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CAD Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the goal LDL reduction in patients with SIHD?

A

► 50% LDL reduction

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2
Q

What medication can be added in very high-risk patients with SIHD already on maximal statin therapy including:

  • multiple major events
  • one major and multiple risk factors

and

  • LDL ► 70
A
  • Ezetemibe (non-statin therapy)

or

  • PCSK-9 inhibitor
    • proprotein convertase subtilisin/kexin type 9 inhibitor
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3
Q

What trial demonstrated the benefit of Ezetemibe in high risk patients with SIHD?

A

IMPROVE-IT (2015)

  • Simvastatin + Ezetemibe vs. Simvastatin alone
  • associated with reduction in CV mortality, major CV event, nonfatal stroke
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4
Q

How is the intensity of statin therapy defined?

A
  • High = ► 50% LDL reduction
  • Moderate = 30 - 50% LDL reduction
  • Low = < 30% LDL reduction
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5
Q

In regards to “very high risk” features of future ASCVD event,

What are the high risk conditions?

A
  • CHF (history of)
  • CKD (GFR 15-59)
  • HTN
  • Heterozygous familial hypercholesterolemia
  • History of CABG or PCI outside of major ASCVD event
  • Age ► 65 years
  • DM
  • Persistently elevated LDL
    • ► 100 LDL
    • despite maximally tolerated statin therapy + Ezetemibe
  • Tobacco abuse (current)
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6
Q

In regards to those who are “Very High Risk” of Future ASCVD events,

What are the major ASCVD events?

A
  • Recent ACS (within the past 12 months)
  • History of MI (other than recent ACS listed above)
  • History of ischemic stroke
  • Symptomatic PAD
    • history of claudication with ABI < 0.85 or
    • previous revascularization or amputation
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7
Q

What patients should undergo stress imaging as the initial testing modality?

A
  • Inability to exercise with requirement for pharmacologic stress
  • EKG abnormalities (which preclude interpretation of stress EKG)
  • High pre-test probability of CAD
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8
Q

What are the mechanisms responsible for SCAD?

A
  • intimal tear with blood subsequently entering a false lumen

or

  • spontaneous hemorrhage of the vaso vasorum –> intramural hematoma within the coronary arteries
    • network of small blood vessels that supply the walls of large blood vessels, such as elastic arteries (e.g., the aorta) and large veins (e.g., the venae cavae).
    • name derives from Latin, meaning “the vessels of the vessels”
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9
Q

Describe features of the TIMI risk score (NSTE-ACS)

A
  • ST changes ► 0.5 mV
  • ► 2 episodes of angina within 24 hours
  • 3 or more CAD risk factors
    • DM, Tobacco abuse, HTN, Dyslipidemia, FH CAD
  • Positive cardiac biomarkers
  • Known CAD ( ► 50% stenosis)
  • Age ► 65 years
  • ASA use in prior 7 days
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10
Q

What are two well known, clinically validated multivariable risk score algorithms for ACS?

A
  • TIMI
    • Thrombolysis in Myocardial Infarction
    • separate scores for STEMI and NSTE-ACS
  • GRACE
    • Global Registry of Acute Coronary events
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11
Q

What does the TIMI risk score predict?

A
  • Clinically validated risk score which predicts the
  • risk of …. within 14 days
    • all-cause mortality
    • new or recurrent MI
    • severe recurrent ischemia prompting ugent revascularization
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12
Q

Describe the GRACE risk score

A
  • Originally developed across the whole spectrum of ACS (with and without ST elevation) in 17, 142 patients from GRACE registry
  • Predicts in-hospital mortality and death or MI
  • Identifies patients who will benefit from early invasive approach
  • 8 variables included:
    • Age
    • Cardiac arrest at presentation
    • SBP
    • ST-segment deviation
    • Serum creatinine level
    • HR at admission
    • Positive initial cardiac biomarkers
    • Killip class
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13
Q

What risk factor is the strongest predictor of future cardiovascular event?

