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Cardiology > Acute Coronary Syndrome II > Flashcards

Acute Coronary Syndrome II Flashcards

1
Q

ACS Demographics & Statistics

A
  • Middle age: men > women
  • Elderly: men = women
  • 1/2 of patients who die w/ AMI do so due to sudden death before they reach the hospital
  • Up to 10% of survivors die in the year after hte MI
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2
Q

Unstable Angina Pectoris

  • Symptoms of MI or impending MI
  • Physical exam
A
  • Symptoms of MI or impending MI
    • New onset of chest discomfort suggestive of MI occuring at rest or w/ ordinary activities
    • Angina changes
      • –> more frequent, severe, prolonged, or difficult to relieve w/ rest or nitroglycerin
      • Occurs at rest for the first time
    • Chest discomfort suggestive of MI in a pt w/ coronary heart disease that’s unrelieved by rest or nitroglycerin
  • Physical exam
    • Less valuable in ACS than history & ECG
    • S4 sometimes present form stiff LV
    • If S3 is present, indicates LV dysfunction
    • Short systolic murmurs may suggest MR from ischemic papipllary muscle dysfunction
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3
Q

ECG

  • Places pt into 1 of 2 categories
  • Transmural injury
  • Subendocardial injury/ischemia
  • Infarction patterns
  • Leads
  • “Strictly” / “True” posterior wall
  • Silent MI
  • Caution
A
  • Places pt into 1 of 2 categories
    • ST elevation MI (STEMI)
    • Unstable angina pectoris (UA) / Non-ST elevation MI (NSTEMI)
  • Transmural injury
    • ST elevation + injury pattern
    • J-point elevation w/ an ST segment that’s lost its normal concave upward appearance & has a straight or concave downwards appearance
  • Subendocardial injury/ischemia
    • ST segment depression or T wave inversion or both
  • Infarction patterns
    • Pathological Q wave / QS complex (old = prior infarction)
    • Likely to develop after ST elevation
  • Leads
    • V1-V5: anterior wall
    • V1-V4: anteroseptum
    • V3-V6: anterolateral
    • V3 &/or V4: apex
    • I, aVL, & V6: lateral wall
    • II, III, & aVF: inferior wall
  • “Strictly” / “True” posterior wall
    • Inferred in the presence of deep ST depression in leads V1 & V2
  • Silent MI
    • Not associated w/ classical symptoms
    • > 25% of Q-wave infarctions
    • In pts at risk for coronary heart disease, presentation w/ pulmonary edema or stroke should be considered as due to AMI
  • Caution
    • ECG is near normal in some cases early in the event
      • Esp when the circumflex coronary artery is the “culprit”
    • In pts w/ ongoing symptoms, ST depression, & T wave changes in lateral leads: NSTEMI may mask an STEMI
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4
Q

Cardiac Biomarker Measurements for Myocardial Necrosis

  • Cardiac markers
  • Cardiac troponins I (inhibitory) & T (tropomyosin-binding)
  • CK & CK-MB (its subunit)
  • Using cardiac markers
A
  • Cardiac markers
    • Measrued in the peripheral blood to document MI & determine infarct size
  • Cardiac troponins I (inhibitory) & T (tropomyosin-binding)
    • Appear in the bloodstream 8 hours after MI, peak at 24 hours, & gradually decline over a week
    • Highly sensitive & specific for myocardial necrosis
    • Useful for detecting MI in patients who present early & late
    • Caution: MI damage from any cause –> troponin elevation, so doesn’t diagnosis ACS
  • CK & CK-MB (its subunit)
    • CK naturally occurs in 3 forms
      • MM: skeletal muscle (100%) & cardiac muscle (80-85%)
      • BB: CNS (100%)
      • MB: cardiac muscle (15-20%), presence in serum –> AMI
    • Appear in bloodstream 8 hours after MI, peak in 24-48 hours, return to normal in 3-5 days
    • Diagnosis of MI w/ CK requires elevated CK/CK-MB w/ characteristic peaking pattern
  • Using cardiac markers
    • Toponin I or T: measure at admission, 8-12 hours later, & 24 hours later
      • Most reasonable & cost-effective
    • CK & CK-MB: measure every 8 hours for > 3 samples until (trending values) until peak CK is established
      • Reserved for pts w/ suspected recurrent MI w/ known troponin elevation
    • Negative troponin or CK in first 6-8 hours doesn’t rule out MI
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5
Q

