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NAPLEX Review > Acute Coronary Syndromes > Flashcards

Acute Coronary Syndromes Flashcards

1
Q

What causes an acute coronary syndrome?

A

An acute coronary syndrome (ACS) results from plaque building up in the coronary arteries (coronary atherosclerosis). The plaques are made up of fatty deposits that cause the arteries to narrow, making blood flow more difficult

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2
Q

What is the danger of acute coronary syndrome?

A

The plaque can rupture, leading to clot (thrombus) formation and sudden, reduced blood flow (ischemia) to the heart. This causes an imbalance between myocardial oxygen supply and demand. Ischemia can cause cardiac muscle cell death (myocardial necrosis)

*ACS is a medical emergency

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3
Q

What are some risk factors that can lead to the plaque buildup that causes an ACS?

A
  • Age: mean > 45 years, women > 55 years (or early hysterectomy)
  • Family history: 1st degree relative with coronary event before 55 years (men) or 65 years (women)
  • Smoking
  • Hypertension
  • Known coronary artery disease
  • Dyslipidemia
  • Diabetes
  • Chronic angina
  • Lack of exercise
  • Excessive alcohol
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4
Q

What are the classic symptoms of ACS?

A

Chest pain (often described as discomfort, pressure and squeezing), lasting >10 minutes, severe dyspnea, diaphoresis, syncope/presyncope and/or palpitations. The pain can radiate to arms, back, neck, jaw or epigastric region

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5
Q

Who is less likely to experience the classic symptoms of ACS?

A

Females, the elderly and patients with diabetes are less likely to experience the classic symptoms

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6
Q

When can symptoms of ACS occur?

A

Symptoms can occur at rest, or may be precipitated by minimal exertion, exercise, cold weather, extreme emotions, stress or sexual intercourse

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7
Q

What should patients with nitroglycerin (NTG) do if they experience chest pain?

A

Patients with prescription for sublingual nitroglycerin (NTG) should use one dose every 5 minutes for up to three doses to relieve chest pain. If the chest pain or discomfort is not improved or is worse five minutes after the first dose, call 911 immediately

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8
Q

What does ACS encompass?

A

ACS encompasses non-ST segment elevation acute coronary syndromes (NSTE-ACS) and ST-segment elevation myocardial infarction (STEMI)

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9
Q

What does NSTE-ACS describe?

A

NSTE-ACS describes both unstable angina (UA) and non-ST segment elevation myocardial infarction (NSTEMI), which are indistinguishable upon presentation

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10
Q

How are the types of ACS differentiated?

A

The types of ACS are differentiated by ECG changes (ST segment elevation with STEMI), the presence of cardiac enzymes (occurs in NSTEMI and STEMI) and the extent of blockage in the affected artery (partial blockage in UA and NSTEMI and complete blockage with STEMI)

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11
Q

What should be done in patients with ACS at the site of first medical contact?

A

A 12-lead ECG should be performed and evaluated within 10 minutes at the site of first medical contact. Patients with an acute MI (STEMI or NSTEMI) should be urgently transported to a hospital with percutaneous intervention (PCI) capability, if possible

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12
Q

What are the most sensitive and specific biomarkers for ACS?

A

Biochemical markers (enzymes) are released into the bloodstream when myocardial cells die. Cardiac troponins I and T (TnI and TnT) are the most specific and sensitive biomarkers for ACS

*Creatinine kinase myocardial isoenzyme (CK-MB) and myoglobin are less sensitive markers but may still be monitored in clinical practice

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13
Q

When are TnI and TnT detectable and when should levels be obtained?

A

They are detectable in the blood within 2-12 hours, and for up to 5-14 days, after myocardial necrosis. Levels should be obtained at presentation and 3-6 hours after symptom onset in all patients with ACS syndrome

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14
Q

How can NSTE-ACS be treated?

A

NSTE-ACS can be treated with medications alone (referred to as medical management) or with PCI (preferred to as an early invasive strategy)

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15
Q

What is PCI?

A

PCI is a coronary revascularization procedure that involves inflating a small balloon inside a coronary artery to widen it and improve blood flow. Usually, metal mesh, called a stent, is placed into the artery afterward to keep the artery open

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16
Q

What is a STEMI?