A

Prior ischemic event (MI or CVA)

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14
Q

Define coronary artery vasospasm

A
  • transient, sudden, intense vasoconstriction of an epicardial coronary artery resulting in vessel occlusion or near occlusion
  • MOA
    • hyper-reactivity of coronary vascular smooth muscle cells to constrictor stimuli
  • Most notable risk factor:
    • smoking (tobacco abuse)
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15
Q

What is the most prominent risk factor for coronary vasospasm?

A

smoking (tobacco abuse)

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16
Q

What is the treatment for coronary vasospasm?

A
  • Avoid provoking agents - Quitting smoking
  • CCB’s
  • Nitrates
  • Statins
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17
Q

When do spontaneous episodes of coronary vasospasm (CAS) typically occur?

A

midnight - early morning hours

  • circadian variation and propensity for early morning
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18
Q

What are additional provoking factors for coronary artery vasospasm (CAS)?

A
  • Hyperventilation
  • Other vasoconstrictors (cold temperatures, exercise)
  • Methamphetamines
  • Ephedrine
  • Alcohol
  • Catecholamines (Epinephrine, Norepinephrine)
  • Cocaine
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19
Q

How is coronary artery vasospasm diagnosis made?

A
  • Clinical findings/suspicion
  • Coronary angiography:
    • observed spasm –> resolves with intracoronary NTG
    • provocative testing with intracoronary acetylcholine or methylergonovine
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20
Q

Describe the findings and increased future risk:

  • 80 year old male presents to establish care
  • PMH: CAD, DM, HTN, HLD, prior tobacco abuse
  • prior anterior MI 10 years ago without revascularization
A
  • Echo –> LV apical aneurysm​
    • ​discrete, dyskinetic area of the LV wall with a broad neck
  • VT
    • ​LV aneurysm occurs in < 5% of STEMI patients
    • most common after anterior MI
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21
Q

When does ischemic MR typically occur?

Why?

A
  • Inferior MI
  • Restricted motion of the posterior mitral valve leaflet
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22
Q

What are patients at increased risk for, post-MI who develop LV aneurysm?

A
  • Ventricular arrhythmias
  • Heart failure
  • Thromboembolism
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23
Q

Differentiate between LV aneurysm and pseudoaneurysm

A
  • LV aneurysm
    • discrete, dyskinetic area of the LV wall with a broad neck
  • Pseudoaneurysm
    • caused by contained myocardial rupture
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24
Q

When is surgical correction of LV aneurysm considered?

A
  • Refractory ventricular arrhythmias
  • Refractory heart failure
  • Recurrent thromboembolism (LV thrombus)
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25
Q

What are three complications that can occur with acute anteroapical MI’s?

A
  • Dynamic LVOT obstruction
  • LV aneurysm
  • LV thrombus
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26
Q

Describe the findings and next step:

  • 73 year old man who presents with STEMI/total occlusion of LAD –> revascularization with no-reflow phenomenon
  • VS: HR 80, BP 80/60 mmHg
  • Exam: loud late systolic murmur
  • Echo: EF 45% with anterior akinesis, no pericardial effusion
  • RHC: RA 6, PA 40/18, PAWP 15 with v waves to 18, CI 1.8. No step-up on O2 sats.
A
  • Dynamic LVOTO with systolic anterior mitral leaflet motion
  • Normal saline
    • ​treatment is centered around reducing the obstruction:
      • decrease inotropy
      • increase preload
      • increase afterload
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27
Q

What are causes of mitral regurgitation in post-AMI patients?

A
  • LV dilatation
  • Ischemic papillary muscle dysfunction
  • Severe regional wall motion abnormality adjacent to a papillary muscle
  • Papillary muscle rupture
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28
Q

What is the AMI mortality associated with papillary muscle rupture?

A

5% of AMI deaths

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29
Q

Describe blood supply of the papillary muscles

A
  • Anterolateral papillary muscle
    • dual blood supply
      • LAD
      • CFx
  • Posteromedial papillary muscle
    • RCA –> PDA
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30
Q

Describe acute papillary muscle rupture?

