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Flashcards in ICS-STEMI Deck (69):
1

Clinical Scenarios for Chronic Stable Angina

identified by obtaining a detailed history from the patient (patient is usually pain free at the time)
a. Stable angina means the pain is predictable
2. Acute onset of chest pain
a. Rest angina: angina is prolonged (usually > 20 minutes) and occurs at rest
b. New-onset angina: at least CCS Class III severity
c. Increasing angina: previously diagnosed angina that is more frequent, longer in duration, or lower in threshold (increased CCS Class within 2 months to at least CCS Class III)

2

ST-segment elevation requiring immediate reperfusion therapy (STEMI)

AMI

3

ischemia is severe enough to cause sufficient myocardial damage and the release of markers of myocardial injury

NSTEMI

4

Pathophysiology of STEMI

Vulnerable plaque, plaque rupture, thrombus formation

5

Triggers for plaque rupture

physical exertion, mechanical stress, pulse rate, BP, and vasoconstriction

6

Initial Recognition of STEMI in the ED

1. ST-segment elevation  0.1 mV in greater than or equal to 2 contiguous leads indicates STEMI and patients should be considered for immediate reperfusion therapy
- > 90% of patients will have elevated serum cardiac markers
- ST-segment depression indicates UA or NSTEMI
- Biochemical markers distinguish between these diagnoses
- If initial EKG is nondiagnostic, serial EKG at 15-30 minute intervals may be performed

2. Biomarkers of cardiac injury

7

1. Preferred test due to cardiac specificity
2. Low sensitivity early in MI (< 6 hours)
3. Remain elevated for 5-14 days

Cardiac-specific troponins (TnT and TnI)

8

1. Principal serum cardiac marker until recently
2. Lack of cardiac specificity due to many isoforms
3. Useful for early detection of MI (within 4 hours)
4. Peak in 24 hours and may remain elevated for 3-4 days

Creatine kinase isoenzymes (CK-MB)

9

1. Not cardiac specific but is released more rapidly from infarcted myocardium than CK-MB or troponins
2. Detected as early as 2 hours but is elevated for less than 24 hours

Myoglobin

10

When are Serial enzyme sets (CK-MB, troponin, myoglobin) ordered

at 3 to 6 hour intervals

11

Other laboratory tests besides cardiac specific biomarkers

CBC, INR, aPTT, electrolytes and Mg, BUN, creatinine, glucose, serum lipids

12

Initial Management of ACS in the ED

MONA -
1. Morphine (Analgesia)
2. Oxygen for patients with PaO2 < 90%
3. Nitroglycerin
4. Aspirin
5. Beta-blockers

13

Why give Morphine for ACS

Pain contributes to increased sympathomimetic activity
In addition to analgesic and anxiolytic effects, morphine causes venodilation and may further reduce myocardial oxygen demand
- does not decrease mortality

14

Dose of Morphine for ACS

Morphine sulfate 2-4 mg IV repeated at 5 to 15 minute intervals as needed

15

Adverse effects of Morphine

respiratory depression, nausea and vomiting, hypotension

16

AVOID in ACS patients

AVOID NSAIDS and Cox-2 inhibitors (except aspirin

17

When can oxygen be given for ACS

Can be administered for all patients within first 6 hours
- no mortality benefit

18

Dose of Nitroglycerin for ACS

a. SL NTG 0.4 mg q5min X 3 doses then assess the need for IV NTG
b. IV NTG indicated for relief of ongoing ischemia, control of HTN or management of pulmonary congestion
- Titrate until signs of ischemia are relieved or SBP does not tolerate
- no mortality benefit

19

DO NOT ADMINISTER IV Nitroglycerin IF

1. SBP < 90 mm Hg or more than 30 mm Hg below baseline
2. Severe bradycardia (< 50 bpm)
3. Tachycardia (> 100 bpm)
4. Suspected RV infarction
5. Use of PDE for erectile dysfunction within the last 24 hours (48 hours for tadalafil)

20

can be used as an alternative or once patients have been pain free for 12 – 24 hours on IV NTG

Oral or topical nitrates

21

Dose of Aspirin in ACS

162 mg to 325 mg chewed if not taken before presentation to the ED
- Decreases mortality in patients with ACS (23% RRR in 35-day mortality)

22

Contraindications for beta-blockers

1. Signs of heart failure, low output state or risk for cardiogenic shock
2. Active asthma or reactive airway disease
3. Heart block

23

Prompt IV therapy of beta-blockers can be used alternatively if

if tachyarrhythmia or hypertension is present
- decreased mortality in patients with ACS by the end of day 1 (prior to the reperfusion era) (IV or PO)

24

Dose of Metoprolol for ACS

1. 5 mg IV q5min X 3 doses
2. 50 mg PO q6h X 48 hours
3. 100 mg PO twice daily thereafter

25

Dose of atenolol for ACS

1. 5 mg IV q10min X 2 doses
2. 50 mg PO q12h X 2 doses
3. 100 mg PO once daily thereafter

26

In patients with contraindications to beta-blockers, what may be used

diltiazem or verapamil many be used but only if there are no signs of CHF, LV dysfunction or AV block

