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					CORONARY ARTERY
    DISEASE
      OXYGENATION/
      PERFUSION NEEDS
      Nursing Management
      Coronary Artery Disease
      Lewis Ch 34
     Coronary Artery Disease
• Significance
  – Number one cause of death in US.
  – Myocardial infarction
  – increased in those > 60 years
• Etiology/Pathophysiology
  – starts with endothelial injury (HTN, hyperlipid)
     • platelet activation, release of growth factor
     • growth of smooth muscle
     Coronary Artery Disease
     • lipids trapped in tissue
     • calcification begins
• Developmental stages of plaque
  – fatty streak
  – fibrous plaque
  – complicated lesion
             Description
• A type of blood vessel disorder that is
  included in the general category of
  atherosclerosis
• Atherosclerosis
   – Begins as soft deposits of fat that harden
     with age
   – Referred to as the “hardening of
     arteries”
   – Can occur in any artery in the body
   – Atheromas (fatty deposits)
      • Preference for the coronary arteries
             Description
• Atherosclerosis
   – Terms to describe the disease process:
      • Arteriosclerotic heart disease
        (ASHD)
      • Cardiovascular heart disease
        (CHD)
      • CAD
• Cardiovascular diseases are the major
  cause of death in the United States
• Heart attacks are still the leading cause
  of all cardiovascular disease deaths and
  deaths in general
        Etiology and Pathophysiology
      Atherosclerosis is the major cause of CAD
   – Characterized by a focal deposit of cholesterol and
     lipids, primarily within the intimal wall of the
     artery
      Endothelial lining altered as a result of chemical
  injuries
   – Hyperlipidemia
   – Hypertension
 C-reactive protein (CRP)
   – Nonspecific marker of inflammation
   – Increased in many patients with CAD
   – Chronic exposure to CRP triggers the rupture of
     plaques
       Etiology and Pathophysiology
• Endothelial alteration 
  – Platelets are activated
  – Growth factor stimulates smooth muscle
    proliferation
• Endothelial alteration 
  – Cell proliferation entraps lipids, which are
    calcified over time and form an irritant to
    the endothelium on which platelets adhere
    and aggregate
• Endothelial alteration 
  – Thrombin is generated
  – Fibrin formation and thrombi occur
   Etiology and Pathophysiology
        Developmental Stages
• Fatty streak
  – Earliest lesions
  – Characterized by lipid-filled smooth
    muscle cells
  – Yellow tinge appears
  – Reversible
• Raised fibrous plaque
  – Beginning of progressive changes in the
    arterial wall
  – Initiated by chronic endothelial injury
  Etiology and Pathophysiology
      Developmental Stages
• Complicated lesion
  – Final stage in development
  – The most dangerous
  – Plaque consists of a core of lipid
    materials within an area of dead tissue
  – With the incorporation of lipids,
    thrombi, damaged tissue, and
    accumulation of calcium, the growing
    lesion becomes complex
   Etiology and Pathophysiology
       Collateral Circulation

• Normally some arterial branching,
  termed collateral circulation, exists
  within the coronary circulation
  Etiology and Pathophysiology
       Collateral Circulation
• Growth of collateral circulation is
  attributed to two factors:
   – The inherited predisposition to
     develop new vessels
   – The presence of chronic ischemia
• When occlusion of the coronary arteries
  occurs slowly over a long period, there is
  a greater chance of adequate collateral
  circulation developing
Collateral Circulation
     Coronary Artery Disease
• Collateral circulation
• Risk Factors: Unmodifiable
     •   age
     •   gender
     •   race
     •   genetic inheritance
Coronary Artery Disease (CAD)
• Risk factors: Modifiable
  – elevated serum lipids (major)
  – hypertension (major)
  – Tobacco use (major)
  – obesity (major)
  – sedentary life style (major)
  Contributing factors
  – diabetes mellitus
  – stress/behavioral patterns
Coronary Artery Disease (CAD)
• Risk factors: Modifiable
  – elevated homocysteine levels
  – elevations highly sensitive C reactive protein
     • indicates inflammatory response
    CAD: Health promotion and
          maintenance
• Modifiable risk factor management
  – Nutrition
     • normalize weight
     • diet low in saturated fats, cholesterol
  – Pharmacologic management
     • Drugs that increase removal lipoproteins
         – resin-type drugs: cholestyramine, colestipol
     • Drugs that decrease production of lipoproteins
         – HMG-CoA reductase inhibitors or “statins”
              • lovastatin (Mevacor), atorvastatin (Lipitor)
CAD: Health promotion and
      maintenance
•Drugs that decrease production of
lipoproteins
   –nicotinic acid
   –gemfibrozil
   –clofibrate
•Drugs which decrease absorption of
cholesterol
  –ezetimibe (Zetia)
     CAD: Health promotion and
           maintenance

• When are drugs started?
