ACS (Acute)

    Sources:

    1.  MKSAP16 / MKSAP 17

    2.  2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction

    3.  CCS: Management of Patients With Refractory Angina - A Canadian Cardiovascular Society/Canadian Pain Society Joint Guidelines

    4.  2004STEMI: ACC/AHA Guidelines

     

     

    Introduction / Classification

    • "Acute MI is an event of myocardial necrosis caused by an unstable ischemic syndrome" (NEJM 2017)
    • In practice, the disorder is diagnosed and assessed on the basis of clinical evaluation, the electrocardiogram (ECG), biochemical testing, invasive and noninvasive imaging, and pathological evaluation.
    • All patients suspected of having an ACS should be referred to an Emergency Department with the goal of making an evaluation within 10min (AHA/ACC guidelines).
    • During initial evaluation, the clinician must determine if an ACS is present, and whether it fits one of the following clinical syndromes: (important for management)
    • (taken from Anderson et al NEJM 2017)

       

    • NEJM MI diagram.jpeg

     

    • Decide if STEMI or NSTEMI, differentiation is important because:
      • STEMI
        • = EMERGENCY!
        • Represents a complete occlusion of a coronary vessel.
        • Clear mortality benefit of EARLIEST POSSIBLE reperfusion in STEMI, (<90min of chest discomfort) with thrombolytic therapy or primary PCI.
      • Unstable Angina or NSTEMI
        • Have some time to work up and treat patient
        • Represents as narrowing of a coronary vessel or an unstable plaque at high risk of rupturing.
        • Should undergo risk stratification if early invasive strategy (angiography) vs. medical therapy
        • Often initiate medical therapy, use TIMI risk score to find risk of future CV events, symptoms, LV dysfunction, etc.. All these high risk features can drive earlier intervention.
          • Use TIMI risk score to risk-stratify
    • General Pathway for ACS:
    • ACSPathway2.png
    • Physical Exam:    
      • Look for direct evidence of MI, as well as possible precipitants, risk factors, and consequences (i.e. HF)
      • Inspection:
        • Obesity?
        • Evidence of hyperlipidemia (Xanthelasma/xanthomata)
        • Herpes Zoster
      • Vital signs
      • Cardiac Exam:
        • JVP
        • Heart Sounds/ Murmurs
        • Reproducible on palpation? 
      • Presence of PVD
        • Carotid/renal/femoral bruit
        • Peripheral pulses
        • Abdominal Aneurysm
     

    Unstable Angina / NSTEMI

    Risk Stratification

    • For NSTEMI, use TIMI risk score to determine in-patient risk of CV events.
    • Many TIMI trials... finally came up with:
      • TIMI Prognostic Variables (each = one point)

        Age ≥65 years

        ≥3 Traditional CAD risk factors (HTN, DMII, Hyperlipidemia, FMhx, Smoking)

        Documented CAD with ≥50% diameter stenosis

        ST-segment deviation

        ≥2 Anginal episodes in the past 24 hours

        Aspirin use in the past week

        Elevated cardiac biomarkers (CK MB or troponin)

        TIMI Risk Score (Sum of Prognostic Variables)

        0-2 Low risk

        3-4 Intermediate risk

        5-7 High risk

     

    • NOTE: ASA --> highlights having active ischemia despite being on therapy. 
    • NOTE FOR U.S. EXAMS: GpIIAIIIB inhibitors
      • Often useful in elevated cardiac markers, and ongoing ischemia (high risk TIMI ≥5)... particuarly useful in early invasive strategy.
      • Rarely used in Canada.

     

    NSTEMItimi.png

    (Source: MKSAP 16)

     

    • In above table, the term "Early coronary angiography" timing is unclear.
      • TIMCS and ISAR-COWL studies have conflicting data. 
      • Usually for clinically stable patients unclear when the best time to do the invasive procedure.
      • No clear indication for benefit of a very rapid vs. delayed strategy (few days after presentation). 

     

    Treatment

    • Treat all patients with:
    • Tx

      Comments

      Controls

      ASA-160mg PO chewed

      • Up to 21% decrease in mortality

      Antiplatelet

      B-blocker

      • Usually metoprolol PO 25mg BID
      • In past used IV as well (not anymore)
      • Not if HR <60-70 or CHF
      • Careful with conduction problems on ECG
      • If already on B-B give extra dose
      • (Lately: controversial, IV dose can increase incidence of cardiogenic shock in MI pts).