General Pathophysiologic, Diagnostic, & Therapeutic Considerations

  • Evaluation & ECG monitoring
  • IV access
  • Oxygen therapy
  • Pain relief
A
  • Evaluation & ECG monitoring
    • Immediate ECG monitoring
      • High incidence of life-threatening rate & rhythm disorders in early ACS
    • Chest pain –> ECG interpretation within 10 mins
      • Determines ACS &, if so, ST elevation vs. depression &/or T wave abnormalities
  • IV access
    • Facilitates immediate pharmacological therapy
  • Oxygen therapy
    • For all MI pts until normal oxygen saturation is documented
    • Hypoxia w/ AMI is common & caused by ventilation-perfusion abnormalities & LV failure
  • Pain relief
    • High priority b/c ongoing pain can worsen ischemia & necrosis
    • (1) Sublingual nitroglycerin (unless contraindicated) b/c difficult to distinguish ischemia from infarction
    • (2) Opiate analgesics if chest pain & ECG abnormalities don’t resolve w/ 3 nitroglycerin administrations
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6
Q

Assessing Risk w/ ACS: Determinants of Mortality

  • Determinants of mortality following AMI
  • Why mortality risk is important
  • Intermediate/high risk category
    • Includes…
    • Intervention
      • Intermediate
      • High
      • Both
A
  • Determinants of mortality following AMI
    • LV size & function
    • Hemodynamic status (HR, BP, CHF, CVP, PCW/PA diastolic pressure, CO)
    • Size of infarct
    • Gender (women worse)
    • Age (older worse)
    • Ventricular rhythm disorders
    • Spontaneous or provoked (stress-test) ischemia
  • Why mortality risk is important
    • Place UA/NSTEMI pts in low, intermediate, or high risk categories to dermine need for early coronary arteriography & coronray revascularization therapy
    • Higher risk –> greater benefit of interventions
    • Continue risk eval for > 24 hours after admission b/c low risk can –> high risk
  • Intermediate/high risk category
    • Includes…
      • CAD
      • Unstable angina
      • Ongoing chest discomfort
      • New or dynamic ST changes or T wave changes
      • Positive biomarkers for MI
      • Hemodynamic instability
      • Ventricular rhythm abnormalities (“electrical instability”)
    • Intervention
      • Intermediate: admission to hospital in a step-down monitored unit
      • High: admission to coronary intensive care unit
      • Both: strong consideration for early (24-48 hours) but not emergency coronary arteriography
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7
Q

Ventricular Tachyarrhythmias: Early VT, VF, & Sudden Cardiac Death (First 2 Days)

  • AMI associated w/…
  • VT abnormalities
  • Likelihood of these abnormalities
  • Prognosis w/ VT or VFib in the first two days of MI
A
  • AMI associated w/…
    • Increased incidence of VT
    • Decreased threshold for VFib
    • Most common causes of SCD in 1st day of ACS
  • VT abnormalities
    • “Warning” premature ventricular complexes (PVCs) –> higher risk for VFib
      • Frequent, coupled, multiform, or falling on the T wave of the proceeding complex (“R on T phenomenon”)
    • “Primary” VFib w/o warning PVCs
    • (Non)-Sustained VT
      • Esp polymorphic VT w/o torsades de pointes
    • VFib due to deterioration from VT
  • Likelihood of these abnormalities
    • Highest risk in the first minutes after AMI onset
    • Increased risk for ventricular rhythm disorders persists for 24-48 hours & can return w/ recurrent MI
  • Prognosis w/ VT or VFib in the first two days of MI
    • Doesn’t worsen long term prognosis as long as the rhythm disorders are promptly reversed w/ antiarrhythmic therapy for 6-24 hours –> watchful waiting
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8
Q

