Acute Coronary Syndromes

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Acute Coronary Syndromes

• By Dr azimian

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The motion of the heart is best understood by God
alone. - Harvey
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Time lost life lost
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Definitions

• Acute coronary syndrome is defined as myocardial
  ischemia due to myocardial infarction (NSTEMI or
  STEMI) or unstable angina or Sudden cardiac death

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• 23.8 of admissions to resus. unit for chest
  pain/acs related (stats 1Jan 2009 28 Feb 2009)
  150/628 entries.
• In US 1.56 million admissions for ACS 669 000
  for unstable angina, 896 000 for MI
• Higher prevelance for NSTEMI.

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• CAD is a continuum of disease.
• Angina -gt unstable angina -gt AMI -gt sudden
  cardiac death
• Acute coronary syndrome encompasses unstable
  angina, NSTEMI, STEMI
• Stable angina transient episodic chest pain d/t
  myocardial ischaemia, reproducible, frequency
  constant over time.usually relieved with
  rest/NTG.
• Classification of angina Canadian
  Cardiovascular Society classification.

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Canadian Cardiovascular Association
Classification of Angina
CLASS 1 NO PAIN WITH ORDINARY PHYSICAL ACTIVITY
CLASS 2 SLIGHT LIMITATION OF PHYSICAL ACTIVITY PAIN OCCURS WITH WALKING, CLIMBING STAIRS,STRESS
CLASS 3 SEVERE LIMITATION OF DAILY ACTIVITY PAIN OCCURS ON MINIMAL EXERTION
CLASS 4 UNABLE TO CONDUCT ANY ACTIVITY WITHOUT PAIN, PAIN AT REST
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• WHY IS IT IMPORTANT TO RECOGNISE PATIENTS WITH
  UNSTABLE ANGINA??
• 5 -17 suffer an MI within a week after
  admission.
• 3 -15 die within a year.

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• UNSTABLE ANGINA
• Pain occurring at rest duration gt 20min, within
  one week of first visit
• New onset angina Class 2 severity, onset with
  last 2 months
• Worsening of chest pain increase by at least 1
  class, increases in frequency, duration
• Angina becoming resistance to drugs that
  previously gave good control.
• NB! ECG normal, ST depression(gt0.5mm), T wave
  changes

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Pathophysiology of ACS

• Plaque rupture and subsequent formation of
  thrombus this can be either occlusive or
  non-occlusive (STEMI, NSTEMI, USA)
• Vasospasm such as that seen in Prinzmetals
  angina, cocaine use (STEMI, NSTEMI, USA)
• Progression of obstructive coronary
  atherosclerotic disease (USA)
• In-stent thrombosis (early post PCI)
• In-stent restenosis (late post PCI
• Poor surgical technique (post CABG)

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ATHEROSCLEROSIS
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Pathophysiology of ACS

• Acute coronary syndromes can also be due to
  secondary causes
• Thyrotoxicosis
• Anemia
• Tachycardia
• Hypotension
• Hypoxemia
• Aterial inflammation (infection, arteritis)

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Assesment

• 1. Hx
• 2. Physical Exam
• 3. EKG
• 4. Exercise EKG
• 5. Thallium Scan
• 6. Coronary Angiography
• 7. Cardiac Enzymes

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Diagnosis

• Dx of acute coronary syndrome is based on
  history, physical exam, ECG, cardiac enzymes
• Patients can then be divided into several groups
• Non-cardiac chest pain (i.e., Gastrointestinal,
  musculoskeletal, pulmonary embolus)
• Stable angina
• Unstable angina
• Myocardial infarction (STEMI or NSTEMI)
• Other cardiac causes of chest pain (i.e., aortic
  dissection, pericarditis)

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ECG for acute chest pain

• Not a perfect diagnostic tool (specificity-sensiti
  vity)
• 10 of new ST-elevations are not caused by MI
• Up to 50 of MI patients present with normal or
  inconclusive ECG (e.g. previous MI, LV
  hypertrophy)
• 2 of patients with normal ECG will develop MI
• 15-lead ECG for right ventricular or posterior MI
  
• Request previous ECG for comparison
• Serial ECGs (and continuous ST-monitoring?)
  improve sensitivity

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Ischemia ,Acute Injury, Infarction
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Ischemia

• T wave inversion, ST segment depression
• Acute injury ST segment elevation
• Dead tissue Q wave

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Gender Differences in MI

• Females, when compared to males
• -present with MI later in life
• -have poorer prognosis and high morbidity
• -are 2x as likely to die in the first weeks
• -are more likely to die from the first MI
• -have higher rates of unrecognized MI
• -NSTEMI MI vs STEMI

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The perfect marker

• Marker for myocardial necrosis, and also for
  cardiac ischemia
• Linear relationship between blood levels and
  extent of myocardial injury (and prognosis)
• 100 sensitive
• 100 specific
• Immediate increase ( constant blood level for
  hours to days)
• Test kits reliable, rapid, universally
  available and inexpensive

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What about troponin T and I ?