  • Incidence and timing
  • Presentation
  • Diagnosis
  • Treatment
A
  • Incidence and timing
    • Occurs 2-7 days after inferior MI (usually)
    • 1% of patients with AMI
  • Presentation
    • Acute Pulmonary Edema and
    • Cardiogenic Shock
  • Diagnosis
    • Echo
      • flail segment of the mitral valve and the ruptured papillary muscle head moving feely within the LV and often prolapsing into the left atrium
    • RHC
      • large v waves in the PAWP measurements
  • Treatment
    • Initial stabilization –> Afterload reduction
      • Sodium nitroprusside
      • IABP
      • Inotropic support
    • ​Definitive treatment –> early surgical repair
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31
Q

What is the pattern of LGE on cMRI:

  • Stress Cardiomyopathy
A

No LGE

  • no myocardial scarring and therefore no LGE
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32
Q

What is the pattern of LGE on cMRI:

  • Myocarditis
A

Mid myocardial LGE

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33
Q

What is the pattern of LGE on cMRI:

  • Cardiac amyloidosis
A

Diffuse, subendocardial LGE

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34
Q

EKG Definition:

  • ST and/or T wave abnormalities suggesting myocardial ischemia
A
  • > 1 mm of horizontal or downsloping ST-T segment depression

and/or

  • T wave inversion ► 2 mm
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35
Q

Describe acute free wall rupture?

  • Incidence and timing
  • Presentation
  • Diagnosis
  • Treatment
A
  • Incidence and timing
    • 2-5 days after anterior MI (usually)
      • usually « 48 hours
    • 1-6% of patients with AMI
  • Presentation
    • Cardiac tamponade
    • PEA
    • Death
  • Diagnosis: Echo
    • pericardial effusion with clots
    • ► 10 mm pericardial effusion post-STEMI –> high risk of rupture
    • cardiac tamponade
  • Treatment
    • Initial stabilization
      • IV fluids
      • Inotropes
      • Emergent pericardiocentesis
    • Emergent surgical repair
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36
Q

Describe ventricular septal rupture?

  • Incidence and timing
  • Presentation
  • Diagnosis
  • Treatment
A
  • Incidence and timing
    • 1-3% of patients with AMI
      • 0.2% of patients enrolled in GUSTO-1 trial
    • day 1 (if reperfused) or 3-5 days (not reperfused) after MI
      • Anterior infarct –> apical septum
      • Inferior infarct –> posterobasal septum
  • Presentation
    • Loud holosystolic murmur
      • ​thrill or RV lift may also be present
    • Chest pain
    • Dyspnea
    • Cardiogenic Shock
  • Diagnosis:
    • Echo
      • Doppler –> Left-to-Right shunt through septum
    • RHC:
      • “step-up” in O2 sat at level of RV
      • prominent V wave on PCWP tracing in supine position
  • Treatment
    • Initial stabilization
      • IV Nitroprusside
      • Inotropes
      • IABP
    • Emergent surgical repair
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37
Q

What leads to formation of pseudoaneurysm?

A
  • Anterior MI –> free wall rupture
  • Organizing thrombus and hematoma, together with pericardium –> sealing a rupture of the LV
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38
Q

What is the classic RVMI presentation?

A

Hypotension + Clear Lungs

  • relative bradycardia
    • may be a clue to enhanced vagal tone
    • can also be seen in this setting
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39
Q

What is the differential diagnosis:

  • post ACS patient with recurrent chest pain
  • revascularized with PCI
A
  • Mechanical complication
  • Non cardiac
    • GERD, PTX
  • Coronary perforation –> pericardial effusion
  • Pericarditis (postinfarction)
  • Recurrent coronary occlusion or high-grade stenosis
    • either in the previously treated vessel/lesion or another vessel
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40
Q

What is the differential diagnosis:

  • post ACS patient with recurrent chest pain
  • revascularized with thrombolytics
A

failed reperfusion and recurrent coronary occlusion

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41
Q

What is the first step in patients with:

  • recent ACS with PCI
  • post-ACS exertional chest pain
A

Optimize antianginal therapy

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42
Q

Describe the findings:

A
  • Pseudoaneurysm (false aneurysm) of LV
    • contained rupture of the LV following AMI
    • narrow neck which communicated from the LV cavity into a cavity contained by pericardial adhesions
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43
Q

Define “no-reflow”

A
  • characterized by suboptimal myocardial perfusion despite restoration of lumen patency in the infarct related artery
  • angiographically is associated with TIMI flow « 2
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44
Q

What is one test that should be performed post-ACS?