Ventricular Tachyarrhythmias: Later VT & VF (After First 2 Days)

  • Prognosis of VFib or sustained VT after first 2 days
  • Scar VT
  • Important differentiations in late VT following MI
  • Antiarrhythmic therapy
  • Pts after MI that have a better outcome if treated w/ an ICD
A
  • Prognosis of VFib or sustained VT after first 2 days
    • Substantially worsens long term prognosis
  • Scar VT
    • Life-threatening ventricualr rhythm disorder that MI survivors are at risk for
    • Monomorphic VT due to micro-reentrant circuits in the LV
    • Develop b/n infarcted & viable myocardium
    • Most common after large, anterior wall MIs w/ LVEF < 40%
    • Can deteriorate to VF
    • Account for many SCDs in MI survivors
  • Important differentiations in late VT following MI
    • Polymorphic VT: indicates ongoing ischemia, non-torsade
    • Monomorphic VT: indicates development of a reentrant “scar” VT
  • Antiarrhythmic therapy
    • Not helpful, can be harmful
  • Pts after MI that have a better outcome if treated w/ an ICD
    • Most benefit: sustained monomorphic VT + poor LV contraction
    • Moderate benefit: non-sustained monomorphic VT + inducible VT + LVEF < 35%
    • Least benefit: LVEF < 35% + full recovery from MI (> 2-3 months)
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9
Q

Accelerated Idioventricular Rhythm (AIVR)

A
  • Commonly seen soon after MI
  • May be a “reperfusion” arrhythmia
  • Rate = 50-120 bpm
  • AIVR stpos immediately when sinus rhythm exceeds its rate
  • Rarely deteriorates to VT
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10
Q

Sinus Bradyarrhythmias

  • Frequency
  • Neurocardiac reflex
  • Effect on AMI
  • Treatment options
A
  • Frequent following MI (esp of posterior & inferior walls)
  • Usually due to neurocardiac reflex
    • State of predominantly parasympathetic tone
    • Short-lived phenomenon (few hours to a day)
    • Simulation of mechano-receptors in the infero-posterior wall –> decrease sympathetic tone –> parasympathetic predominance
  • Mixed effect on AMI
    • Decrease CO
    • Increase likelihood of serious ventricular rhythm disorders
    • Decreases myocardial oxygen demand –> protects jeopardized myocardium
    • Rarely warrants therapy (only when associated w/ hemodynamic consequences)
  • Treatment options
    • Atropine
    • Temporary pacer if atropine fails
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11
Q

Bradyarrhythmias Associated w/ AV & Intraventricular Conduction Delays:
Block at the Level of the AV Node (Supra-Hisian)

  • Frequency
  • Cause
  • Duration
  • Heart block
  • QRS
  • Hemodynamic compromise
  • Therapy
A
  • Most common w/ inferior & posterior MIs
  • Usually due to the neurocardiac reflex
  • Usually short-lived (few hours to a day)
  • Heart block
    • 2nd degree block is usually Mobitz Type I
    • 3rd degree (complete) block
      • Often preceeded by 1st or 2nd degree (Motibtz type I) block
      • Often not associated w/ hemodynamic compromise
  • Normal QRS
  • Hemodynamic compromise is usually HR related
  • Therapy
    • No hemodynamic compromise: not required
    • Hemodynamic compromise or persistunacceptable bradycardia: temporary pacing
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12
Q

Bradyarrhythmias Associated w/ AV & Intraventricular Conduction Delays:
Block Below the AV Node (Infra-Hisian, within the His-Purkinje System)

  • Heart block
  • Hemodynamic compromise
A
  • Heart block
    • Block is usually associated w/ a large anterior infarction
    • Frequently associated w/ a prolonged QRS &/or BBB/fasicular block
    • 2nd degree block is usually Mobitz type II
    • 3rd degree (complete) block may occur precipitously w/o warning w/ lesser degree block
  • Severe hemodynamic compromise is almost always associated w/ complete heart block
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13
Q