      B-blocker

      Heparin

      • UFH if >75, obese or sig renal failure
      • LMWH otherwise
      • Fondaparinux also an option
      • Bivalirudin can be used if history of HIT.
      • For UA or NSTEMI:

        • Enoxaparin for 8 days or until discharged [ESSENCE trial] - preferred to UFH
        • UFH x 48hrs if not revascularized (longer if still chest pain)
      • For STEMI:
        • UFH or LMWH (no difference) if NOT reperfused
        • UFH preferred over LMWH for PCI or lytic therapy

      Anticoag.

      Second Antiplatelet

      Plavix (Clopidogrel)

        (Given with ASA - dual anti-plt)

         - NSTEMI: 300mg load + 75mg

          po daily

         - STEMI: 600mg load.

      OR

      Prasugrel OR Ticagrelor

      • Proven with STEMI when added to ASA
      • The only issue is if you suspect triple-vessel disease, patient may need CV surgery, do not give plavix (will delay OR).

      Antiplatelet

      Gp IIb/IIIa inhibitors

      If TIMI ≥5 (in NSTEMI)

      Antiplatelet

      Nitroglycerin 0.3mg SL q5min x3

      (IF NO RV Infarct!)

      • Give sublingual nitrates to all patients except pts in inferior MI and evidence of RV involvement.
      • Suspect RV infarct on all inferior infarcts - do 15 lead ECG to confirm (ST elevation in V4R lead)
        (SEE BELOW)
      • Mechanism: reduce preload, drops venous capacitance, improves coronary flow
      • If continued chest pain, start nitro drip.

      Pain

      Morphine(1-2mg IV/SC x1)

      • Suppresses heightened sympathetic response, helps beyond pain

      Pain

      O2

      (Only if hypoxemia)

      • Only if hypoxemia, but all patients end up getting it.

       

      **Red – Improves survival

      **Green – Symptom Management

      **Blue - Longer Term management:

      •  
    • NOTE: No indication for antiarrhythmics (like lidocaine) to prevent ventricular arrhythmias.

     

    Special: RV Involvement

    • In RV infarcts, must give lots of volume to push blood through weak RV. (think of it as if it becomes a "passage chamber").  
    • Giving nitrates will decreases passage, LV preload, leading to hypotension and cardiogenic shock.  This is called "preload dependent".
    • If R-sided HF (high JVP etc) with clear lung fields, hypotension --> suspect RV infarct, give fluids
      • Ask for 15 Lead ECG for V3R and V4R leads (look for 1mm STE)

    Mortality Benefit

    • 1. ASA + clopidogrel/prasugrel/ticagrelor
    • 2. B-Blocker (if heart rate and BP permit)
    • 3. Anticoagulation
      • Examples:
        • Heparins (used in low TIMI risk, but provides more benefit in medium+high risk groups).
          • Unfractionated Heparin (early invasive approach,  in setting of kidney disease)
          • LMWH (Twice daily SC injection).
            OR
        • Direct Thrombin Inhibitors (Bivalirudin)
          • Used as an alternative to heparins.
          • ACUITY Trial: evaluated moderate-to-high risk unstable angina or NSTEMI treated with bivalirudin + GIIBIIIA vs. UFH+GpIIBIIIA vs. bivalirudin, undergoing early invasive strategy to evaluate coronary arteries.
            • Rates of death, MI, repeat revascularization was similar, but lower risk of bleeding complications in bivalirudin monotherapy group.
      • Decision to use them based on TIMI risk, timing of cath, consideration of risk of bleed etc.
    • Statins
      • Clearly has role in primary and secondary prevention.
      • Benefit of intense lipid lowering in early phase is unknown. 
      • Studies (MIRACL and PROVE IT trials): high dose statin therapy soon after ACS (i.e. within 24-96hrs), reduces long-term CV events at 18mo and 2 years.
      • 80mg of atorvastatin typically regarded as "intensive therapy" with a composite benefit (mortality, CV events etc..)
      • Current consensus: High dose statin, with an LDL target of (<100mg/dL or <2.59mmol/L).
        • I.e. 40 or 80mg of atorvastatin.

     

    Thrombolysis?

    • Use of thrombolytics studied, worsens outcomes in NSTEMI.