  – try dietary modification and exercise first
     • 6 months
  – drugs typically taken for the rest of one’s life to
    keep lipids under control.
Stable Angina
  Results when the lack of oxygen supply is temporary
  and reversible
Acute Coronary Syndrome (ACS)
  Develops when the oxygen supply is prolonged and
  not immediately reversible
ACS encompasses:
  Unstable angina
  Non-ST-segment-elevation myocardial infarction
  (NSTEMI)
  ST-segment-elevation (STEMI)
Clinical Manifestations of CAD

 • Angina Pectoris
 • Acute Coronary Syndrome
 • Sudden Cardiac Death
  Clinical Manifestations
• Stable Angina
   – Results when the lack of oxygen supply is
     temporary and reversible
• Acute Coronary Syndrome (ACS)
   – Develops when the oxygen supply is
     prolonged and not immediately
     reversible
• ACS encompasses:
   – Unstable angina
   – Non-ST-segment-elevation myocardial
     infarction (NSTEMI)
   – ST-segment-elevation (STEMI)
   CAD: Clinical Manifestations
• Angina pectoris
  – when demand exceeds supply of myocardial
    oxygen? ISCHEMIA
     • usually due to insufficient flow of
       oxygenated blood
         – narrowed arteries
         – coronary spasm
     • cellular metabolism changes to anaerobic
       and causes buildup of lactic acid which
       irritates nerves and transmits pain to cardiac
       nerves and thoracic nerve roots.
              CAD: Angina
• Precipitating factors
      • physical exertion (↑ heart rate)
      • strong emotions (↑ catecholamines)
      • consumption of a heavy meal (blood
        diverted)
      • temperature extremes
      • cigarette smoking
      • sexual activity
      • stimulants (cocaine, caffeine)
      • circadian rhythm patterns
               CAD: Angina
• Types of angina
   – stable
   – unstable (USA) or acute coronary syndrome
      • AKA progressive, crescendo, pre-infarction
        angina
   – variant or Prinzmetal’s
   – nocturnal angina?
• Clinical manifestations
   – Pain: squeezing, cramping, choking, burning
        Types of Angina
    Stable Angina Pectoris
• Chest pain occurring intermittently over a
  long period with the same pattern of onset,
  duration, and intensity of symptoms
• Pain usually lasts 3 to 5 minutes
   – Subsides when the precipitating factor is
     relieved
   – Pain at rest is unusual
   – ECG reveals ST segment depression
• Stable angina can be controlled with
  medications on an outpatient basis
  Canadian Cardiovascular Society
       Angina Classification
  Class 0: Asymptomatic
• Class 1: Angina with strenuous Exercise
• Class 2: Angina with moderate exertion
• Class 3: Angina with mild exertion
  – Walking 1-2 level blocks at normal pace
  – Climbing 1 flight of stairs at normal pace
• Class 4: Angina at any level of physical
  exertion
      Types of Angina
       Silent Ischemia


• Up to 80% of patients with
  myocardial ischemia are
  asymptomatic
• Associated with diabetes mellitus and
  hypertension
           Types of Angina
         Prinzmetal’s Angina
• “Variant angina”
• Occurs at rest usually in response to spasm
  of major coronary artery
• Seen in patients with a history of migraine
  headaches and Raynaud’s phenomenon
• Spasm may occur in the absence of CAD
• When spasm occurs:
   – Pain
   – Marked, transient ST segment elevation
   – May occur during REM sleep
           Types of Angina
Nocturnal Angina and Angina Decubitus

  • Nocturnal Angina
    – Occurs only at night but not
      necessarily during sleep
  • Angina Decubitus
    – Chest pain that occurs only while
      lying down
    – Relieved by standing or sitting
    Types of Angina
     Unstable Angina
• Angina that is:
   – New in onset
   – Occurs at rest
   – Has a worsening pattern
   – Unpredictable
   – Considered to be an acute
     coronary syndrome
• Associated with deterioration of a
  once stable atherosclerotic plaque
        Clinical Manifestations
                Angina
• Most common clinical manifestation is chest pain
  or discomfort
• Exact cause of the pain is unknown
• Neurogenic pain at the site of ischemia is most
  likely
• Referred to as a vague sensation, a strange
  feeling, pressure, or ache in the chest