A

A STEMI results from a complete blockage of one or more coronary arteries, and the blocked arteries need to be opened as quickly as possible

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17
Q

What is the preferred approach for patients with a STEMI?

A

PCI is the preferred approach, but if it cannot be done in a reasonable time frame, fibrinolytics should be given. Patients may also go directly for urgent coronary artery bypass graft (CABG) surgery if there is significant multi-vessel disease within the coronary arteries

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18
Q

What is the goal of acute treatment of ACS?

A

Immediate relief of ischemia and preventing MI expansion and death

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19
Q

What is the drug treatment included for ACS?

A

Drug treatment includes a combination of antianginal, antiplatelet and anticoagulant medications

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20
Q

What is the purpose of using antianginals and what are some examples?

A

Antianginals (morphine, nitrate, beta-blockers): decrease myocardial oxygen (O2) demand or increase myocardial O2 supply (blood flow) to relieve ischemia

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21
Q

What is the purpose of antiplatelets and what are some examples?

A

Antiplatelets (aspirin, P2Y12 inhibitors, glycoprotein (GP) IIb/IIIa inhibitors) inhibit platelet aggregation to prevent clot formation/growth

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22
Q

What is the purpose of anticoagulants and what are some examples?

A

Anticoagulants (UFH, LMWH, bivalirudin): inhibit clotting factors to prevent clot formation/growth

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23
Q

What are some drugs for ACS that should be given immediately (as needed)?

A

Morphine, oxygen, nitrates, aspirin

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24
Q

What are some clinical notes about Morphine?

A

Morphine sulfate may be used in patients with ongoing chest discomfort despite NTG therapy. Side effects: hypotension, bradycardia, N/V, sedation and respiratory depression

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25
Q

When should oxygen be administered?

A

Administer to patients with arterial oxygen saturation <90% (SaO2 < 90%) or those with respiratory distress

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26
Q

What are some clinical notes about nitrates?

A

Sublingual NTG if not already administered. Start IV NTG for persistent ischemic pain, hypertension, heart failure. Nitrates can reduce blood pressure. Do not use IV NTG if SBP < 90 mmHg, HR < 50 BPM or if patient is experiencing a right ventricular infarction. PDE-5 inhibitors are contraindicated with NTG

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27
Q

What are some clinical notes about aspirin?

A

Non-enteric-coated, chewable aspirin (162-325 mg) should be given to all patients immediately if no contraindications are present (do not use extended-release aspirin products). A maintenance dose of aspirin 81-162 mg daily should be continued indefinitely. If intolerant to aspirin, may use clopidogrel or ticagrelor

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28
Q

What are the drugs for ACS given after depending on the plan?

A

GPIIb/IIIa receptor antagonists, Anticoagulants or P2Y12 inhibitors

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29
Q

What are drugs for ACS that are given within 24 hours and continued as an outpatient medication?

A

Beta blockers and ACE inhibitors

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30
Q

What are some clinical notes about beta-blockers?

A

An oral, low dose beta-blocker (beta-1-selective blocker without intrinsic sympathomimetic activity preferred) should be started within the first 24 hours unless contraindicated (e.g. decompensated heart failure, cardiogenic shock, HR < 45 BPM). If the patient has concomitant HFrEF that is stable, choose bisoprolol, metoprolol succinate or carvedilol. An IV beta-blocker or an oral long-acting non-DHP CCB are alternative options used in some situations

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31
Q

What are some clinical notes about ACE inhibitors?

A

An oral ACE inhibitor should be started within the first 24 hours and continued indefinitely in all patients with left ventricular ejection fraction (LVEF < 40%), those with HTN, DM or stable CKD unless contraindicated (use ARB if the patient is ACE inhibitor tolerant). Use in other patients may be reasonable. Do not use an IV ACE inhibitor within the first 24 hours due to risk of hypotension

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32
Q

What are medications to avoid in acute setting with patients with ACS?

A
  • NSAIDs (except aspirin), whether nonselective or COX-2-selective, should not be administered during hospitalization due to increased risk of mortality, reinfarction, hypertension, cardiac rupture, renal insufficiency and heart failure
  • Immediate release nifedipine should not be used due to increased risk of mortality
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33
Q

What is the MOA of aspirin?

