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Cardiology > Acute Coronary Syndrome I > Flashcards

Acute Coronary Syndrome I Flashcards

1
Q

Acute Coronary Syndromes

  • aka
  • Refers to…
  • Result of…
  • Associated w/…
A
  • aka
    • ACS, syndromes of acute myocardial ischemia, or unstable coronary syndrome
  • Refers to…
    • ST elevation myocaridal infarction (STEMI)
    • Non-ST segment myocardial infarction (STEMI)
    • Unstable angina pectoris (UA): syndrome of threatening MI
  • Result of…
    • Tissue death
    • Necrosis
    • Hypoxia
  • Associated w/…
    • Increased risk of systemic or pulmonary embolism
    • Supports role of anti-thrombotic therapy as part of therapy
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2
Q

Plaque Disruption (“Unstable Plaque”) & the Pathophysiology of the ACS

  • Acute myocardial ischemia in most cases is the result of…
  • Underlying pathophysiology
  • Plaque
A
  • Acute myocardial ischemia in most cases is the result of…
    • Dynamic limitations in coronary blod flow (a “supply” problem)
      • Not a “demand” problem that causes chronic stable MI
    • Can occur at any time in the course of coronray atherosclerosis
  • Underlying pathophysiology
    • Deterioration & disruption of an atherosclerotic plaque –> sudden occlusion of coronary artery
  • Plaque
    • Mildly narrowing & flow-limiting
    • Porr in calcium & fibrous tissue
    • Rich in lipids
    • May become inflamed due to…
      • Attaining a certain threshold level of oxidized lipid
      • Infection of a plaque
      • Involvement in the plaque by a systemic inflammatory process
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3
Q

Dynamic & Transient Limitations in Coronary Blood Flow & the Pathophysiology of the ACS

  • Inflammation, “self-digestion,” & ateriosclerotic plaque disruption lead to…
  • Transient limitations in coronary blood flow result in…
  • Eventual outcome of this process determines…
  • If this process is kept in check…
A
  • Inflammation, “self-digestion,” & ateriosclerotic plaque disruption lead to…
    • Varying degrees of plaque disruption (prothrombotic)
    • Endothelial cell dysfunction
    • Abnormal vasoconstriction in the region of the deteriorating plaque
  • Transient limitations in coronary blood flow result in…
    • Clot & abnormal vasoconstriction wax & wane in the coronary vessel
    • Can occur for hours, days, or weeks
    • Accounts for the development of MI following unstable angina
  • Eventual outcome of this process determines…
    • The worst clinical syndrome that will afflict the patient (UA, NSTEMI, or STEMI)
  • If this process is kept in check…
    • By the normal governing process of thrombosis & thrombolysis
    • Total or near-total occlusion of the involved coronary doesn’t occur or is brief
    • Unstable plaque may heal
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4
Q

Clots, Occlusion, & MI Timing

  • White clots (platelet plugs) vs. red clots
  • Partial / short duration total vs. long duration total occlusion
  • Timing of acute MIs
A
  • White clots (platelet plugs) vs. red clots
    • White clots
      • –> unstable angina
      • Prone to dispersal in the arteries
    • Red clots
      • –> MI
      • More stable & less prone to dispersal
  • Partial vs. total occlusion
    • Partial occlusion w/ thrombus or total occlusion for a short time (<20 mins)
      • –> NSTEMI
    • Total & persistent occlusion (>20 mins)
      • –> STEMI
  • Timing of acute MIs
    • >1/2 of acute MIs occur during sleep or during mild to moderate physical activity
    • Circadian rhythm to time of acute MIs –> greatest frequency b/n 6am & noon
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5
Q