• An unpleasant feeling described as constrictive,
  squeezing, heaving, choking, or suffocating
  sensation
• Almost never sharp or stabbing
• Usually does not change with position or
  breathing
• May complain of severe indigestion or burning
   Treatment/Education for Stable
              Angina
• A-ASA and antianginal therapy- nitro imdur
• B-Beta Blocker and Blood Pressure tx
• C-Cigarette Smoking (stop) and Cholesterol
  (lower)
• D-Diet and Diabetes
• E-Education and Exercise
              CAD: Angina
• Complications
      • arrhythmias
      • ↓ myocardial contractility
• Diagnostic studies
  – thorough history and physical
  – chest X-ray
  – lipid levels
  – cardiac enzymes (isoenzymes), proteins
  – ECG: compare to previous readings
              CAD: Angina
• Diagnostic studies (continued)
  – treadmill exercise testing
  – 24-hour ECG monitoring
  – nuclear imaging
      • thallium/radioisotope, Dobutamine Stress
        echo
  – positron emission tomography (PET scan)
  – angiography
              CAD: Angina

• Diagnostic studies (continued)
  – echocardiography (exercise vs. meds)
  – transesophageal echocardiography (TEE)
  – positron emission tomography (PET)
  – electron beam computed tomography
    (EBCT)
     • can ID patients with risk factors but no
       S/S
               CAD: Angina
• Therapeutic management: Pharmacologic
   – #1 Antiplatelet aggregation therapy
      • ASA 50% reduction in progression USA to
        MI
   – Antianginals – short and long acting Nitrates
      • dilates peripheral vessels and coronaries
      ACE inhibitors or ARBs
   – Beta-adrenergic blockers
      • cardioprotective, < morbidity and mortality
      • lessens cardiac workload
      Management of Angina

  – Calcium channel blockers
• Therapeutic Management:Reperfusion
  – Percutaneous coronary intervention (PCI)
     • benefits
     • complications
  – Balloon dilation
  – Stent placement
  – Atherectomy
  – CABG coronary artery bypass grafting
       Collaborative Care
               Angina
• Treatment for stable angina:
  –  oxygen demand and/or  oxygen
    supply
  – Nitrate therapy
  – Stent placement
  – Percutaneous coronary intervention
  – Atherectomy
  – Laser angioplasty
  – Myocardial revascularization
      Collaborative Care
                Angina
• Percutaneous coronary intervention
   – Surgical intervention alternative
   – Performed with local anesthesia
   – Ambulatory 24 hours after the
     procedure
• Stent placement
   – Used to treat abrupt or threatened
     abrupt closure and restenosis following
     PCI
    Collaborative Care
              Angina
• Atherectomy
  – The plaque is shaved off using a type of
    rotational blade
  – Decreases the incidence of abrupt
    closure as compared with PCI
• Laser angioplasty
  – Performed with a catheter containing
    fibers that carry laser energy
  – Used to precisely dissolve the blockage
    Collaborative Care
            Angina
• Myocardial revascularization (CABG)
  – Primary surgical treatment for CAD
  – Patient with CAD who has failed
    medical management or has advanced
    disease is considered a candidate
• MIDCABG procedure
  – Minimally invasive direct coronary
    artery bypass grafting (MIDCABG)
  – Alternative to traditional CABG
  Angina: Nursing Management
• Assessment
  – history
  – risk factors
  – pain characteristics (PQRST), (OLDCART)
• Nursing diagnoses
      • pain r/t ischemic myocardium
      • anxiety r/t diagnosis, pain, uncertainty about
        future
      • decreased cardiac output r/t myocardial
        ischemia
      • activity intolerance r/t myocardial ischemia
  Angina: Nursing Management
• Planning
      • pain relief
      • decrease anxiety
      • verbalize adequate knowledge of
        problem, treatment
      • modify risk factors
• Interventions
   – Emergency treatment chest pain
      • ABCs
     Angina: Nursing Management
– Emergency treatment chest pain (MONA)
   • Morphine sulfate if pain unrelieved
   • Oxygen
   • NTG spray, or sublingual or IV if indicated
   • ASA 325mg
   • 2 large gauge IV lines
   • cardiac monitor, 12-lead ECG (gold
     standard) soon as possible, VS
   • history when able or family present.
