg IV bolus followed by 1 mg/kg throughout the index hospitalization) or UFH (60 U bolus followed by 12 U/kg/h for 48 hours). The primary endpoint of death or reinfarction at 30 days occurred in 12.0% (UFH) and 9.9% (enoxaparin) P<0.001. TIMI major bleeding was increased in the enoxaparin group vs UFH (2.1% vs 1.4%, P<0.001) whilst rates of ICH were similar (0.8% vs 0.7% respectively..P=0.14).

Impaired Renal function ((CrCl<90 mL/min) were a/w increased bleeding

So…..LMWHs are a useful alternative to UFH in STEMI in conjunction with FT and should be administered throughout the index hospitalization (up to eight days) ( Class I, Level A).

LMWH in pts Rxed with primary PCI : There are limited data regarding the safety and efficacy of LMWHs during PCI in the context of STEMI.

[LMWHs are a reasonable alternative to UFH in patients with STEMI undergoing primary PCI ( Class IIb, Level B).]

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Direct Thrombin InhibitorsBivalirudin : HERO-1 trial..412 pts… UFH vs low dose bivalirudin

(0.125mg/kg bolus followed by a 0.25 mg/ kg/h infusion for 12 h, then 0.125 mg/kg/h) vs high - dose bivalirudin (0.25 mg/kg bolus followed by a 0.5 mg/kg/h infusion for 12 h, then 0.25 mg/kg/h).

TIMI 3 flow at 90 – 120 mts was higher following bivalirudin than UFH (48% with high dose bivalirudin, 46% with low dose bivalirudin and 35% with UFH, P=0.024).

Larger HERO - 2 trial randomized 17073 pts to receive a bolus and 48 h infusion of bivalirudin or UFH immediately prior to SK. At 30 days, mortality was similar.

ARGAMI-2 trial….1001 pts to UFH or argatroban (Univalent DTI) (120µg bolus followed by a 4µg/kg/ min infusion for 72h) in addition to fibrinolysis with SK or alteplase. A third treatment arm consisting of half - dose argatroban was terminated prematurely due to lack of effi cacy. Mortality at 30 days was similar (5.5% in the argatroban group versus 5.7% in UFH group,P=ns).

Meta -analysis of DTI trials[UFH vs DTI] (by DTI Trialists Collaborative Group)…. No diff in mort was seen at cessation of Rx/7d/30d/6 months, but signif reduction in incidence of reinfarction /combined incidence of death/MI were seen.

So Bivalirudin is a useful alternative to UFH in STEMI along with FT..Class I

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DTI in primary PCIHORIZONS-AMI trial….3600 STEMI pts undergoing primary PCI …UFH

+ GpIIbIIIa- VS Bivalirudin. There was a reduction in overall clinical events (a composite of major bleeding and MACE) in the bivalirudin group at 30 days compared to the UFH and glycoprotein IIb/IIIa receptor antagonist group (12.1% versus 9.2% respectively, P = 0.006).

Major bleeding alone at 30 days was also substantially reduced (8.3% versus 4.9%, P<0.0001) and there was a signifi cant reduction in cardiac death at 30 days (2.9% versus 1.8%, P = 0.035).

The initial data demonstrate an excess in adverse events with bivalirudin only within the first 24 hours, probably related to an excess incidence of early stent thrombosis (1.3% versus 0.3% with UFH and glycoprotein IIb/IIIa receptor antagonist). However, the subsequent reduction in events seen in those treated with bivalirudin results in an overall benefit in favor of bivalirudin at 30 days, likely to be driven by a reduction in bleeding complications.

Bivalirudin is a reasonable alternative to the combination of UFH and a glycoprotein IIb/IIIa receptor antagonist in patients with STEMI undergoing primary PCI ( Class IIa, Level B ).