    Timing of Angiography

    • Optimal timing unclear for clinically stable patients.
    • TIMCS trial and ISARCOOL have conflicting information.
    • No clear indication for rapid strategy vs. more delayed (i.e. few days after presentation). 8

    STEMI

    • Important to triage patients to early reperfusion.
    • EMS do ECGs and triage patients
    • As for 2014 up to 1/3 of STEMI patients don't receive reperfusion therapy!!!
    • Rapid Assessment: (Many causes of CP and ECG STEMI including:)
      • Pericarditis
      • PE
      • Aortic dissection (inferior wall ST elevation) if dissection plane extends into RCA.
      • Must perform focused history (type of pain, prev CAD etc..).
        • Note: some patients (Diabetes with neuropathy, Elderly) come in with non-specific symptoms (SOB, confusion).
        • I.e. Longstanding diabetic presenting with DKA --> look for acute MI.
    • Step 1 - Decide if reperfusion therapy is indicated:
      • Symptom onset <12hrs -->  YES (Class I-A)
      • Symptom onset 12-24hrs --> USUALLY (Class IIa-B) - if evidence of ongoing ischemia (clinical/ecg)
      • Cardiogenic Shock, Severe HF (regardless of time from MI) --> (Class I Level B)

     

    • Step 2 - Decide if reperfusion therapy is Thrombolysis vs. PCI
      • FMC-to-Device would be > 2hrs ?   (FMC = First Medical Contact)
        • If >2hrs --> Thrombolysis  (perform within door-to-needle time of 30min)
        • If <2hrs --> PCI (transfer with door-in-door-out time of 30min) 
    • AHAACC2013 STEMI Guidelines.png

    Thrombolysis

    • Adjunctive therapy to support Thrombolysis
      • ASA 162mg before thrombolysis
      • Clopidogrel 300mg before thrombolysis (75mg dose for pts ≥ 75yo) --> continue for 2w to 1yr
      • Anticoagulation for at least 48hrs
        (duration: until end of hospitalization, up to 8 days, or until revascularized)
        • UFH (weight-based IV bolus + infusion, monitor aPPT 1.5-2.0 times control)
          • Continue x48hrs or until revasc
        • Enoxaparin (weight, age, CrCl dosing) IV bolus then in 15min SC injection
          • Continue for duration of hospitalization or until revasc
        • Fondaparinux initial IV dose, then in 24hrs daily SC injections (if CrCl > 30)
          • Continue for duration of hospitalization, up to 8 days, or until revasc
        • NOTE: All Class I indications evidence level B, but enox has level A.

     

    • Steps After thrombolysis:
      • Did Thrombolytics Work? 
        • Successful Reperfusion Indicators:

          1. Resolution of Chest Pain

          2. >70% ST-segment resolution on ECG (some say 50%)

          3. Reperfusion arrhythmias (such as AIVR)

        • If reperfused:
          • Risk stratify the patient based on risk of future CV events.
          • Arrange transfer to PCI center
          • Poor prognostic features requiring PCI transfer (based on old guidelines):
            • Cardiogenic Shock
            • Severe HF
            • Failed Reperfusion
            • Or other high-risk features (i.e.. low EF, hypotension, HF, shock)
            • (B/c concern large patient myocardium at risk, patient won't tolerate future MI.)  
        • If NOT reperfused
          • Urgent transfer to PCI-capable center for "rescue PCI"
    • Transfer to PCI Center:
      • NEW Evidence: Transfer to PCI center whether or not they reperfused, regardless if they have hemodynamic instability etc..
        • NEJM 2009 TRANSFER-AMI Trial --> RCT comparing delayed angiography vs. early coronary angiography post-thrombolysis: early angiography = lower risk of reinfarction and recurrent ischemia (no diff in mortality)

     

    • Fibrinolytic Therapy (Circulation 2004;110:588)

      Absolute Contraindications

      • Any prior ICH
      • Known structural cerebral vascular lesion (ie. AVM)
      • Known malignant intracranial neoplasm
      • Ischemic stroke within 3mo (except acute ischemic stroke within 3h)
      • Suspected aortic dissection
      • Active bleeding (excluding menses)
      • Significant closed head/face trauma in last 3mo

      Relative Contraindications

      • History of chronic/severe/poorly controlled HTN
      • Severe uncontrolled HTN at presentation
        (sBP > 180 mmHg, or dBP > 110 mmHg)
      • History of ischemic stroke >3mo or known other intracranial pathology
      • Traumatic prolonged (>10min) CPR, or Major Surgery within <3 weeks
      • Recent (<4w) internal bleeding
      • Non-Compressible vascular puncture
      • Pregnancy
      • Active petic Ulcer
      • Current use of anticoagulants (the higher INR, the greater bleeding risk)

     