   • assess contraindications thrombolytic therapy
   • send to cardiac cath lab within 30 minutes
  Angina: Nursing Management
  – Assessment of pain, response to meds
     • get detail pain characteristics
     • use pain scale
  – Monitor blood pressure, heart tones
• Chronic management of angina
     • Teach nitroglycerin
       administration/storage
     • precipitating factors, S/S angina vs. MI
     • personal risk factors
     • diet and exercise
    Myocardial Infarction (MI)
• Pathophysiology acute coronary syndrome
   – ischemia irreversible
      • cellular death, necrosis
   – increased mortality first 24 hours
      • 30-50% pre-hospital mortality from
        lethal arrhythmias.
   – Cell death (cellular contents spill out)
      • ST elevation MI
      • non ST elevation MI
      • many MIs involve left ventricle
Etiology and Pathophysiology
 • Coronary spasm - The constriction is
   transient and reversible Causes either
   subtotal or total narrowing
 • Myocardial cyanosis occurs within
   the 1st 10 seconds of coronary
   occlusion
 • ECG changes
 • Total occlusion  anaerobic
   metabolism and lactic acid
   accumulation
               Time is Tissue
•   4-6 hours without O2 for tissue to die
•   Apoptosis
•   Stunned Myocardium
•   Hibernating Myocardium
Etiology and Pathophysiology
 • Myocardial Infarction
   – Occurs as a result of sustained ischemia,
     causing irreversible cellular death
 • Myocardial Infarction
   – The degree of altered function depends
     on the area of the heart involved and the
     size of the infarct
Etiology and Pathophysiology
 • Myocardial Infarction
   – Contractile function of the heart
     stops in the areas of myocardial
     necrosis
   – Most involve the left ventricle
     (LV)
 • Types of Myocardial Infarction
   – Transmural MI
      • Involves the entire thickness of
        the myocardium
Etiology and Pathophysiology
 • Myocardial Infarction
   – Subendocardial MI
      • The damage has not penetrated
        through the entire thickness
   – Infarctions are described by the
     area of occurrence
    Etiology and Pathophysiology
           Healing Process
• Within 24 hours, leukocytes infiltrate the area
  of cell death
• Enzymes are released from the dead cardiac
  cells (important indicators of MI)
• Proteolytic enzymes of neutrophils and
  macrophages remove all necrotic tissue by 2nd
  or 3rd day
• Development of collateral circulation improves
  areas of poor perfusion
• Necrotic zone identifiable by ECG changes and
  nuclear scanning
• 10 to 14 days after MI, scar tissue is still weak
Etiology and Pathophysiology
         Healing Process
 • By 6 weeks after MI, scar tissue has
   replaced necrotic tissue
    – Area is said to be healed
 • Ventricular remodeling
    – In an attempt to compensate for the
      infarcted muscle, the normal
      myocardium will hypertrophy and
      dilate
    Clinical Manifestations
       Myocardial Infarction
• Pain
   – Severe, immobilizing chest pain not relieved by
     rest, position change, or nitrate administration
      • The hallmark of an MI
• Nausea and vomiting
   – Can result from reflex stimulation of the
     vomiting center by the severe pain
• Sympathetic nervous system stimulation
   –  catecholamines released during initial phases
     of MI
   – Results in diaphoresis and vasoconstriction
   Clinical Manifestations
      Myocardial Infarction
• Pain
   – Severe, immobilizing chest pain not relieved
     by rest, position change, or nitrate
     administration
      • The hallmark of an MI
• Nausea and vomiting
   – Can result from reflex stimulation of the
     vomiting center by the severe pain
• Sympathetic nervous system stimulation
   –  catecholamines released during initial
     phases of MI
   – Results in diaphoresis and vasoconstriction
         Clinical Manifestations
         Myocardial Infarction
• Fever
   – May  within 1st 24 hours up to 100.4°
   – May last as long as 1 week
   – Systemic manifestation of the inflammatory
     process caused by cell death
• Cardiovascular manifestations
   –  BP and heart rate initially