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Fondaparinux: Based upon the results from OASIS trials….Fondaparinux is a useful

alternative to UFH in STEMI patients who have received fibrinolytic therapy ( Class I, Level B )

Fondaparinux should not be used as the sole anticoagulant in patients with STEMI undergoing primary PCI ( Class III, Level B)…

OASIS-6 trial1) benefit of fondaparinux vs UFH or placebo on the primary

endpoints of death and recurrent MI in pts on FTwas not seen in patients undergoing primary PCI

2)d/t higher rate of guiding catheter thrombosis & more coronary complications (abrupt coronary closure,new angiographic thrombus,catheter thrombus,no reflow,dissection or perforation)

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• Ancillary Therapy to ReperfusionAncillary Therapy to Reperfusion

UFH should be given [CLASSCLASS I] intravenously in: Patients undergoing PCI or surgical revascularization [C] After alteplase, reteplase, tenecteplase [C] After streptokinase, anistreplase, urokinase in patients at high risk

for systemic emboli [B]

CLASSCLASS I Platelet counts should be monitored daily in pts taking UFH [C]

CLASSCLASS IIb LMWH might be considered an acceptable alternative to UFH in pts less than 75 years who are receiving fibrinolytic therapy in the absence of significant renal dysfunction. [B]…..Enoxaparin used with tenecteplase is the most comprehensively studied.

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• Other Pharmacological MeasuresOther Pharmacological Measures• Angiotensin converting enzyme inhibitors

• Angiotensin receptor blockers (ARB)

• Aldosterone blockers

• Glucose control

• Magnesium

• Calcium channel blockers

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• ACE/ARB: Within 24 HoursACE/ARB: Within 24 Hours• An ACE inhibitor should be administered orally within the first 24

hours of STEMI to the following patients without hypotension or known class of contraindications:Anterior infarction,

pulmonary congestion,

LVEF < 0.40.• An ARB should be given to ACE-intolerant patients with either

clinical or radiological signs of HF or LVEF < 0.40.

• An intravenous ACE inhibitor should not be given to patients within the first 24 hours of STEMI because of the risk of hypotension

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III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

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• Strict Glucose Control During STEMIStrict Glucose Control During STEMI• An insulin infusion to normalize blood glucose is recommended for

patients and complicated courses.

• It is reasonable to administer an insulin infusion to normalize blood glucose even in patients with an uncomplicated course.

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III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

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Hemodynamics: Increased RA pressure (y descent)Square root sign in RV tracing

Rx:Maintain RV preloadLower RV afterload (PA---PCW)Inotropic supportReperfusion

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Right Ventricular InfarctionRight Ventricular Infarction

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• Secondary Prevention and Long Term Management

• Smoking Goal: Complete Cessation• Blood pressure control:• Goal: < 140/90 mm Hg or <130/80 mm

Hg if chronic kidney disease or diabetes• Physical activity:Minimum goal:30

minutes 3 to 4 days per week;Optimal daily

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• Weight management:• Goal: BMI 18.5 to 24.9 kg/m2

• Waist circumference: Women: < 35 in. Men: < 40 in.• Diabetes management: Goal: HbA1c <

7%

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Lipid management:TG <200 mg/dLPrimary goal:LDL-C << than 100 mg/dLStart dietary therapy in all patients (< 7% of total calories as saturated fat and < 200 mg/d cholesterol). Promote physical activity and weight management. Encourage increased consumption of omega-3 fatty acids. Assess fasting lipid profile in all patients, preferably within 24 hours of STEMI.

TG 200 mg/dL or greater : Primary goal: Non–HDL-C << 130 mg/dL

TGs ≥ 150 mg/dL or HDL-C < 40 mg/dL:Emphasize weight mgt and physical activity. Advise smoking cessation.TG 200 to 499 mg/dL: After LDL-C–lowering therapy, consider adding fibrate or niacin.TG ≥ 500 mg/dL: Consider fibrate or niacin before LDL-C–lowering therapy.Consider omega-3 fatty acids as adjunct for high TG.

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• Hormone therapy with estrogen plus progestin should not be given de novo to postmenopausal women after STEMI for secondary prevention

of coronary events.

• Postmenopausal women who are already taking estrogen plus

progestin at the time of STEMI should not continue hormone

therapy.

• However, women who are beyond 1 to 2 years after initiation

of hormone therapy who wish to continue such therapy for

another compelling indication should weigh the risks and benefits.

• Antioxidant vitamins such as vitamin E and/or vitamin C

supplements should not be prescribed to patients recovering from

STEMI to prevent cardiovascular disease. 68

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

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• The psychosocial status of the patient should be evaluated, including inquiries regarding symptoms of depression, anxiety, or sleep disorders and the social support environment.

• Treatment with cognitive-behavioral therapy and selective serotonin reuptake inhibitors can be useful for STEMI patients with depression that occurs in the year after hospital discharge.

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III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

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HAPPY NEW YEAR

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