Bradyarrhythmias Associated w/ AV & Intraventricular Conduction Delays

A
  • 2nd degree heart block, Mobitz type II &/or trifasicular block within the His-Purkinje system
    • Associated w/ AMI
    • Frequent harbinger of 3rd degree heart block
  • ECG evidence
    • 2nd degree heart block, Mobitz type II
    • RBB or LBBB + 1st degree AV block
    • RBBB + left anterior or posterior fasicular block
    • Alternating BBB
  • Treatment
    • Temporary ventricular pacer
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14
Q

Sinus Tachycardia

A
  • If complicates AMI, usually has an underlying cause
    • Pain, anxiety, low CO, anemai, hypovolemia, infection, etc.
  • Cause –> proper therapy
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15
Q

Atrial Tachyarrhythmias

  • Types
  • Cause
  • Mortality
  • Therapy
A
  • Types: AFib, atrial flutter, & supraventricular tachycardia
  • Usually due to larger infarcts & increased atrial pressure (not atrial damage)
  • Associated w/ higher mortality w/ MI due to abnormal rhythm
  • Therapy
    • Type III antiarrhythmic for 6-12 weeks (period of greatest recurrence risk)
    • Conventional therapies for rate control & anti-thrombin therapy to prevent stroke & thromboembolism (for AFib & atrial flutter)
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16
Q

Systolic LV Dysfunction

  • Important in pts w/ AMI
  • Most easily measured variables
  • Myocyte loss
A
  • Important in pts w/ AMI
    • Size of infarct & ischemia
    • Resulting effects on regional & global systolic LV performance
  • Most easily measured variables
    • Global & segmental systolic LV performance (assessed by cardiac imaging)
    • Forward CO
  • Myocyte loss
    • More myocytes lost –> more prfound global LV systolic dysfunction –> larger infarct –> more likely HF & cardiogenic shock
17
Q

“Stunned Myocardium” w/ ACS

A
  • LV dysfunction can be reversed if blood flow is restored promptly
    • Brief MI form a short coronary occlusion –> prompt abnormality resolution
  • Repetitive or prolonged ischemia (UA, MI)
    • Ischemic areas may require days to weeks to recover
    • Tissue often seen within an infarct zone & at the margin of the infarct zone
    • This tissue = “stunned myocardium”
18
Q

Diastolic LV Dysfunction

  • Frequency
  • Testing
  • PV curves
  • Chief cause of…
  • Cardiac relaxation
A
  • Frequent during MI (esp in pts w/ LVH &/or DM) due to a stiff LV
  • Testing is inferoir to testing for systolic dysfunction
  • PV curves are shifted so LVEDP, LA pressures, & pulmonary venous pressures are elevated
  • Chief cause of pulmonary edema w/ AMI when systolic funciton is normal
  • Cardiac relaxation
    • Energy requiring
    • Affected as quickly as contraction
    • Impaired relaxation adds to problems from underlying stiff LV
19
Q

Therapy of HF & Optimizing Volume Status

  • All
  • Mild HF
  • Severe cases
  • Pulmonary edema
  • BP
    • Normal or hypertensive
    • Hypotensive
  • Severe HF or hypotension requiring inotropic agents
A
  • All: continuous positive pressure administration
  • Mild HF: conventional diuretic therapy
  • Severe cases: endotracheal intubation & assisted ventilation
  • Pulmonary edema: prompt & vigorous diuretics, IV morphine
  • BP
    • Normal or hypertensive: nitroglycerin reduces preload & afterload
    • Hypotensive: IV inotropic &/or pressor agents for diuresis w/o compromising arterial BP or CO
  • Severe HF or hypotension requiring inotropic agents
    • Manage volume status w/ indwelling pulmonary artery cathether
    • Slightly elevated pulmonary capillary wedge pressure: target value range that optimizes CO & minimizes pulmonary edema risk
20
Q

