Acute Coronary Syndrome II

Question 1

ACS Demographics & Statistics

Answer 1

• 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

Question 2

Unstable Angina Pectoris

• Symptoms of MI or impending MI
• Physical exam

Answer 2

• 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

Question 3

ECG

• Places pt into 1 of 2 categories
• Transmural injury
• Subendocardial injury/ischemia
• Infarction patterns
• Leads
• “Strictly” / “True” posterior wall
• Silent MI
• Caution

Answer 3

• 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

Question 4

Cardiac Biomarker Measurements for Myocardial Necrosis

• Cardiac markers
• Cardiac troponins I (inhibitory) & T (tropomyosin-binding)
• CK & CK-MB (its subunit)
• Using cardiac markers

Answer 4

• 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

Question 5

General Pathophysiologic, Diagnostic, & Therapeutic Considerations

• Evaluation & ECG monitoring
• IV access
• Oxygen therapy
• Pain relief

Answer 5

• 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

Question 6

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

Answer 6

• 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

Question 7

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

Answer 7

• 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

Question 8

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

Answer 8

• 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)

Question 9

Accelerated Idioventricular Rhythm (AIVR)

Answer 9

• 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

Question 10

Sinus Bradyarrhythmias

• Frequency
• Neurocardiac reflex
• Effect on AMI
• Treatment options

Answer 10

• 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

Question 11

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

Answer 11

• 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

Question 12

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

• Heart block
• Hemodynamic compromise

Answer 12

• 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

Question 13

Bradyarrhythmias Associated w/ AV & Intraventricular Conduction Delays

Answer 13

• 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

Question 14

Sinus Tachycardia

Answer 14

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

Question 15

Atrial Tachyarrhythmias

• Types
• Cause
• Mortality
• Therapy

Answer 15

• 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)

Question 16

Systolic LV Dysfunction

• Important in pts w/ AMI
• Most easily measured variables
• Myocyte loss

Answer 16

• 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

Question 17

“Stunned Myocardium” w/ ACS

Answer 17

• 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”

Question 18

Diastolic LV Dysfunction

• Frequency
• Testing
• PV curves
• Chief cause of…
• Cardiac relaxation

Answer 18

• 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

Question 19

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

Answer 19

• 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

Question 20

Mechanical Complications: Typical Cardiogenic Shock

• When typical cardiogenic shock may complicate AMI
• Features
• Therapy
• When to consider early coronary revascularization

Answer 20

• 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

Question 21

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

Answer 21

• 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

Question 22

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

Answer 22

• ~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

Question 23

Mechanical Complications: Free Wall Rupture of the LV

• Frequency
• Risk factors
• Casue
• Features
• Sub-acute rupture (“pseudo-aneurysm in evolution”)

Answer 23

• ~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

Question 24

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

Answer 24

• 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

Question 25

Mechanical Complications: LV Aneurysm & Thrombus

• LV aneurysm
• LV thrombus

Answer 25

• 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

Question 26

Emergency Reperfusion Therapy

• STEMI
• UA/NSTEMI

Answer 26

• 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

Question 27

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

• High risk UA/NSTEMI
• Low risk UA/NSTEMI

Answer 27

• 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

Question 28

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

Answer 28

• 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

Question 29

Nitrates & Calcium Channel Blockers

• Nitrate use
• Calcium channel blocker use
  
  • General
  • Strongly vasodilating dihydropyridines
  • HR-limiting & negatively inotropic verapamil & diltiazem

Answer 29

• 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)

Question 30

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

Answer 30

• 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

Question 31

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…

Answer 31

• 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

Question 32

“Plaque Stabilization” w/ Lipid-Lowering Therapy

• Cholesterol-lowering therapy
• LDL-cholesterol lowering therapy
• Effect on preventing coronary syndromes due to…
• Guidelines

Answer 32

• 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