    Primary PCI

    • Adjunctive therapy to support Primary PCI
      • ASA 162mg given before PCI(continue indefinitely post-PCI)
      • P2Y12 receptor inhibitor(continue x1 year regardless of BMS/DES stent)
        • Clopidogrel 600mg --> continue 75mg daily x1 year
        • Prasugrel 60mg  --> continue 10mg daily x1yr  (contraind. if prior stroke/TIA)
        • Ticagrelor 180mg --> continue 90mg bid x1yr
      • Consider IV GP IIb/IIIa (large thrombus burden, inadequate P2Y12 loading)
        • inhibitors before PCI (+/- stent, +/- clopidogrel) who are receiving UFH.
        • Not used with bivalirudin
          • Abciximab, high-bolus-dose tirofiban, or double-bolus ptifibatide
          • Can give them in ED, EMS, cath lab (only if the decision to do PCI is made!!!)
          • intracoronary abciximab can be used
          • Can continue GP IIb/IIIa beyond 1yr in pts with DES
      • Anticoagulation (consider in case-by-case basis)
        • Options:
          • UFH (with boluses to keep aPTT therapeutic) [be careful if GP IIb/IIIa is used]
          • Bivalirudin (with or without prior tx with UFH)
        • If bleeding risk is HIGH, use bivalirudin montherapy instead of UFH+GP IIb/IIIa)
        • NOTE: Do not use fondaparinux (catheter thrombosis risk)

     

    • Angiography in STEMI NOTES:
      • PCI should NOT be performed in non-infarct artery at the time of primary PCI in hemodynamically stable STEMI patients (Class III-B) --> EVIDENCE OF HARM. (conflicting studies) [Unless cardiogenic shock]
      • "No Reflow" Phenomenon --> occurs when poor perfusion despite restoration of epicardial flow
        • Thought to be due to inflammation, endothelial injury, edema, atheroembolization, vasospasm, reperfusion injury 
        • Associated with poor survival rate
        • Possible treatment/prevention: (all have inconsistent effect)
          • Use of GP IIb/IIIa antagonist (abciximab)
          • Vasodilators (nitroprusside, verapamil, adenosine)
          • Metabolism Inhibitors (nicorandil, pexelizumab) 
          • Manual thrombus aspiration (positive studies, but not all showed positive results)
      • Manual aspiration thrombectomy is reasonable undergoing primary PCI (4 studies - Class IIa-B)
      • Do not PCI of CTO (total occlusion) infarct artery >24hrs after STEMI (Class III Level B)
        • If stable, no severe ischemia, and 1 or 2-vessel disease)
        • OAT Trial (Occluded Artery Trial) - higher re-infarction rates if try to open a CTO >24hrs occluded.
      • Non-Infarct Artery PCI: (AFTER primary PCI)
        • DO NOT open at time of primary PCI.
        • Only if spontaneous symptoms of ischemia (Class I, Level C)
        • Intermediate or high-risk findings on non-invasive testing (Class IIA, Level B)

     

     

     

     

     

     

    • Other Notes:

     

    • Blood sugar control
      •  Study: Intense glucose control (4.5-6mmol/L) ass'd with increased mortality!!! (hypoglycemica) This is a new guideline: glucose <10mmol/L. (ICU patients, but included ACS)
      • Study: ACS patients with high glucose = worse outcomes.
      • DIGAMI: mortality at 1 year, 28% RRR, and 11% absolute if randomized to aggressive glucose control. (not acute ICU, but for recovery).
      • Hence, this is a long-term outcome measure, acutely can be lenient (<10) but chronically in recovery should be more strict.

     

    • Balloon pumps
      • If cardiogenic shock, or decreased LV function, can put in balloon pump.

     

    Other STEMI Syndromes

    • Other disease can give same syndrome:
      • Vasospastic Prinzmetal Angina (uncommon) - Classically at rest associated with transiet ST segment elevation/depression, occurs in normal or near-normal coronary artery segments.
        • Treated with vasodilator therapy long-term such as CCB or long-acting nitrates.
        • Provoked by use of ilict drugs (cocaine, methamphetamine). 
        • Presence of the plaque in coronary artery is a strong precipitant of vasospasm at the same site.
      • Takotsubo
        • Japanese octupus trap that shaped like LV when have apical ballooning. 
        • Aka Stress-Induced Cardiomyopathy - significant impairment of LV contractility in typical pattern (distal anterior wall, apex, distal inferiour wall) with preserved function in basal segments of the heart. 
        • No obstructive coronary lesions....usually present with mild elevation of enzymes, but not to the degree that affects so much of the LV. 
        • Supportive care --> Almost always reversible.