Less Common Causes of ACS

A
  • Thrombus downstream of a chronic high-grade stenosis (~10%)
    • Rheological factors associated w/ abnormal blood flow –> thrombosis at site of chornically & critically stenosed coronary artery –> MI
  • Greatly increased myocardial oxygen demand
  • Hyperadrenergic state
  • Acute plaque disruption
    • In the presence of fixed & stable atherosclerotic coronary narrowing
  • Coronary spasm
    • Spontaneous (Prinzmetal’s angina) or due to drugs
    • W/ or w/o atherosclerotic coronary heart disease
  • Embolism to a coronary artery
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6
Q

Non Q Wave vs. Q Wave Infarction & the Wave Front of Myocardial Necrosis

  • Tissue most at risk when myocardial blood flow is limited: subendocardial tissue
  • Transmural vs. subendocardial infarction
  • 2 categoreis of patients in the 1st hours of acute coronary syndromes
  • Coronary vessel occlusion +
    • Artery isn’t opened
    • Artery is opened within an hour of occlusion
    • Artery isn’t opened within 6-12 hours
    • 3-4 hours of occlusion
  • Factors in necrosis that speed propagation of the wave front
A
  • Tissue most at risk when myocardial blood flow is limited: subendocardial tissue
    • Large epicardial vessels give off nutirent mycoardial branches directly from subenpicardial to subendocardial tissue
    • Vessel is constricted during systole by the tension from the contracting myocardium
  • Transmural vs. subendocardial infarction
    • Transmural: necrosis reaches epicardium, Q wave devlops
    • Subendocardial: necrosis doesn’t reach epicardium, Q wave doesn’t develop
  • 2 categoreis of patients in the 1st hours of acute coronary syndromes
    • STEMI
    • UA / NSTEMI
  • Coronary vessel occlusion +
    • Artery isn’t opened
      • Tissue in jeopardy gradually undergoes irreversible damage in a wave front fashion moving from endocardium to epicardium
      • Irreversible injury begins within 20 mins
    • Artery is opened within an hour of occlusion
      • Much of the muscle will survive
    • Artery isn’t opened within 6-12 hours
      • Little to none of the myocardium will survive
    • 3-4 hours of occlusion
      • About half of the jeopardized myocardium will be irreversibly damaged
  • Factors in necrosis that speed propagation of the wave front
    • Presence & magnitude of coronray collateral vessels to the involved vessel
    • Metabolic state of the myocardium
    • Presence of anti-thrombotic therapy
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7
Q

Normal Hemostasis & Control of Hemostasis

  • Blood clot formation
  • Hemostasis
  • Too much vs. too little hemostasis (clot control)
  • Following successful clotting…
  • 2 essential elements for hemostasis
A
  • Blood clot formation
    • Occurs at the site of an injured vessel
  • Hemostasis
    • Must occur rapidly
    • Limited to the local site of disruption / thrombus formation
    • Must be under good control
  • Too much vs. too little hemostasis (clot control)
    • Too much –> severe hemorrhage
    • Too little –> occlude
  • Following successful clotting…
    • The clot must be removed by thrombolysis (fribrinolysis) & the damaged tissue must be healed
  • 2 essential elements for hemostasis
    • Platelet plug
    • Fibrin formation
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8
Q

Platelet Plug Formation

A
  • Platelets: small, plate-like codies that aren’t adherent
  • Platelets are activated by thrombin or exposed to collagen
  • –> change from a rounded to plate-like shape w/ multiple sticky pseudopods
  • –> adhere to the subendothelial matrix
  • –> secrete platelet granule products
  • –> enhance thrombin generation
  • –> activate other platelets
    • Feed back loop involving platelet ADP release & platelet generation of thromboxane A-2
  • –> aggregate w/ other platelets into a platelet plug
  • –> expose the platelet glycoprotein IIb/IIia complex (integrin)
    • Site of fibrinogen & fibrin binding at the platelet surface
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9
Q