   – Later the BP may drop from  CO
   –  urine output
   – Crackles
   – Hepatic engorgement
   – Peripheral edema
      Myocardial Infarction (MI)
• Complications post-MI
    • Arrhythmias occur in 80%
    • CHF
    • cardiogenic shock
    • papillary muscle dysfunction
    • ventricular aneurysm
    • pericarditis
    • Dressler syndrome (post-MI syndrome)
    • right ventricular infarction
Complications of Myocardial
        Infarction
• Arrhythmias
  – Most common complication
  – Present in 80% of MI patients
  – Most common cause of death in the
    prehospital period
• Congestive heart failure
  – A complication that occurs when the
    pumping power of the heart has
    diminished
Complications of Myocardial
        Infarction
 • Cardiogenic shock
    – Occurs when inadequate oxygen and
      nutrients are supplied to the tissues
      because of severe LV failure
    – Requires aggressive management
 • Papillary muscle dysfunction
    – Causes mitral valve regurgitation
    – Condition aggravates an already
      compromised LV
Complications of Myocardial
        Infarction
• Ventricular aneurysm
  – Results when the infarcted
    myocardial wall becomes thinned
    and bulges out during contraction
• Pericarditis
  – An inflammation of the visceral
    and/or parietal pericardium
  – May result in cardiac compression, 
    LV filling and emptying, and cardiac
    failure
Complications of Myocardial
        Infarction
• Dressler syndrome
  – Characterized by pericarditis with
    effusion and fever that develops 1 to
    4 weeks after MI
• Pulmonary embolism
  – Source of the thrombus may be the
    roughened endocardium or leg veins
    Myocardial Infarction (MI)
• Complications post-MI (continued)
     • pulmonary embolism
• Diagnostic studies
  – rapid assessment
     • 12-lead ECG, (ST elevation in at least
       2 leads)
     • serial measurement of cardiac markers
        –troponin: very sensitive
        –CK-MB
     • albumin cobalt-binding (ACB)
    Myocardial Infarction (MI)
• Therapeutic Management
  – CCU care
     • continuous monitoring for arrhythmias
       and treatment when they occur
     • morphine sulfate IVP
     • oxygen by nasal cannula 2-4 lpm
     • IV lidocaine or amiodarone
     • VS every 1-2 hours
     • PA catheter, arterial line if LV
       dysfunction
          Therapeutic Management MI
•    Therapeutic Management
    – CCU care
      • anti-platelet aggregation tx. (start in ER or cath
        lab)
          – decrease incidence of new MI, death,
            refractory ischemia
          – tirofiban (Aggrastat) intravenous
          – abciximab (Reopro) intravenous
          – eptifibatide (Integrilin)
          – give with aspirin, heparin, lovenox
            concurrently
      • thrombolytic therapy (start in ER or cath lab)
          – contraindications?
   Therapeutic Management MI
• Other pharmacologic management
  – IV nitroglycerin, antiarrhythmics
  – positive inotropic agents
  – beta-adrenergic blockers
  – calcium-channel blockers
  – angiotensin-converting enzyme inhibitors
  – stool softeners
• Nutritional management
   Therapeutic Management MI
• Nursing Management
  – Assessment
         – thorough history
         – physical, test results
  – Nursing diagnosis
     • Acute pain r/t lactic acid production and
       altered MVO2
     • Altered cardiac tissue perfusion r/t
       myocardial damage, decreased cardiac
       output
     • Anxiety related to pain, perceived threat of
       death
   Therapeutic Management MI

• Nursing Management (continued)
     • Impaired gas exchange r/t ineffective
       breathing,, decreased systemic tissue
       perfusion
     • Activity intolerance r/t fatigue d/t decreased
       cardiac output, poor tissue perfusion
     • Self-esteem disturbance r/t lack of control,
       illness, and perceived role changes
     • Constipation r/t immobility, change in diet,
       fluid restriction, meds
   Therapeutic Management MI
• Nursing Management (continued)
     • Ineffective management of therapeutic
       regimen r/t lack of knowledge.