27

Additional Therapies for STEMI

1. Reperfusion therapy
2. Anticoagulation therapy
3. Additional antiplatelet therapy
4. Inhibitors of renin-angiotensin-aldosterone-system
5. Lipid Management

28

in the first 6 to 12 hours while the affected myocardial zone is undergoing necrosis majority of patients have

Majority of patients have persistent occlusion of the infarct artery

29

Goal of reperfusion therapy

restore blood flow to the infarct zone as soon as possible

30

Recommended for ALL patients with STEMI due to evidence of improved survival (reperfusion therapy)

Fibrinolytic therapy

31

Mechanism of fibrinolytic therapy

initiate thrombolysis by converting plasminogen to plasmin (a fibrinolytic enzyme that dissolves the fibrin clot)

32

Efficacy of fibrinolytic therapy

a. 35-day mortality reduction (18% RR)
b. Survival benefit maintained up to 10 years

33

Door-to-needle time for fibrinolytic therapy

30 minutes
- May also be administered in the pre-hospital setting by EMS

34

Fibrinolytic agents

Streptokinase, Alteplase, Reteplase, Tenectoplase-tPA

35

Contraindications (absolute) of Fibrinolytic therapy

a. Any prior intracerebral hemorrhage
b. Active bleeding (excluding menses)
c. Significant trauma or ischemic stroke within three months
i. Except acute ischemic stroke within 4.5 hr
d. Uncontrolled hypertension

36

1. Suitable for 90% of patients
2. Should be performed within 90 minutes of first medical contact (otherwise fibrinolytic therapy is preferred)

Percutaneous coronary angiography (PCI)
- Preferred reperfusion strategy

37

PCI preferred, especially if

1. Patient is at a high risk of bleeding
2. STEMI diagnosis is questionable
3. Lower mortality rates
4. Opens 90% of occluded arteries

38

Fibrinolytic therapy is preferred if

PCI is unavailable and patient cannot be transferred to an alternate center with PCI performed within 120 minutes of initial medical contact
- opens <60% of occluded arteries

39

Goal of anticoagulant therapy

establish and maintain patency of the infarcted artery, prevent DVT/PE, LV mural thrombus and/or cerebral embolism

40

UFH for STEMI

- Used in conjunction with fibrinolysis or PCI
Dose:
1. 60 U/kg bolus (max = 4000 units)
2. 12 U/kg/hr (max = 1000 units/hr)
- Duration: minimum of 48 hours and preferably for the length of hospitalization or up to 8 days

41

Enoxaparin for STEMI

Evidence for use with fibrinolytic therapy

42

ASSENT-3 Trial for Enoxaparin

a. TNK + UFH 60 units/kg bolus then 12 units/kg/hr was compared to TNK + enoxaparin 30 mg IV bolus then 1 mg/kg SC q12h
b. Primary endpoint: composite of 30-day mortality, in-hospital reinfarction, or in-hospital refractory ischemia
i. 15.4% UFH vs. 11.4% enoxaparin (p < 0.0001)
c. Non-cerebral major bleeding was greater in patients > 75 years of age

43

Extract-TIMI 25 Trial for Enoxaparin

a. Thrombolytic therapy with either:
i. UFH 60 units/kg bolus then 12 units/kg/hr
ii. Enoxaparin 30 mg IV bolus then 1 mg/kg SC q12h in patients < 75 years of age
iii. Enoxaparin 0.75 mg/kg SC q12h in patients > 75 years of age
iv. Enoxaparin 1 mg/kg SC q24h in patients with CrCl < 30 ml/min
b. Primary endpoint: composite of death or non-fatal recurrent MI in the first 30 days after randomization
i. 12% UFH vs. 9.9% enoxaparin (p< 0.001)
c. Rates of major bleeding were greater in patients treated with enoxaparin

44

Dosing options for Enoxaparin

a. Patients < 75 years of age: 30 mg IV bolus then 1 mg/kg SC q12h (current guideline recommendation)
b. Patients > 75 years of age: 0.75 mg/kg SC q12h (NO BOLUS)
c. Patients with CrCl < 30 ml/min: 1 mg/kg SC q24h
d. Treat for the length of hospitalization up to 8 days

45

OASIS-6 trial

Fondaparinux
- Not indicated for PCI – it is recommended to use an anticoagulant with anti-IIa activity

46

Dosing of Fondaparinux if fibrinolytic strategy is used

1. 2.5 mg IV, then 2.5 mg SC q24h
2. Continue for length of hospitalization
3. NOT FDA approved for this indication at this time

47

HORIZONS-AMI trial

Bivalirudin
- May be used as an alternative anticoagulant in select patients undergoing PCI
- Reasonable to use in patients with high bleeding risk

48

ADP Inhibitors

i. May be used as an alternative to aspirin if the patient has a true aspirin allergy
ii. Should be used in combination with aspirin in ALL patients who receive PCI with stent implantation

49

Duration of therapy of ADP inhibitors

a. 12 months of dual antiplatelet therapy for bare metal stents implanted
b. Continue therapy beyond 12 months if a drug eluting stent (sirolimus or paclitaxel-eluting stent) is used