     

    Thrombolytics

    • If time to PCI > 120min, and no contraindications, can give thrombolytic threapy:
      • Within 12 hours (Class I, Level A)
      • Within 12-24 hours (Class IIa, Level C) - if ongoing ischemia (ecg or clinical) and large area of myocardium at risk (or hemodynamic instability)
    • DO NOT give fibrinolytics to ST depressions
      • Unless posterior (inferobasal) MI suspected, (or associated STE in aVR)

     

    • Adjunctive Therapy
      • All thrombolyzed patients should receive:
        • ASA (162mg) + 80mg daily indefinitely
          AND
        • Clopidogrel (300mg if ≤ 75yo and 75mg if >75yo) + 75mg daily  for at least 14 days (level A) to 1yr. (Level C)
        • Anticoagulation at least >48hrs up to 8 days (or until revascularized)
          • UFH (wt-adjusted IV bolus+infusion to aPTT 1.5-2.0x control) x48hrs or revasc
          • Enoxaparin (age, wt, CrCl) IV bolus + in 15min by SC injection up to 8 days or until revasc.
          • Fondaparinux (if CrCl > 30mL/min) IV dose, followed in 24hrs by daily SC up to 8 days or until revasc.
          • (helps vessel patency, prevents reocclusion)
    • Post-Thrombolysis Transfer
      • Immediate transfer to PCI center for angiography if: (SHOCK Trial - STEMI+shock --> revasc improves mort)
        • Acute Severe HF
        • Cardiogenic Shock (Class I Level B)
      • Urgent transfer to PCI center for angiography if:
        • Evidence of failed reperfusion (or reocclusion)  (Class IIA, Level B)
      • Routine Transfer for "routine early coronary angiography" (even if stable, and successful reperfusion)
        • For Angiography within 24hrs (but not within 2-3hrs post-lytics - to monitor for bleeding)  (Grade IIa, Level B)
        • TRANSFER-AMI Trial (less recurrence ischemia/infarction)

     

     

    • Post-Thrombolysis PCI
      • ASA indefinitely
      • Clopidogrel
        • 300mg load (if no prev load, and within 24hrs of lysis)
        • 600mg load (if no prev load, and >24hrs of lysis)
        • (Followed by 75mg daily)
      • Prasugrel
        • 60mg load (once coronary anatomy is known, and no prev plavix load)
        • DO NOT give within 24hrs of fibrin-specific agent
        • DO NOT give within 48hrs of non-fibrin-specific agent. 
        • Follow by 10mg load. 
        • DO NOT give if prior storke/TIA
      •  

     

     

     

    • In absence of contraindications, can give thrombolytic therapy to pts with STEMI and onset of symptoms in previous 12hrs.
      (When antidipcated time to PCI > 120min)
    • Patient receiving fibrin-specific fibrinolytics --> also give UFHeparin (prevent re-occlusion of infarct artery).  Half-life of fibrinolytics is short (LMWH can also be used)
    • Agents available:

    Characteristics of Thrombolytic Agents Used in the Treatment of STEMI  (RED: more common)

    Characteristic

    Streptokinase (SK)

    Alteplase (tPA)

    Reteplase (rPA)

    Tenecteplase (TNK)

    Dose

    1.5 million units

    over 30-60 min

    15mg IV bolus,

    +0.75 mg/kg over 30m

    +0.5 mg/kg over 60m

    (Total = 90m)

    Halflife 5min

    10 units × 2

         (30 min apart)

    each over 2 min

    30-50 mg (wt based)

    60kg = 30mg

    60-69kg = 35mg

    70-79kg = 40mg

    80-89kg = 45mg

    ≥ 90kg = 50mg

    Bolus administration

    No

    No

    Yes

    Yes

    Allergic reaction possible on

    repeat exposure

    Yes

    No

    No

    No

    TIMI flow grade 2/3b

    ~55%

    ~75%

    ~83%

    ~83%

    Rate of intracerebral hemorrhage

    ~0.4%

    ~0.4-0.7%

    ~0.8%

    ~0.9%

    Fibrin specificity (theoretically

    reduce bleeding)

    None

    +++

    +

    ++++

    Mechanism (all convert plasminogen

    to plasmin --> break down fibrin)

    Acts on circulating 

    fibrinogen (systemic

    lytic state)

    Acts on fibrin-

    bound plasminogen

    (more specific)

       
    Notes:

    - bacterial protein

    - Produces fever in

    20-40%, can get

    neutralizing antibod.