A

Inhibits platelet aggregation/clot formation by inhibiting production of thromboxane A2 (TXA2) via irreversible COX 1 and COX 2 inhibition

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34
Q

What is the MOA of P2Y12 inhibitors?

A

Bind to adenosine disphosphate (ADP) P2Y12 receptor on the platelet surface, which prevents ADP-mediated activation of the GPIIb/IIIa receptor complex, thereby reducing platelet aggregation

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35
Q

What is the MOA GPIIb/IIIa receptor antagonists?

A

Block the platelet glycoprotein IIb/IIIa receptor, which is the binding site for fibrinogen, von Willebrand factor and other ligands, thereby reducing platelet aggregation and further thrombosis

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36
Q

What is the MOA of Vorapaxar?

A

Protease-activated receptor-1 (PAR-1) antagonist that reversibly binds to the PAR-1 expressed on platelets, preventing thrombin-induced and thrombin receptor agonist peptide-induced platelet aggregation

37
Q

Describe the structure and mechanism of Clopidogrel and Prasugrel

A

Clopidogrel and Prasugrel are structurally similar and are classified as thienopyridines. They are prodrugs that irreversibly bind to the receptor

38
Q

What is DAPT?

A

P2Y12 inhibitors are commonly used with aspirin after an ACS, which is called dual antiplatelet therapy (DAPT)

39
Q

What are some examples of P2Y12 inhibitors?

A

Clopidogrel, Prasugrel, Ticagrelor, Cangrelor

40
Q

What is the boxed warning for Clopidogrel?

A

Clopidogrel is a prodrug. Effectiveness depends on the conversion to an active metabolite, mainly by CYP450 2C19. Poor metabolizers of CYP2C19 exhibit higher cardiovascular events than patients with normal CYP2C19 function. Tests to check CYP2C19 genotype can be used as an aid in determining a therapeutic strategy. Consider alternative treatments in patients identified as CYP2C19 poor metabolizers.

41
Q

What are the contraindications of Clopidogrel?

A

Active serious bleeding

42
Q

What are some warnings associated with Clopidogrel?

A

Bleeding risk, stop 5 days prior to elective surgery, do not use with omeprazole or esomeprazole, premature discontinuation (increased risk of thrombosis), thrombotic thrombocytopenic purpura (TTP)

43
Q

What are some side effects of Clopidogrel?

A

Generally well tolerated, unless bleeding occurs

44
Q

What are the boxed warnings with Prasugrel?

A

Significant and sometimes fatal bleeding; not recommended in patients > 75 years due to high bleeding risk, unless patient is considered high risk (DM or prior MI); do not initiate if CABG likely, stop at least 7 days prior to elective surgery

45
Q

What are contraindications of Prasugrel?

A

Active serious bleeding, history of TIA or stroke

46
Q

What are some warnings associated with Prasugrel?

A

Bleeding risk, premature discontinuation (increased risk of thrombosis), thrombotic thrombocytopenic purpura (TTP)

47
Q

What are some side effects associated with Prasugrel?

A

Generally well-tolerated, unless bleeding occurs (higher risk than clopidogrel)

48
Q

What are the boxed warnings associated with Ticagrelor?

A

Significant, sometimes fatal, bleeding; after the initial dose of 162-325 mg, do not exceed aspirin 100 mg for maintenance doses because higher daily doses reduce the effectiveness of ticagrelor; avoid use when CABG likely, stop 5 days before any surgery

49
Q

What are contraindications of Ticagrelor?

A

Active serious bleeding, history of intracranial hemorrhage

50
Q

What are some warnings of Ticagrelor?

A

Bleeding risk, severe hepatic impairment, bradyarrhythmias, premature discontinuation (increased risk of thrombosis), thrombotic thrombocytopenic purpura (TTP)

51
Q

What are some side effects of Ticagrelor?

A

Bleeding, dyspnea (> 10%), increased SCr, increased uric acid

52
Q

What are the contraindications of Cangrelor?

A

Significant active bleeding

53
Q

What is a side effect of Cangrelor?