50

Prasugrel clinical trial

b. TRITON-TIMI 38:
i. 13, 608 patients with ACS managed by PCI randomized to prasugrel at doses above or clopidogrel 300 mg loading dose then 75 mg daily
ii. Primary efficacy endpoint (composite of death due to CV causes, nonfatal MI or non-fatal stroke) was significantly less with prasugrel (2.2% absolute reduction, 19% relative reduction)
iii. Rates of major bleeding were higher with prasugrel and net-harm was observed in 3 subgroups:
1. Patients with history of TIA or stroke
2. Patients > 75 years of age
3. Patients with body weight < 60 kg

51

Dose of Prasugrel

60 mg loading dose then 10 mg once daily

52

Dose of Clopidogrel

600 mg loading dose before or when PCI is performed then 75 mg once daily

53

PPI controversy with Plavix

1. 2C19 inhibitors: inhibit breakdown of clopidogrel to its active form
2. Strong inhibitors: Omeprazole, lansoprazole, rabeprazole
3. ACC does not prohibit use of PPIs with clopidogrel

54

2 clinical trials with Plavix in pts receiving fibrinolytic therapy

a. CLARITY-TIMI 28: 300 mg loading dose followed by 75 mg daily for a maximum of 8 days demonstrated a significant 36% relative reduction in a composite endpoint
b. COMMIT: 75 mg daily until hospital discharge or up to 4 weeks demonstrated a significant 9% relative reduction in a composite endpoint

55

Recommendation for Short-term use of clopidogrel in STEMI patients who receive fibrinolytic therapy, aspirin and anticoagulation with heparin or LMWH

75 mg once daily for at least 14 days (300 mg loading dose may be given to patients < 75 years of age)
- Any patient needing CABG should have clopidogrel discontinued for at least 5 days prior to the procedure

56

Oral, reversible, direct-acting inhibitor of the ADP receptor that has a more rapid onset and more pronounced platelet inhibition than clopidogrel

Ticagrelor

57

Dose of Ticagrelor

Load 180 mg followed by 90 mg bid

58

Clinical trial for Ticagrelor

d. PLATO trial
i. Ticagrelor vs clopidogrel in ACS patients
ii. Resulted in reduced rates of death 9.8% ticagrelor vs 11.7% clopidogrel

59

ASA dose with Ticagrelor

81 mg

60

Duration of therapy of ticagrelor

a. 12 months of dual antiplatelet therapy for bare metal stents implanted
b. Continue therapy beyond 12 months if a drug eluting stent (sirolimus or paclitaxel-eluting stent) is used

61

Any patient needing CABG should have clopidogrel discontinued when

at least 5 days prior to the procedure

62

MOA of GP IIb/IIIa inhibitors

block GP IIb/IIIa receptor on platelet surfaces and prevent binding of fibrinogen during platelet aggregation
for STEMI patients undergoing PCI (abciximab has strongest evidence)

63

GP IIb/IIIa inhibitors

Abciximab (ReoPro)
Eptifibatide (Integrelin)
Tirofiban (Aggrastat)
- Agents: not interchangeable

64

Leads to pts developing HF after MI

a. Left ventricular remodeling: alterations in ventricular mass, chamber size and shape due to myocardial injury
i. Myocyte hypertrophy, fibroblast hyperplasia and collagen deposition in non-infarcted myocardium
ii. Acute dilatation and thinning on infarcted area resulting in extra workload on residual function myocardium (leading to hypertrophy)
iii. RAAS and local production of angiotensin II within the endothelium are important stimuli for the remodeling process

65

Which ARB to use post MI


valsartan according to VALIANT trial

66

clinical trial for aldosterone antagonists

i. EPHESUS Trial
1. Compared eplerenone 25-50 mg daily vs. placebo in 6642 patients within 3-14 days of AMI
2. Patients required documented LVEF  0.4 plus one documented sign of heart failure
3. Results:
a. 15% RR in all-cause mortality
b. 13% reduction in CV death or hospitalization for CV causes
c. Significantly higher rates of hyperkalemia (especially with CrCl < 50 mL/min)

67

e. ACC/AHA recommendation for post-STEMI

i. Initiate oral ACEI therapy within 24 hours of STEMI and continue indefinitely
ii. Initiate valsartan in patients intolerant to ACEI who have clinical or radiological signs of heart failure or LVEF  0.4
1. May also be used as alternative in patients tolerant of ACEI
iii. Long-term aldosterone blockade for post-STEMI patients who are receiving therapeutic doses of ACEI, have an LVEF  0.4, and have either symptomatic heart failure or diabetes
1. SCr should be < 2.5 mg/dL in men and < 2.0 mg/dL in women
2. Potassium level should be < 5 mEq/mL

68

Secondary Prevention for all pts

Smoking cessation
HTN (goal is <130/80 per JNC-8)
Lipid management
Physical activity
Weight management
Diabetes management
Influenza vaccination

69

should be initiated or continued in all patients with STEMI and no contraindications

High intensity statin therapy