    - No longer used

    - More common

    - Survival benefit over

      SK

    - Newer agents act 

     faster, infuse faster.

    - Variant of tPA (alteplase)

    - Developed for more rapid

      clot lysis (but in trials 

      does not have better 

      outcomes than tPA

    - faster clot lysis time

      but mortality rate

      same as other 

      agents

    Any of above can be used (except Streptokinase), but rPA and TNK preferred due to bolus dosing and faster

    clot lysis (even though has no mortality benefit)

    aBased on body weight.

    bTIMI flow grade 2/3 refers to mildly impaired flow through the coronary artery involved in the myocardial infarction. The higher the percentage of TIMI 2/3 flow, the more effective the thrombolytic agent.

     

    Boden et al. J Am Coll Cardiol. 2007;50(10):917-929. PMID: 17765117

    Urokinase = used only for PE.  T

     

     

    • Adverse effects:
      • Complication Rate
        Intracranial Hemorrhage (most feared)  0.5 - 1.0 % (risk same with tPA, rPA, and TNK)
        Bleed requiring transfusion 5-15% 

         
    • Thrombolytic reversal: Replete fibrinogen levels with cryoprecipitate (10-15 bags needed) to raise fibrinogen level to 1 g/L
      • Can also infuse FFP up to 6 units for additional fibrinogen and volume!
      • Antifibrinolytic agents such as epsilon-aminocaproic acid (5g over 15-30m IV), discouraged due to widespread thrombosis.
         

    Contraindications to Thrombolytic Therapy for ST-Elevation Myocardial Infarction

     

    Absolute Contraindications

    Any previous intracerebral hemorrhage

    Known cerebrovascular lesion (e.g., arteriovenous malformation)

    Ischemic stroke within 3 months

    Suspected aortic dissection

    Active bleeding or bleeding diathesis (excluding menses)

    Significant closed head or facial trauma within 3 months

    Relative Contraindications

    History of chronic, severe, poorly controlled hypertension

    Severe uncontrolled hypertension on presentation (SBP >180 mm Hg or DBP >110 mm Hg) 

    (OK if can lower to <140/90)

    History of ischemic stroke (>3 months), dementia, or known intracranial pathology

    Traumatic or prolonged (>10 minutes) CPR or major surgery (<3 weeks)

    Recent (within 2-4 weeks) internal bleeding

    Noncompressible vascular puncture site

    For streptokinase/anistreplase: previous exposure (>5 days) or previous allergic reaction to these agents

    Pregnancy

    Active peptic ulcer disease

    Current use of anticoagulants: the higher the INR, the higher the bleeding risk

     

    • NOTE: If has relative contraindications, usually PCI transfer is preferred to lytics.
    • "Facilitated PCI" - Sometimes have pre-treatment lytics followed by PCI, but recent studies indicated increased adverse events (bleeding).

     

     

    CABG for STEMI

    • Urgent CABG for STEMI and coronary anatomy not amenable to PCI:
      • IF ongoing or recurrent ischemia, shock, severe HF, or other high risk features (Class I, Level B)
      • IF no shock, not candidates for PCI or lytic therapy --> CABG within 6hrs (Class IIb, Level C)
    • CABG is recommended in pts with STEMI if repairing mechanical defects. (Class I, Level B)
    • Use of mechanical support is reasonable for STEMI, hemodynamically unstable, and need urgent CABG.
    • Managing Antiplatelets around CABG
      • ASA should not be withheld before urgent CABG (Class I, Level C)
      • Clopidogrel or ticagrelor should be d/c at least 24hrs before urgent on-pump CABG if possible (Class I, Level B)
      • IV GP IIB/IIIA
        • Eptifibatide, tirofiban d/c 2-4hrs before urgent CABG (Class I)
        • Abciximab at least 12hrs before urgent CABG (Class I)
      • Urgent off-pump CABG within 24hrs of plavix/ticagrelor can be considered (Class IIb, Level B)
        • (esp if benefits of revasc outweigh risks of bleeding)
      • Urgent CABG within 5 days of clopidogrel or ticagrelor (or 7 days after prasugrel) can be considered (Class IIB, Level C)  [benefits vs. risks]
      • Summary: Plavix+Ticagrelor d/c 24hrs before urgent CABG (Class I) or 5 days before CABG (Class IIb)
        Prasugrel = 7 days. 