Mechanical Complications: Typical Cardiogenic Shock

  • When typical cardiogenic shock may complicate AMI
  • Features
  • Therapy
  • When to consider early coronary revascularization
A
  • When typical cardiogenic shock may complicate AMI
    • When >35-40% of LV myocardium has been damaged by AMI or cumulatively from a current + previous MIs
  • Features
    • Severe hypotension
    • Elevated LV filling pressure
    • Reduced CO
      • Clinical signs: oliguria/anuria, mental obtundation, cold clammy extremities, pallor, sweating, tachycardia
  • Therapy
    • ​Optomize volume status
    • Inotropic & vasopressor agents
    • LV assistance device
    • Goal of MAP = 60 mmHG & CI = 2.5
  • When to consider early coronary revascularization
    • Large amoutn of stunned but not necrotic myocardium
    • Correctable abnromality like acute MR, acute VSD, or a LV
21
Q

Mechanical Complications: Shock Associated w/ Major RV Involvement in Inferoposterior MI

  • Acute inferoposterior MI: RV vs. LV
  • Acute inferoposterior MI
    • Occlusion
    • Clinical importance
    • RV SV
    • Electrocardiography
    • Echo
    • Right-heart cath
    • Recovery
    • Death rates
  • Therapy
A
  • Acute inferoposterior MI: RV vs. LV
    • Thin, low pressure RV is mroe resilient to diminished blood flow than RV
    • But RV ischemia, infarction, & stunning can contribute to acute inferoposterior MI
  • Acute inferoposterior MI
    • Occlusion of the proximal right coronray artery prior to its acute marginal branch (major artery to the RV)
    • Uncommon clinically important involvement
    • Inadequate RV SV –> imapired LV filling –> decreased LV SV & BP
    • Right-sided electrocardiography detects RV injury
      • ST elevation compatible w/ a current of injury in V1-V6
    • Echo determines RV size & contraction
    • Right-heart (Swan-Ganz) cath shows depressed CO & elevated RA pressure
    • Most cases have nearly full recovery of RV contraction in ~3 days
    • Death rates up to 50%
  • Therapy
    • Fluid administration –> slightly elevate left sided filling pressures
      • Don’t elevate RA (central venous) pressure b/c an overly distended RV can impinge on the LV & decrease LV SV
    • Positive inotropic agents to return RV function to normal
    • Avoid vasodilator therapy (nitrates & ACE-Is or ARBs) & beta blockers until RV contraction has improved
22
Q

Mechanical Complications: Shock Associated w/ Rupture of the Papillary Muscles or the Interventricular Septum

  • Papillary muscle involvement
  • Interventricular septum involvement
  • Both conditions
  • Therapy
    • First line
    • If BP allows it
    • Surgical candidates
A
  • ~10% of myocardial rupture cases involve papillary muscles
    • Immediate acute MR
  • ~10% of myocardial rupture cases involve the interventricular septum
    • Immediate VSD w/ left to right shunt
  • Both MR & VSD –> HF –> murmur & cardiogenic shock
    • Echo or right heart cath –> prompt differentiation b/n these murmurs
  • Therapy
    • First line: LV assistance w/ inotropic agents & vasopressors
    • If BP allows it: ACE-Is, ARBs, or nitrates + hydralazine for LV unloading
    • Surgical candidates: early (<24 hours) coronary bypass surgery
      • Prognosis: poorer for VSD than MR, better than w/o surgery
23
Q

Mechanical Complications: Free Wall Rupture of the LV

  • Frequency
  • Risk factors
  • Casue
  • Features
  • Sub-acute rupture (“pseudo-aneurysm in evolution”)
A
  • ~90% of myocardial ruptures are of the free wall
  • Risk factors: elderly, women, HTN
  • Cause: dissection through the myocardium at the junciton of infarcted & normal myocardium
  • Features: hemopericardium –> pericardial tamponade –> death within minutes
  • Sub-acute rupture (“pseudo-aneurysm in evolution”): rare
    • Clot, fibrous tissue, & surrounding structures provid ethe “walls” for the pseudoaneurysm
    • Eventual rupture of a pseudoaneurysm occurs w/o surgery
24
Q