A

Echo to assess LV function

  • one of the most powerful predictors of short and long-term outcomes
  • carries therapeutic implications for revasculrization and device-based therapies
  • should be assessed in all patients with SIHD with/without signs/symptoms of heart failure
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45
Q

What test carries the highest negative predictive value for myocardial infarction?

A

Troponin I

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46
Q

What are the treatment stategies for NST-ACS as determined by risk stratification scores?

A
  • Invasive
    • Immediate (within 2 hours)
    • Early (within 24 hours)
    • Delayed (25-72 hours)
  • Ischemia guided strategy
    • noninvasive strategy first
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47
Q

In the setting of NST-ACS, what are the indications for an:

  • Immediate Invasive ( « 2 hours) treatment strategy
A
  • Refractory angina
    • at rest or with low-level activities (despite intensive medical therapy)
  • Hemodynamic instability
  • Electrical instability
    • sustained VT or VF
  • Heart failure
    • new or worsening MR
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48
Q

In the setting of NST-ACS, what are the indications for an:

  • Early Invasive ( < 24 hours) treatment strategy
A
  • Criteria not met for “Immediate invasive” strategy
  • Risk scores:
    • Grace score > 140
    • TIMI 3-4
  • ST depression
    • new or presumably new
  • Temporal change in Troponin
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49
Q

In the setting of NST-ACS, what are the indications for an:

  • Delayed Invasive ( 25-72 hours) treatment strategy
A
  • Criteria for “Immediate” and “Early” invasive strategies not met
  • Risk scores
    • Grace 109-140
    • TIMI ► 2
  • PCI within 6 months
  • Prior CABG
  • CKD
    • GFR < 60
  • DM
  • Early postinfarction angina
  • Reduced LVEF < 40%
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50
Q

In the setting of NST-ACS, what are the indications for an:

  • Ischemia guided treatment strategy
A
  • Low risk score
    • TIMI 0-1
    • Grace < 109
  • Low-risk, troponin negative, female patients
  • Absence of high risk features + patient or physician preference
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51
Q

What is the effect of TTS on mortality?

A

Higher long-term mortality

  • higher compared with general age-matched population
  • outcomes resemble those of patients with ACS
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52
Q

What are TTS features which are associated with unfavorable long-term prognosis?

A
  • Older age
  • Physical stressors
  • Atypical ballooning
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53
Q

What is the recurrence rate of TTS?

A

10-20% recurrence rate

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54
Q

What are potential cardiovascular complications associated with TTS?

A
  • MR
  • LVOT obstruction
  • Cardiogenic shock
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55
Q

What is the recovery time for TTS?

A

hours - weeks

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56
Q

What are the treatment recommendations for antiplatelet therapy in SIHD?

A

Class I - ASA 75-162 mg daily

  • Comprehensive meta-analysis
    • 37% reduction in risk of serious vascular events
    • 46% decrease in risk for UA
    • 53% reduction in the need for revascularization

*****ASA allergy –> Clopidogrel is a reasonable alternative

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57
Q

What trial compared ASA and Clopidogrel in patients with ASCVD?

A

CAPRIE TRIAL (2003)

  • Clopidogrel provided superior secondary prevention of atherosclerotic vascular events by a small margin
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58
Q

What are contraindications to ASA use?

A
  • ASA allergy
  • NSAID allergy
  • Samter’s syndrome
    • asthma
    • rhinitis
    • nasal polyps
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59
Q

What test should be performed after the patient is stable?