• Very high sensitivity for myocardial necrosis
• Related to prognosis
• Not 100 specific for atherosclerotic coronary
  artery disease
• (myocarditis, cardiomyopathy, myocardial
  contusion, renal failure, auto-immune diseases,
  ...)
• Up to 6 hours before raised blood levels no
  early MI diagnosis possible
• Raised blood levels for many days troublesome
  diagnosis of re-infarction

BUT
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TROPONINS T/I

• Troponin T vs I
• both equivalent in diagnostic and prognostic
  abilities ( except in renal failure Trop T less
  sensitive)
• Elevation 2hrs to 12hrs
• 30 40 of ACS patients without ST elevation
  had normal CKMB but elevated troponins on
  presentation
• Meta-analysis (Heindereich et al) odds of death
  increased 3 to 8 fold with positive troponin

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Role for myoglobin ?

• Initial elevation 1 to 4h after onset better
  early marker than troponins
• BUT early myoglobin is less sensitive and
  less specific (due to skeletal muscle trauma)
  than late troponin decisions mainly based on
  clinical skills, ECG and late troponin
  (except rarely for reperfusion therapy)
• Duration of elevation 24 48h useful for
  re-infarction diagnosis

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Role for CK-MB ?

• Initial elevation comparable with troponins
• Less sensitive than troponins
• High specificity (comparable with troponins)
• Rapid rise and fall (instead of gradual fall for
  troponins) allowing more accurate estimation of
  MI extent

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MYOGLOBIN

• Rapid release within 2 hours
• Not cardiac specific
• Rule out for NSTEMI rather than rule in.
• CKMB
• Used in conjunction with troponins
• Useful in diagnosing re-infarction

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Pre-test Probability

• In the absence of abnormal findings on physical
  exam, ECG, or enzymes, the pre-test probability
  of acute coronary syndrome must be determined by
  the clinician
• A good history is crucial (is the chest pain
  typical or atypical what are the associated
  symptoms)
• Determination of risk factors is also crucial
  (male, age gt55, smoking, DM, HTN, FamHx,
  hyperlipidemia, known CAD)

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Angiogram pre/post PTCA
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imaging
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Treatment of ACS Aspirin

• Aspirin is an antiplatelet agent that initiates
  the irreversible inhibition of cyclooxygenase,
  thereby preventing platelet production of
  thromboxane A2 and decreasing platelet
  aggregation
• Administration of ASA in ACS reduces cardiac
  endpoints

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ACC/AHA Guidelines for Aspirin Therapy

• Aspirin should be given in a dose of 75-325
  mg/day to all patients with ACS unless there is a
  contraindication (in which case, clopidogrel
  should be given)
• Newest guidline clopidogrel asprin

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Treatment of ACS Nitrates

• Nitroglycerin is considered a cornerstone of
  anti-anginal therapy, despite little objective
  evidence for its benefit
• Benefit is thought to occur via reduction in
  myocardial O2 demand secondary to venodilation
  induced reduction in preload as well as coronary
  vasodilation and afterload reduction
• Titrate to relief of chest pain chest pain
  death of myocardial cells
• No documented mortality benefit

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Side/Adverse Effects

• Vascular HA (may be severe)
• Hypotension (may be marked)
• Tachycardia
• Palpitations

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Treatment of ACS Beta Blockers

• Beta Blockers reduce myocardial oxygen demand by
  reducing heart rate, contractility, and
  ventricular wall tension
• Administration of beta blockers in ACS reduces
  cardiac endpoints

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Beta Blocker Trials

• HINT (metoprolol)
• Beta Blocker Heart Attack Trial (propranolol)
• Esmolol vs. placebo
• Carvedilol vs. placebo
• Propranolol vs. placebo
• Overall, treatment with beta blockers reduces
  primary endpoints when compared to placebo

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AHA/ACC Guidelines for Beta Blocker Therapy

• Intravenous beta blockers should be used
  initially in all patients (without
  contraindication) followed by oral beta blockers
  with the goal being decrease in heart rate to 60
  beats per minute
• A combination of beta blockers and nitrates can
  be viewed as first line therapy in all patients
  with ACS

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Treatment of ACS Heparin

• Heparin (unfractionated heparin or UFH) has
  traditionally been the mainstay of therapy in
  acute coronary syndromes as its efficacy has been
  documented in several large, randomized trials