Fibrin Formation

A
  • Activated factor II (IIa) –> thrombin
  • Thrombin releases tissue factor
  • Tissue factor + activated coagulation factor VII (VIIa) –> activated factor X (Xa)
  • Xa: prothrombin (II) –> thrombin (IIa)
  • Thrombin (IIa): fibrinogen (soluble) –> fibrin (insoluble)
    • Feedback loop creates more thrombin
  • Thrombin (IIa) –> activated factor XIII (XIIIa)
    • Aids in crosslinking & stabliizing fibrin into a web
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10
Q

Formation & Propagation of Thrombus

A
  • Fibrin web attach to & stabilize platelet plugs at the glycoprotein (BP) IIb/IIIa complex
  • Incorporation fo platelet plug into fibrin –> stabilization of fibrin web –> traps RBCs & WBCs
  • Platelet plugs (white clots) quickly convert into propagating, resilient red clots
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11
Q

Control of Platelet Activation & Fibrin Formation

  • Platelet activation & aggregation are inhibited locally by…
  • Antithrombin/heparin system
A
  • Platelet activation & aggregation are inhibited locally by…
    • Local endotehlial production of prostacyclin
    • NO (EDRF)
  • Antithrombin/heparin system
    • Controls fibrin formation
    • Antithrombin (AT)
      • Circulating plasma protease inhibitor
      • Inhibits thrombin, Xa, & 3 other coagulation factors
    • AT binds w/ endogenous heparin, polymeric chains of monosaccarides, & endothelial heparin sulfate moities –> enhances inactivation
    • Heparin binds to thrombin & AT simultaneously –> inactivates thrombin
      • Only occurs when heparin contains _>_18 monosaccharide units
        • Shorter units inactivate Xa
      • Heparins have a pentasaccharide unit important in AT binding
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12
Q

Thrombolysis

  • Controlled vs. uncontrolled
  • Controlled by…
  • Caused by…
  • Tissue-type plasminogen activator (t-PA)
A
  • Controlled vs. uncontrolled
    • Controlled: removes clots
    • Uncontrolled: hemorrhage
  • Controlled by…
    • Thrombolytic inhibitors (local process)
    • 4 inhibitory mechanisms
  • Caused by…
    • t-PA activation of circulating plasminogen to plasmin
  • Tissue-type plasminogen activator (t-PA)
    • One of two native plasminogen activators in circulation
    • Product of endothelium
    • Binds to fibrin to maximally activate plasminogen
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13
Q

Anti-thrombotic Drugs

  • Treats…
  • Categories
A
  • Treat ACS
    • Open acutely closed coronary arteries
    • Prevent further thrombosis
    • Prevent thrombotic & thromboembolic complications
  • Categories
    • Anti-platelet agents
    • Anti-thrombin agents (“anticoagulatns”)
      • Local & systemic effects
      • Problem: bleeding
    • Thrombolytic (fibrinolytic) agents (plasminogen activates)
      • Local & systemic effects
      • Problem: bleeding
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14
Q

Anti-platelet Agents

A
  • Anti-thrombotic drugs
  • 4 types
    • Aspirin
    • Platelet P2Y12 protein (ADP binding) inhibitors
      • Thienopyridines
      • Cyclo-pentyl-triazolo-pyrimidines (CPTPs)
    • Platelet GPIIb/IIIa blockers
    • Protease-activated receptor-1 (PAR-1), thrombin-binding inhibitors
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15
Q

Aspirin

  • Type
  • General
  • Low dose
A
  • Type
    • Anti-thrombotic anti-platelet agents
  • General
    • Irreversible COX-1 inhibitor for the anuclear platelet
    • Permanently decreases thromboxane A2 synthesis in the affected platelet
    • Decreases teh positive feedbacl loop of thromboxane A2 in recruiting more activated platelets
  • Low dose
    • Max inhibition of thromboxane production
    • Min decrease on prostacyclin production by endothelial cells
      • Endothelial cells have nuclei & can make new COX-1 molecules
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16
Q