A

Bleeding

54
Q

What are some notes about Cangrelor?

A

Effects are gone 1 hour after drug discontinuation and transition to one of the oral P2Y12 inhibitors after PCI

55
Q

What are some general drug interactions for all P2Y12 inhibitors?

A

Most drug interactions are due to additive effects with other drugs that can increase bleeding risk. If an ACS patient experiences bleeding while on a P2Y12 inhibitor, it should be managed without discontinuing the P2Y12 inhibitor, if possible. Stopping the P2Y12 inhibitor (particularly within the first few months after ACS) increase the risk of subsequent cardiovascular events

*NSAIDs, warfarin, SSRIs and SNRIs increase the bleeding risk

56
Q

What are drug interactions specific to Clopidogrel?

A

Avoid in combination with the CP2C19 inhibitors esomeprazole and omeprazole due to the risk of decreased antiplatelet effect. Use with caution with other CYP2C19 inhibitors. Clopidogrel increases the effect of repaglinide, which can cause hypoglycemia

57
Q

What are some drug interactions specific to Ticagrelor?

A

Ticagrelor is a CYP3A4 (major) substrate; avoid use with strong CYP3A4 inhibitors and inducers. Avoid simvastatin and lovastatin doses greater than 40 mg/day. Monitor digoxin levels with initiation of or any change in ticagrelor dose

58
Q

What are examples of Glyoprotein IIb/IIIa receptor antagonists and describe their MOAs?

A

Eptifibatide and tirofiban have reversible blockade of the GPIIb/IIIa receptor. Abciximab has irreversible blockade of the receptor and is only indicated for PCI with or without stent

59
Q

What is a Glycoprotein IIb/IIIa receptor antagonist always given with?

A

Heparin

60
Q

What are some contraindications of GPIIb/IIIa receptor antagonists?

A

Thrombocytopenia (platelets < 100,000/mm3), history of bleeding diathesis (predisposition), active internal bleeding, severe uncontrolled HTN, recent major surgery or trauma (within 4 past weeks for tirofiban, past 6 weeks for abciximab/eptifibatide), history of stroke within 2 years (abxicimab), history of stroke within 30 days or any history or hemorrhagic stroke

61
Q

What are some contraindications specific for abciximab?

A

Recent (within 6 weeks) GI or GU bleeding of clinical significance, increased prothrombin time, hypersensitivity to murine proteins, intracranial neoplasm, arteriovenous malformation or aneurysm

62
Q

What is a contraindication specific for eptifibatide?

A

Dependency on renal dialysis

63
Q

What are some side effects of GPIIb/IIIa receptor antagonists?

A

Bleeding, thrombocytopenia (especially abciximab)

64
Q

What are some monitoring parameters of GP IIb/IIIa receptor antagonists?

A

Hgb, Hct, platelets, s/sx of bleeding, renal function

65
Q

What are some notes of GP IIb/IIIa receptor antagonists?

A
  • Do not shake vials
  • Must filter abciximab
  • Platelet function returns in about 24-48 hours after stopping abxicimab and about 4-8 hours after stopping eptifibatide/tirofiban
66
Q

What is Vorapaxar indicated for?

A

Vorapaxar is indicated in patients with a history of MI or peripheral arterial disease (PAD) to reduce thrombotic cardiovascular events (CV death, MI, stroke and urgent coronary revascularization)

67
Q

What is a boxed warning of Vorapaxar?

A

Bleeding risk (include ICH and fatal bleeding); do not use in patients with a history of stroke, TIA, ICH or active serious bleeding

68
Q

What is a warning associated with Vorapaxar?

A

Do not use in severe liver impairment

69
Q

What are some side effects of Vorapaxar?

A

Bleeding, anemia

70
Q

What is a major drug interaction of Vorapaxar?

A

Vorapaxar is a substrate of CYP3A4 and an inhibitor of P-gp. Avoid use with strong CYP3A4 inhibitors and strong CYP3A4 inducers

71
Q

How do fibrinolytics work?

A

These medications cause fibrinolysis (clot breakdown) by binding to fibrin and converting plasminogen to plasmin

72
Q

When are fibrinolytics used?