     

    Post-STEMI

    • B-Blocker within 24hrs (Class I)
      • Continue during and after hospitalization
        • Contra-indications:
          • HF
          • Low output state
          • High risk of cardogenic shock
          • Other (AV block >240ms, asthma, 2nd or 3rd deg AVB)
        • If contra-indicated, re-evaluate later.
      • Acutely: Can consider IV BB if ongoing ischemia (Class IIa, Level B)
    • ACEi within 24hrs:
      • Class I, Level B -> Anterior STEMI, HF, LVEF < 40%
      • Class IIa, Level A --> TO ALL PATIENTS WITH STEMI
    • ARB if intolerant to ACE.
    • Aldosterone antagonist with BB and ACEi if EF < 40% AND:
      • Symptomatic HF
      • DMII
    •  

     

    Compl ications

     

    Status: Under Construction: PENDING REVIEW

    • Look for shock, new murmurs, HF, which often occur several days post-MI when necrosis happens
    • LV systolic dysfunction
      • Heart failure --> reduce preload (for symptoms), afterload reduction w/ ACEi to reduce work load and adverse LV remodeling.
      • Cardiogenic shock
        • Very high risk of death! 
        • Very common with RV infarct, which requires fluid resuscitation (no preload reduction!)
      • Note on RV Infarcts:
        • Clinical Features of RV Infarct 

          • Hypotension
          • Clear lung fields
          • Elevated JVP

           

        •  
        • Get a RIGHT-sided ECG (V3R and V4R leads -> look for >1mm ST Elevation)
        • Treatment:
          • Give FLUIDS to fill the RV, give dopamine or dobutamine if hypotension persists.
          • Can take up to 3 days for RV to recover, even if revascularized.
    • Mechanical complications
      • VSD (ischemic/necrotic myocardium)
        • Anterior or Inferior MI (transmural affecting septum).
        • Often requires VSD closure, with very high surgical/medical mortality (50%). 
        • Difficult due to necrotic tissue around the defect.
      • Papillary muscle rupture (i.e. severe acute MR)
        • Several days after MI
        • Present with acute pulmonary edema & loud systolic murmur with no thrill (pressure equilibrates rapidly) --> shock.
        • Get echo!  (differentiates between VSD and papillary rupture -both loud systolic murmurs).
          • Often balloon pump is advised.
          • Nitroprusside to reduce afterload, diuretics.
          • Emergency surgery required!
        • NOTE: MR common post-MI (wall motion affecting leaflet coaptation), especially inferior wall.
      • LV free wall rupture
        • High mortality, often catastrophic (Pericardial tamponade & death)
        • High Risk Features:
          • Females, first MI, elderly, anterior location.
        • Symptoms:
          • Sudden feeling un unwell, nauseated, restless.
          • Echo findings
        • If recognize early, can salvage (pericardiocentesis, surgery).
        • Can get LV pseudoaneurism, which is a rupture contained by pericardium
          • Often requires surgery
      • Pericarditis
        • Dressler syndrome, pericarditis 1mo post-mi.
        • OR acute pericarditis with transmural infarct.
      • Aneurism
        • Anterior or rarely inferior infarct.
        • 3 complictions:
          • Refratory HF, Clot, VT arrhythmia
        • DOES NOT RUPTURE, has all 3 layers.
        • CLOT:
          • Anticoagulation of warfarin for 3-6mo (high risk embolism).
            • 10-20% of pts with anterior STEMI will have LV thrombus.
            • Anterior wall MI used to get anticoagulation (not advised anymore).  Nowadays risk is low with dual antiplatelet therapy.
      • Pseudoaneurism
        • Very narrow neck, and very thin.
        • Can occur anywhere.
        • Higher risk of rupture

    LV thrombus2.png

    • NOTE: Bezold-Jarisch Reflex:

       

      Mechanoreceptor reflex triggered by mechanoreceptors in LV, trigger response of sinus bradycardia+hypotension.

       