Platelet P2Y12 Inhibitors

  • Type
  • General
  • Thienopyridines
    • General
    • Ticlopidine
    • Clopidogrel
    • Pasulgrel
  • Cyclo-pentyl-triazolo-pyrimidines
    • General
    • Ticagrelor
A
  • Type
    • Anti-thrombotic anti-platelet agents
  • General
    • Block the binding of ADP to the adenosine binding protein P2Y12
    • Decrease the positive feedback loop of ADP in recruiting more activated platelets
  • Thienopyridines
    • Metabolites of these drugs irreversibly block the platelet protein P2Y12
    • Ticlopidine
    • Clopidogrel
      • Fewer side effects
      • Used more frequently
    • Pasulgrel
      • More potent
      • Great bleeding risks
      • Superior to clonidine in early ACS
  • Cyclo-pentyl-triazolo-pyrimidines
    • Bind directly to & reversible to P2Y12 –> block ADP binding
    • Ticagrelor
      • Superior to clopidogrelin in early ACS but only at low doses
17
Q

Platelet GPIIb/IIIa Blockers

  • Type
  • General
    • Abciximab
    • Eptifibatide & tirofiban
A
  • Type
    • Anti-thrombotic anti-platelet agents
  • General
    • Given IV
    • Abciximab
      • Non-specific antibody that binds to many integrins
      • Long acting (up to 24-48 hours)
    • Eptifibatide & tirofiban
      • Small moleucles
      • Highly specific for GPIIb/IIIa
      • Short-acting (~4-6 hours)
18
Q

Protease-Activated Receptor-1 (PAR-1), Thrombin-Binding Inhibitors

  • Type
  • General
  • Mechanism of action
A
  • Type
    • Anti-thrombotic anti-platelet agents
  • General
    • First agent: vorapaxar sulfate
    • For initial ACS recovery to prevent subsequent cardiac ischemic events
    • Potent, orally active, tricyclic himbacine-derived, selective PAR-1 antagonist
  • Mechanism of action
    • Thrombon activates platelets by binding & activating PAR-1 & PAR-4 receptors
      • PAR-1 receptros are activated at lower thrombin concentrations & elicit a more rapid platelet response than PAR-4
    • PAR-1 inhibitors limit thrombin-activation of platelets
      • Competitively block PAR-1 –> inhibit thrombin-induced platelet aggregation
19
Q

Anti-thrombin Agents

A
  • Anti-thrombotic drugs
  • Block the formation of thrombin &/or inhibit thrombin action
  • 3 types
    • Heparin (or heparin-like) agents
    • Direct thrombin inhibitors (hirudin-like agents)
    • Oral vitamin K antagonists (VKAs)
20
Q

Heparins

  • Type
  • Unfracitonated heparin
  • Low-molecular weight heparins
  • Fondaparinux
A
  • Type
    • Anti-thrombotic anti-thrombin agents
  • Unfractionated Heparin
    • Biological product
      • Ginds to antithrombin
      • –> makes antithrombin more active
      • –> inhibits thrombin , Xa, & other coagulaiton factors
    • Molecules > 18 polysaccharide units –> greater effect on thrombin
    • Given IV
    • Blood clot testing required
  • Low-molecular weight heparins
    • Created by breaking down larger heparin chains into lower MW chains
      • –> inhibits thrombin & Xa
    • Molecules < 18 polysaccharide units –> greater effect on Xa
    • Given subcutaneously
    • Blood clot testing not required
  • Fondaparinux
    • Pentasaccharide heparin analog
      • Effect in ACS but cost limits it to patients who can’t receive heparin
    • Blocks Xa w/ no effect on thrombin
    • Given subcutaneously
    • Blood clot testing not required
21
Q

Direct Thrombin Inhibitors (Hirudin-Like Agents)