A

Fibrinolytics are used only for STEMI

73
Q

What is preferred when a STEMI is confirmed?

A

PCI is preferred f it can be performed within 90 minutes (optimal door-to-balloon time) or within 120 minutes fo first medical contact (which could be in an ambulance)

74
Q

What is recommended if PCI is not possible within 120 minutes of first medical contact?

A

Fibrinolytic therapy is recommended and should be given within 30 minutes of hospital arrival (door-to-needle time)

*In the absence of contraindications, and when PCI is not available, fibrinolytic therapy is reasonable in STEMI patients who are still symptomatic within 12-24 hours of symptom onset

75
Q

What are some examples of fibrinolytics?

A

Alteplase, Cathflo Activase, Tenecteplase, Reteplase

76
Q

What are contraindications fo fibrinolytics?

A

Active internal bleeding or bleeding diathesis, history of recent stroke, any prior intracranial hemorrhage (ICH), recent intracranial or intraspinal surgery or trauma (last 2-3 months), intracranial neoplasm, arteriovenous malformation or aneurysm, severe uncontrolled hypertension (unresponsive to emergency therapy)

77
Q

What are some side effects associated with fibrinolytics?

A

Bleeding (including ICH)

78
Q

What are some monitoring parameters of fibrinolytics?

A

Hgb, Hct, s/sx of bleeding

79
Q

What are some notes associated with fibrinolytics?

A

Alteplase contraindications and dosing differ when used for ischemic stroke

80
Q

What drugs are used for secondary prevention after ACS?

A

Aspirin, P2Y12 inhibitor, Nitroglycerin, Beta-blocker, ACE inhibitor, Aldosterone Antagonist, Statin

81
Q

How long should a patient use Aspirin for secondary prevention?

A

Indefinitely (81 mg per day), unless contraindicated

82
Q

How long should a patient use a P2Y12 inhibitor for secondary prevention?

A
  • Medical therapy patients: ticagrelor or clopidogrel with aspirin 81 mg for at least 12 months
  • PCI treated patients (including any type of stent): clopidogrel, prasugrel or ticagrelor with aspirin 81 mg for at least 12 months
  • Continuation of DAPT beyond 12 months may be considered in patients who are tolerating DAPT and are not at high risk of bleeding followign coronary stent placement
83
Q

How long should a patient use Nitroglycerin for secondary prevention?

A

Indefinitely (SL tabs or spray PRN)

84
Q

How long should a patient use beta-blockers as secondary prevention?

A

3 years; continue indefinitely if HF or if needed for management of HTN

85
Q

How long should you use an ACE inhibitor for secondary prevention?

A

Indefinitely if EF < 40%, HTN, CKD or diabetes; consider for all MI patients with no contraindications

86
Q

When and how long should a patient use aldosterone antagonists for secondary prevention?

A
  • indefinitely if EF < 40% and either symptomatic HF or DM receiving target doses of an ACE inhibitor and beta-blocker
  • Contraindications: significant renal impairment (SCr > 2.5 mg/dL in men, > 2 mg/dL in women) or hyperkalemia (K > 5 mEq/L)
87
Q

How long should you use statins for secondary prevention?

A
  • Indefinitely
  • High-intensity
  • Patients > 75 years of age: consider moderate or high intensity statin
88
Q

What should be recommended for patients with after ACS with needed pain relief?

A

Patients with chronic musculoskeletal pain should use APAP, nonacetylated salicylates, tramadol or small doses of narcotics before considering the use of NSAIDs. If these options are insufficient, it is reasonable to use nonselective NSAIDs such as Naproxen (lowest CV risk). COX-2 selective NSAIDs have high CV risk and should be avoided.

89
Q

What is recommended for patients with ACS and Afib?

A

Dual or triple antithrombotic therapy can be used in patients who require anticoagulation for Afib and have had a PCI with stenting. If using triple therapy, use it for the shortest time possible. Clopidogrel is teh preferred P2Y12 inhibitor for triple therapy and a transition to dual therapy (anticoagulant + P2Y12 inhibitor) can be consider after 4-6 weeks. PPI should be prescribed in any patient with a history of GI bleeding while taking triple antithrombotic therapy.

NAPLEX Review (45 decks)

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