      • Successful reperfusion triggers this reflex to increase contractility, but results in bradycardia and hypotension.
      • IV nitrates can cause this as well.
      • Treatment:
        • IV fluids
        • Turn off IV nitroglycerin
        • Use dopamine as a temporizing measure (maintain BP until response resolves).  
        • Can use atropine if bradycardia persists.
    • Arrhythmias:
      • Transient complete heart block with aternior or inferior wall MI.  (usually transient).
        • Inferior MI + 3deg AV block
          • Usually transient - may require temporary transvenous pacing.
          • Theory: inferior wall sits on diaphragm (close proximity to vegas nerve) causing complete heart block.
        • Anterior MI + 3deg AV block
          • Poor prognostic sign!!! 
          • Permanent pacer usually needed.
          • Theory: LAD blocked, infarct proximal to HIS bundle.
      • Ventricular Tachycardia
        • Early: (within 24hrs)
          • Usually self-limited, may not be prognostically significant.
          • Monomorphic
            • Scar/Ischemia
          • Polymorphic
            • 1. Eletrolytes
            • 2. Ischemia
              • Use lidocaine- good for acidic environment
              • Repeat Angiography?
              • Beta-blocker (raises threshold)
        • Late:
          • More concerning
      • Ventricular Fibrillation
        • Often VT degenerates into VF.
      • AIVR
        • Patients with successful reperfusion can develop a wide-complex rhythm.
        • ECG shows a regular wide complex rhythm at 92/min with no clearly discernible atrial activity
        • AIVR is postulated to result from abnormal automaticity in the subendocardial Purkinje fibers.
          • Observed in up to 15% of patients who undergo reperfusion.
          • HR almost always < 120/min and can be < 100/min.
        • Most studies have shown that it is a benign rhythm when it occurs within 24 hours of reperfusion.
        • Management:
          • No intervetion! (usually a good sign)
          • Consider Beta-Blocker if not already on one. 
          • Possible to give atropine for SA node to overtake, but usually not necessary.
      • Atrial Fibrillation
        • Poor prognostic sign.
        • May be caused by acutely increased left atrial pressure

    Notes on Diabetes

    • Pts with diabetes: AHA recommends exercise stress testing for asymptomatic DM patients undergoing an exercise program. (No need for exercise stress testing for other pts who are asymptomatic).
    • CAD and diabetes: Dibetes with triple vessel diseases need less repeat revascularization with CABG when compared to PCI.
      • Many diabetic patients with triple vessel disease and LV systolic dysfunction are adviced to undergo CABG rather than PCI.
      • If PCI is pursued, most will favour DES stents because BMS have a higher rate of in-stent stenosis in DMII patients. 

    Notes on Women

    • WISE study
      • Finding normal coronaries on angio in female patient that has had an abnormal stress test --> still risk.
      • This study compared 540 women with suspected ischemia but no angiographic evidence of obstructive CAD with 1000 age- and race-matched asymptomatic cohorts. The 5-year annualized event rate for cardiovascular events was 16% in women with nonobstructive CAD (stenosis in any coronary artery of 1%-49%), 7.9% in those with normal coronary vessels (no stenosis in any coronary artery), and 2.4% in the asymptomatic cohort (P < 0.002).
    • Exercise testing in women has lower sensitivity and specificity than men.  (although recommendations are the same)
    • Women with positive stress tests and normal coronaries can show microvascular and endothelial disfunction. 
    • Reynold's Risk Score sometimes used as an alternative to Framingham's Risk Score
      • Includes additional risk factors (family hx, and hsCRP).
      • 40% of women in intermediate risk group reclassified with Reynold's Risk Score.
    • Postmenopausal: no benefit of estrogen therapy to reduce CV risk, and no known harm.  There is a signal for breast cancer.
    • Women with ACS are more likely than men to have atypical anginal symptoms (fatigue, dyspnea, nausea)

    Other Important Concepts

    Cardiac Enzymes

    • Cardiac Enzyme Types:
      • Myoglobin (old, poor area under curve)
      • CK-MB (MB isoenzyme of Creatine Kinase) - previously gold standard, but 2003 Heart study removed it 
      • Troponin I (cTnI) (more sensitive and specific than CK-MB)
      • Troponin T (cTnT)
    • Troponin may not be detectable until 2hrs post-onset of chest pain.  (may not be detectable for up to 12h)
    • Some hospitals do the new high-sensitivity troponin (something like that) hsTrp, which goes up earlier?

    TroponinCKincrease.pngTNsensitivity.png

    • Reading:
      • MERIT Study: Collinson PO et al (2002) Heart  (compared biomarkers)

    Differential for Troponin Elevation

    • Myocardial Infarct
      • Rise and/or fall of cardiac biomarkers (trop) with evidence of ischmia (one of):
             1. Ischemic symptoms
             2. ECG: new ischemic changes or new pathologic Q-waves
             3. Imaging: loss of viable myocardium (MIBI) or wall motion abnormality (Echocardiography).
    • Type II:
      • Ischemia due to increase oxygen demand or decreased vascular supply.
        • Increased demand:
          • Arrhythmias, Sepsis
        • Decreased supply:
          • Coronary Spasm, Coronary embolism, anemia, arrhythmias, hypertension/hypotension.
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