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Heparin Trials

• Heparin/Atenolol Trial
• The Canadian Heparin/Aspirin Trial
• The RISC Trial
• Overall, UFH therapy generally results in an
  important clinical benefit when compared to
  placebo. It is more effective when given in
  continuous infusion rather than intermittent
  boluses

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Treatment of ACS LMWH

• More recent studies indicate that low molecular
  weight heparin is also effective in the reduction
  of end points such as myocardial infarction or
  death
• Some studies report that LMWH, when used in
  combination with ASA, may be superior to
  continuous infusion of Heparin

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ACC/AHA Guidelines for Heparin Therapy

• All patients with acute coronary syndromes should
  be treated with a combination of ASA (325 mg/day)
  and heparin (bolus followed by continuous
  infusion with goal of PTT 1-2.5X control) or ASA
  and low molecular weight heparin unless one of
  the drugs is contraindicated

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Treatment of ACS ACE-I

• The best documented mechanism by which these
  agents act is to reduce ventricular remodeling
  over days to weeks after myocardial damage.
  However, there is data that a mortality benefit
  exists when these agents are used early in the
  course of ACS
• Administration of ACE-I in ACS reduces cardiac
  endpoints

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AHA/ACC Guidelines for ACE-I Therapy

• ACE-I should be administered to all patients in
  the first 24 hours of ACS provided hypotension
  and other clear cut contraindications are absent

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Treatment of ACS Statins

• Statins may be of benefit in ACS
• Possible mechanisms include plaque stabilization,
  reversal of endothelial dysfunction, decreased
  thrombogenicity, and reduction of inflammation

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TIMI Risk ScoreThrombolysis In Myocardial
Infarction',

• Age gt65 yrs
• Daily ASA Therapy (gt7 days prior to event)
• Symptoms of Unstable Angina
• Documented CAD (stenosis gt 50)
• 3 or more traditional cardiac risk factors
• Elevated cardiac enzymes
• ECG changes

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TIMI Risk Score

• Score of 3 or less low risk
• Score of 4-5 intermediate risk
• Score of 6-7 high risk

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Treatment of ACS Clopidogrel

• Clopidogrel is a potent antiplatelet agent
• It should be administered to all patients who
  cannot take ASA
• The CURE trial suggests a benefit to adding
  Clopidogrel to ASA/Heparin in patients going for
  PCI
• Give 300 mg loading dose followed by 75 mg/day

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AHA/ACC Guidelines for Clopidogrel

• Clopidogrel should be administered to patients
  who cannot take ASA because of hypersensitivity
  or gastrointestinal intolerance
• In hospitalized patients in whom an early,
  noninterventional approach is planned,
  clopidogrel should be added to ASA as soon as
  possible on admission and administered for at
  least 1 month and up to 9 months. Do not use
  clopidogrel if there is any possibility patient
  may be candidate for CABG

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Treatment of ACS Emergent Revascularization

• In the setting of STEMI primary PCI is associated
  with better outcomes than thrombolysis
• Emergent PCI is also indicated in the setting of
  a new LBBB

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AHA/ACC Guidelines for Primary PCI

• Primary PCI is indicated as an alternative to
  thrombolysis when the following criteria are met
• STEMI or new LBBB
• Can undergo PCI within 12 hours of the onset of
  symptoms
• The MD doing the intervention does more than 75
  PCIs/yr
• The procedure is done in a center that does more
  than 200 PCIs/yr and has surgical backup

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Conclusions Approach to Chest Discomfort

• Good History and Physical (note time and duration
  of symptoms)
• Careful evaluation of ECG (compare to previous
  when possible)
• Check Cardiac Enzymes
• Monitor on Telemetry
• Oxygen

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Acute Angina Treatment

• Goal Enhance 02 supply to myocardium
• M- Morphine for pain
• O- Oxygen 4-6L as ordered
• N- NTG sublingual, repeat q5 minutes x3
• A- Aspirin to prevent platelet aggregation

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Patient education

• Lifestyle modifications for controllable risk
  factors. Support groups are helpful, Example
  Weight watchers,
• Smoke-enders, stress workshops, cardiac
  rehabilitation. Supply patients with
  information, name of contact person and phone
  numbers
• Identify precipitating factors for Anginal pain
• Medication compliance

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Nursing Interventions

• Obtain EKGs
• Monitor mentation
• Assess heart sounds
• Assess lungs
• Assess peripheral circulation/skin
• Assess urinary output
• Assess GI function
• Assess pain

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Nursing Interventions

• Activity
• Safety
• Reduce anxiety
• Patient Education
• Nutrition

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