  • Type
  • General
  • Bivalarudin
  • Argatraban
A
  • Type
    • Anti-thrombotic anti-thrombin agents
  • General
    • Modeled after hirudin (anti-thrombin found in saliva of leaches)
    • Act directly on thrombin
    • Given IV
    • Require blood clot testing
    • Used as alternatives to vitamin K antagonists in longer-term management of ACS patients w/ AFib
  • Bivalarudin
    • Derived from the hirudin molecule
    • Used in ACS…
      • To replace heparin & IIb/IIIa during angioplasty procedures
      • W/ known or suspected heparin-induced thrombocytopenia (HIT)
  • Argatraban
    • Small molecule that contains part of the hirudin molecule that blocks the thrombin active site
    • Used in ACS w/ known or suspected HIT
22
Q

Oral Vitamin K Antagonitsts (VKAs)

  • Type
  • General
A
  • Type
    • Anti-thrombotic anti-thrombin agents
  • General
    • Warfarin (a coumarin)
    • Blocks terminal gamma carboxylation of clotting factor II (prothrombin) & 3 other coagulation factors
      • Decreases normally functioning thrombin & fibrin formation
    • Given orally
    • Slow onset & cessation
    • Blood clot testing required
23
Q

Thrombolytic (Fibrinolytic) Agents (Plasminogen Activators)

A
  • Anti-thrombotic drugs
  • Available drugs
    • Alteplase (recombinant form of t-PA)
    • Tenecteplase & reteplase (alteplase analogs)
      • Derived to allow solely bolus adminstration IV
  • Moderatley selective for fibrinolysis at the site of a clot
  • Little action on fibrinogen
24
Q

Opening Acutely Thrombosed Coronary Arteries: Emergency Reperfusion Therapy for STEMI w/ Thrombolysis (Fibrinolysis)

  • Thrombolytic therapy
    • Restricted to patients w/…
    • STEMI
    • UA/NSTEMI
    • Effectiveness
    • Adverse effects
    • Contraindications
  • Emergency angioplasty & stenting
A
  • Thrombolytic therapy
    • Restricted to patients w/ high risk for adverse outcome & can’t undergo emergency angioplasty & stenting within 90 mins
    • STEMI
      • Within 30 mins of admission
      • Within 6 hours of MI
      • Small benefit b/n 6-12 hours of MI
      • Benefit after 12 hours only w/ recurrent or ongoing ischemia
    • UA/NSTEMI
      • Not beneficial b/c coronary arteyr isn’t totally occluded
      • Risk : benefit ratio isn’t favorable
    • Effectiveness: 50-60%
    • Adverse effects: bleeding (intracranial or other hemorrhage)
    • Contraindications
      • High risk of bleeding & intracranial hemorrhage
      • Elderly, female, small body size, HTN, recent neurosurgery, prior intracranial hemorrhage, vascular risks
  • Emergency angioplasty & stenting
    • Superior to thrombolytic therapy if within 90 mins of admission
25
Q

Aspirin Therapy for ACS

A
  • Antiplatelet w/ low dose following an initial high dose
  • Moderate reduction in 1 month mortality from STEMI & recurrent MI / sudden death when given long-term
  • Marked reduction in death, progression to MI, & recurrent MI in patients w/ UA/NSTEMI
26
Q

Platelet P2Y12 (ADP Binding) Inhibitior Therapy for ACS

  • Use
  • This vs. aspirin
  • Clopidogrel vs. pasugrel & ticagrelor
  • Duration
A
  • Use
    • Adjunctive therapy to aspirin
    • Alternative to aspirin w/ aspirin allergy
    • Small additional benefit to aspirin in UA, NSTEMI, & STEMi w/o angioplasty / stenting procedures
  • This vs. aspirin
    • Mildly effective alone
    • Moderately effective in addition to aspirin
  • Clopidogrel vs. pasugrel & ticagrelor
    • Pasugrel & ticagrelor > clopidogrel in early ACS
    • Clopidogrel used after 1 month for cost
    • Aspirin dose must be < 100 mg when used w/ ticagrelor
  • Duration
    • Use for > 3-12 months in patient sw/ coronary angioplasty & stent placement
    • Use > 12 months in patients w/ drug-eluting stent b/c this slows endothelium recovery time
    • Therapy decreases risk of in-stent thrombosis
27
Q