Mechanical Complications: “Atypical” Shock Patterns that must be Distinguished from More Serious Cases

  • Atypical Cardiogenic Shock due to the Neurocardiac Reflex
    • Mechanism
    • Associations
    • Therapy
  • Atypical Cardiogenic Shock due to Hypovolemia
    • Mechanism
    • Associations
    • Therapy
A
  • Atypical Cardiogenic Shock due to the Neurocardiac Reflex
    • Neurocardiac reflex –> transietn (few hours to a day) peripheral vascular dilation –> acute inferior & posterior wall MI
    • Pattern of hypotension is associated w/ normal or low right- & left-sided ventricular filling pressures
      • Absence of findings indicates low CO & pulmonary edema
    • Therapy
      • Vasoconstriction w/ dopamine, phenylephrine, or NE until systemic vascular resistance returns to normal
  • Atypical Cardiogenic Shock due to Hypovolemia
    • MI –> volume depletion –> LV deteriorates w/ under-filling –> atypical cardiogenic shock
    • Usually associated w/…
      • Normal or low right- & left-sided filling pressures
      • Little to no pulmonary edema
      • Decreased CO
      • Increased systemic vascular resistance
    • Therapy
      • Volume support until hemodynamic state improves
      • Voluem repletion until pulmonary capillayr wedge pressure is normal
25
Q

Mechanical Complications: LV Aneurysm & Thrombus

  • LV aneurysm
  • LV thrombus
A
  • LV aneurysm
    • LV anuerysm formation & LV dilation occur in 12-15% of MIs
    • Almost always a STEMI (90% are anterior or apical)
    • True aneurysms never rupture
      • Cause problems by soaking up contractile energy & contributing to HF
    • Early aneurysms are associated w/ LV thrombus & thromboemoblism
      • Via stagnant blood flow within the aneurysm & inflamed myocardium
  • LV thrombus
    • Complicates the healing in 30% of acute evolving Q wave MIs involving the atnerior wall &/or apex
    • Main risk: thromboembolism & stroke
    • Time of risk: greatest in first few days, subsides over next 3 months
26
Q

Emergency Reperfusion Therapy

  • STEMI
  • UA/NSTEMI
A
  • STEMI
    • All patients within 12 hours of STEMi onset should be considered
    • Percutaneous coronary interventions w/ angiopasty & stenting –> protective effect superior to IV thrombolytic therapy
      • Esp in pts at high risk for adverse outcomes
      • Fewer side effects (ex. intracranial hemorrhage) except for other bleeding (ex. at the cath site)
    • Alternate approaches
      • IV thrombolytic therapy if door-to-dilation time > 100 minutes
      • Primray angioplasty if pts present > 3 hours post-MI
  • UA/NSTEMI
    • Not beneficial b/c these pts don’t have persistent total occlusion of a coronary artery
    • Similarly not beneficial for emergency primary angioplasty therapy
27
Q

Routine Early (within 48 hours) Revascularization Therapy for Patients w/ UA/NSTEMI

  • High risk UA/NSTEMI
  • Low risk UA/NSTEMI
A
  • High risk UA/NSTEMI
    • Pts treated w/ conventional therapy (anti-thrombin, anti-platelet) followed by routine cath & revascularization
    • –> improved outcome compared to non-interventional therapy
  • Low risk UA/NSTEMI
    • Did not benefit from this strategy
    • Treat w/ non-invasve initial approach & watch for development of high-risk features & postivie findings on stress test before –> coronary arteriography
28
Q