     • Grieving r/t actual or perceived losses
       secondary to cardiac condition
  – Planning
         – relief of pain
         – no progression of MI
         – receive immediate, correct treatment
         – effective coping with anxiety
   Therapeutic Management MI
• Nursing Management (continued)
  – Planning
         – compliance with rehabilitation plan
         – alteration of high-risk behaviors
  – Interventions
     • Reduce myocardial oxygen demand
     • Pain: MS, pain scales, nonverbal signs, NTG
       titration
     • Monitoring
         – ECG in CCU, telemetry; tx. arrhythmias
         – ventricular fibrillation most lethal
   Therapeutic Management MI
• Nursing Management (continued)
  – Interventions
     • Monitoring
         – VS, I and O
         – assessment heart and lung sounds
         – oxygenation, fluid retention, thrombosis
     • Rest/comfort
         – bedrest if severe, gradual increase in
           activity
     • Anxiety management
         – teaching only if ready, do not force.
   Therapeutic Management MI
• Chronic/Home management
  – Cardiac rehabilitation
  – Patient education
     • S/S MI vs. angina
     • identification/reduction of modifiable
       risk factors
  – Physical exercise
  – Resumption sexual activity
     • 1-2 flights stairs without symptoms
  Sudden Cardiac Death Pg 817
• Unexpected cardiopulmonary arrest
  – Within minutes to one hour after symptoms
  – 350,000 yearly
     • Poor prognosis, only 10% discharged from
       hospital
  – Multi-vessel coronary arteriosclerosis common
     • Often no previous history
  – Death due to arrhythmias (ventricular
    tachycardia and or ventricular fibrillation)
  – Risk factors same as for CAD and
     • Ejection fraction < 40%
     • History of ventricular arrhythmias
        Sudden Cardiac Death
• Therapeutic management
   – Did they have acute MI?
      • Typical MI workup: enzymes, troponin,
        ECG
      • Cardiac cath to assess degree of problem
         – PTCA vs. CABG
      • Electrophysiology study
         – Possible insertion AICD/ICD
      • Counseling for patient/family
      • Patient/Family education
   Gerontologic considerations
             CAD
• Physiologic changes occur with aging
  –   Increased collagen, fat deposition
  –   Myofibrillar degeneration
  –   Endocardial thickening
  –   Calcification of heart valves
  –   Degeneration conduction system
  –   Loss of elasticity of arteries, > SBP, SVR
  –   Decrease in CO 1% per year
  –   Increase norepinephrine, slowed response
      receptors
    Gerontologic considerations
              CAD
• Considerations
     • Changes in vital signs occur more slowly
     • Atypical symptoms with acute MI
     • Longer warm-up and cool down periods
         – Watch for heat intolerance, decrease in
           sweating
     • Increase in unstable angina, CHF,
       complication related to AMI (arrhythmias!)
  – Watch for early signs/symptoms
     • Treat aggressively
            Women and CAD
• Myocardial infarction #1 killer women
  – CAD symptoms begin about 10 years later than
    men
     • Protective female hormones
  – Women have higher mortality/morbidity with
    fewer returning to work
     • Post-MI, post-CABG
  – Risk factors: diabetes mellitus more influential
     • Smoking is major risk for women in their
       40s
     • Hypertension also of major concern
          Women and CAD
• Typical tests diagnostic for men are not
  useful in women
   – Exercise stress tests not indicative for
     women
   – Thallium treadmill much more sensitive
      • Still not as reliable as EST for men
   – Echocardiogram with exercise even better
• EDUCATE!! Careful assessment when risk
  factors present (Smoking and Oral
  contraceptives use)
              CAD Review
• Stable angina
Pain characteristics, diagnosis, treatment?
  Unstable Angina
Pain characteristic, diagnosis, treatment?
  Myocardial Infarction
Pain characteristic, diagnosis, treatment?
 Drug Review
BB, Morphine, Nitroglycerin,
 antilipemics, ASA, lidocaine,
 amiodarone, thrombolytics
                       CABG
Coronary Artery Bypass Graft
                 • Native vessels
                      Surgery
                  – Saphenous vein
                  – Internal mammary artery
                     • Off–pump CABG
• Transmyocardial laser revascularization

				
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