GP IIb/IIIa Blocker Therapy for ACS

  • Abciximab & eptifibatide
  • Bivalirudin
  • Tirofiban & eptifibatide
A
  • Abciximab & eptifibatide
    • Moderate benefit in patients w/ SteMi undergoing emergency coronary angioplasty procedures (before platelet P2Y12s)
    • Primraily used as an additional anti-platelet agent in high risk patients (coronray dilation & stenting procedures in clot-burdened vessels)
  • Bivalirudin
    • Direc trhombin inhibitor
    • Substitute for both GP IIb/IIIa blocker & heparin for emerggency, high-risk angioplasty procedures
  • Tirofiban & eptifibatide
    • Small molecule glycoprotein IIb/IIIa blockers
    • High benefit in addition to other drug therapy in UA/NSTEMI w/ cardiac cath & angioplasty/stenting therapy (before platelet P2Y12s)
      • Reduce death, MI, & need for urgent repeat vascular procedures
    • If used in UA/NSTEMI, limit to high risk patients w/o cardiac cath & w/ planned angioplsaty /stenting procedures
      • Provide therapy in 12-24 hours b/n initial eval & coronary arteriography
      • Provide therapy in cath lab before dilation or stenting of the coronary arteries
28
Q

PAR-1 Inhibition of Platelets (Vorapaxar) Therapy for ACS

  • Use during active ACS
  • Use > 2 months after ACS
  • Contraindications
A
  • Use during active ACS
    • Unacceptable increased risk of hemorrhage
  • Use > 2 months after ACS + aspirin + P2Y12 inhibitors
    • Mildly further decreaes risk of additional cardiac ischemic episodes, esp recurrent MI
    • Risk fo hemorrhage
  • Contraindications
    • Post-ACS patients w/ a history of stroke or transient cerebrovascular ischemia or other conditoins w/ increased bleeding risk
29
Q

Heparin Therapy for ACS

  • Short term (1-2 day) heparin
  • Low dose heparin
  • In UA/NSTEMI
  • Bivalirudin
A
  • Short term (1-2 day) heparin
    • STEMI: small additional benefits in addition to aspirin & fibrin-selective thrombolytic therapy
    • Necessary for max benefit w/ fibrin-selective thrombolytic agents & emergency angioplasty procedures
  • Low dose heparin
    • Subcutaneous for all MI patients until fully ambulatory
    • Prevent DVT & pulmonary embolism
  • In UA/NSTEMI
    • Unfracitonated heparin, low MW heparin, or fondaprinux + aspirin –> additional protection against death & progression to MI
    • Therapy given for 2 days or until cath & revascularization procedures are complete
  • Bivalirudin
    • Replaces GP IIb/IIia blocker & heparin in STEMI + primary angioplasty procedures
30
Q

Vitamin K Inhibitor Therapy for ACS

A
  • Vitamin K inhibitors vs. aspirin
    • Prevent sudden death & recurrent MI w/o aspirin
    • Additional benefit when added to aspirin
      • But increases hemorrhage risk
    • Prefer aspirin b/c easier, cheaper, & safer longterm
      • Except in patients w/ high risk for peripheral or pulmonary thromboembolism
  • Reduces stroke risk in patients w/ AMI or apical infarctions & persistent wall motion abnormalities
    • 3 months anti-thrombin therapy + shrot-term heparin –> intensive warfarin + low dose aspirin
  • High risk patients after MI
    • Given warfarin to prevent stroke + intensive regimen + low dose aspirin
    • Patients: AFib, large dialted ventricles, prior thromboembolic episodes

Cardiology (40 decks)

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