Beta Adrenergic Blocking Agents

  • Beta blockers for survivors of MI (begun weeks to months post-MI)
  • Early beta blocker IV therapy followed by long term oral therapy post-MI
  • Beta blockers w/ intrinsic sympathomimetic activity (ISA)
  • Carvedilol in post-MI pts w/ LV dysfunciton (LVEF < 40%)
  • Contraindications
A
  • Beta blockers for survivors of MI (begun weeks to months post-MI)
    • –> moderate reduction in recurrent MI & cardiac death
  • Early beta blocker IV therapy followed by long term oral therapy post-MI
    • –> small additional reduction in in-hospital mortality
  • Beta blockers w/ intrinsic sympathomimetic activity (ISA)
    • –> little to no protective effect following MI –> avoid
  • Carvedilol in post-MI pts w/ LV dysfunciton (LVEF < 40%)
    • –> superior results compared to metoprolol
  • Contraindications
    • Severe HF
    • Cardiogenic shock
    • Severe bronchospasm
    • 2nd & 3rd degree AV block
      Bradycardia
    • HoTN
29
Q

Nitrates & Calcium Channel Blockers

  • Nitrate use
  • Calcium channel blocker use
    • General
    • Strongly vasodilating dihydropyridines
    • HR-limiting & negatively inotropic verapamil & diltiazem
A
  • Nitrate use
    • Standard anti-ischemic doses as long as needed for active ongoing ischemia
    • Gradually remove or continue as needed as therapy for chornic MI
  • Calcium channel blocker use
    • Therapy to prevent ischemia
    • Strongly vasodilating dihydropyridines
      • Adjunctive tehrapy w/ beta blockers (otherwise harmful)
    • HR-limiting & negatively inotropic verapamil & diltiazem
      • Replacement for beta blockers in pts who don’t tolerate beta blockers & who have good LV function (LVEF < 40% –> worse outcome)
30
Q

ACE-I or ARB Therapy

  • ACE-Is in high risk pts
  • ACE-Is in low risk pts post-MI
  • ARBs
  • Current guidelines
    • General
    • High risk pts
    • Low risk pts
A
  • ACE-Is in high risk pts
    • Pts: large infarctions, poor LV contraciton, &/or persistent HF
    • –> moderate benefits on limiting HF endpoints & cardoivascular death
    • –> moderate reduction in recurrent coronary events
  • ACE-Is in low risk pts post-MI
    • –> small benefit
  • ARBs
    • Equivalent to ACE-Is in post-MI pts w/ LV dysfunction or CHF
  • Current guidelines
    • Give ACE-Is or ARBs to all pts after ACS
    • High risk pts w/ large MI, poor LV, or HF: start therapy asap following acute reperfusion therapy & recovery of hemodynamic stability
    • Low risk pts: start therapy asap prior to discharge
31
Q

Angiotensin Blocking Therapy

  • Addition of angiotensin blocking therapy to ACEIs in pts w/ large infarctions, LV dysfunction or DM
  • Limited to pts w/…
  • Therapy begins…
A
  • Addition of angiotensin blocking therapy to ACEIs in pts w/ large infarctions, LV dysfunction or DM
    • –> additional small protective effect to ACE-Is alone
  • Limited to pts w/…
    • Minimal or no renal failure
    • No hyperkalemia
  • Therapy begins…
    • Following establishment of ideal dose of an ACE-I or ARB
    • Often delayed until outpatient setting
32
Q

“Plaque Stabilization” w/ Lipid-Lowering Therapy

  • Cholesterol-lowering therapy
  • LDL-cholesterol lowering therapy
  • Effect on preventing coronary syndromes due to…
  • Guidelines
A
  • Cholesterol-lowering therapy
    • Prevents progression of atheroslcerosis
    • Moderate reduction in ACS 7 cardiac death
  • LDL-cholesterol lowering therapy
    • Improved survival & fewer ACS
    • Esp w/ earlier & more aggressive statins
  • Effect on preventing coronary syndromes due to…
    • Re-stabilization of coronray plaques (decreased cholesterol content in the plaque & anti-inflammatory actions)
    • Prevention of endothelial dysfunction –> decreased risk of future plaque destabliziation & recurrent ACS
  • Guidelines
    • All pts w/ ACS & w/o contraindications should be treated asap w/ statins
    • Pts needing additional agents: elevated triglycerides, elevated VLDL, low HDL

Cardiology (40 decks)

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