  • 57 year old post-menopausal women with fevers, back pain –> pyelonephritis –> IVF’s –> pulmonary edema and no chest pain
  • PMH: DM
  • EKG: TWI in V2-V6
  • Echo: apical LV dilation and severe hypokinesis with preserved contractility of the basal segments
  • Troponin (peak) 4.5
A

Cornary angiography

  • stress cardiomyopathy should be considered as a diagnosis of exclusion
  • after excluding CAD in setting of an NSTEMI with decompensated heart failure
  • multiple risk factors for CAD: DM, postmenopausal
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60
Q

Describe the findings and diagnosis:

A
  • Posterior MI - LCx occlusion
  • EKG
    • ST elevations in II, III and I, V5, V6
    • ST depressions in V1-V3
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61
Q

Differentiate between STEMI in RCA and LCx

A

ST-elevation in III > II

and

ST-depression in I, aVL, or both ( > 1mm)

  • Yes –> RCA
    • ST-elevation in V1, V4R, or both –> proximal RCA with RV infarct
  • No –> LCx
    • ST-elevation in I, aVL, V5, V6
    • ST-depression in V1-V3
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62
Q

What is the presentation and EKG findings in LMCA occlsuion?

A
  • Often Fatal
  • Subtotal occlusions / EKG:
    • global ST depressions
    • Variable ST-elevations: V1 and aVR
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63
Q

Describe EKG findings:

  • LAD occlusion
A
  • ST-elevation: V1-V3
  • ST-depressions: II, III, aVF
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64
Q

Describe typical EKG findings:

  • Conus branch occlusion
A

Arrhythmias without significant ST changes

  • depending on size of the branch
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65
Q

Describe the relationship between ST-elevation on EKG and cardiac biomarkers

  • How can this be utilized in patients with a clinical history compelling for ischemia and initial nondiagnostic EKG?
A
  • ST-segment changes precede the release of detectable concentrations of biomarkers of necrosis by hours
  • Serial EKG measurements every 15-30 minutes or until symptom resolution
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66
Q

What are atypical EKG presentations that may prompt emergent coronary angiography?

A
  • BBB
    • positive Sgarbossa criteria
  • Ventricularly paced rhythm
  • Isolated posterior MI
  • LMCA or MVCAD
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67
Q

Describe atypical EKG findings that would prompt emergent angiography:

  • Bundle branch block (LBBB)
  • V-paced rhythm
A
  • Sgarbossa Criteria
    • Concordant ST-elevation ► 1mm in leads with positive QRS complex
    • Concordant ST-depression ► 1mm in V1-V3
    • Discordant ST-elevation ► 5mm in leads with negative QRS complex

**** Presence of RBBB may confound the diagnosis of STEMI

******V-pacing follows the same criteria –> less specific

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68
Q

Describe atypical EKG findings that would prompt emergent angiography:

  • Posterior MI (isolated)
A
  • ST-depression (isolated) ► 0.5mm in V1-V3
  • ST-elevation ► 0.5mm in V7-V9 (posterior leads)
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69
Q

Describe atypical EKG findings that would prompt emergent angiography:

  • LMCA or MVCAD
A

ST-depression ► 1 mm in ► 8 surface leads

and

ST-elevation in aVR and / or V1

****Suggests LMCA, LM-equivalent or severe MVCAD

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70
Q

How many phases of Cardiac Rehabilitaiton are there?

A

4 phases

  • Phase I - Inpatient phase
  • Phase II - Outpatient phase
  • Phase III/IV - Maintenance phase
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71
Q

Describe CR - Phase I

A

Phase I - Inpatient phase

  • PT and education immediately following a cardiac event or intervention
    • Patient assessment:
      • medical history
      • functional status
    • Patient / family education
    • Physical activity
      • advice, support and counseling
    • Follow up plan:
      • goals for secondary prevention
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72
Q

Describe CR - Phase II

A

Phase II - Outpatient phase

  • Individualized exercise prescription
  • Risk-factor reduction

****performed under supervision of a medical team, typically over 36 sessions (thrice-weekly EKG-monitored sessions) over 8-12 weeks.

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73
Q

Describe CR - Phase III / IV

A

Phase III / IV - Maintenance phase

  • emphasize:
    • long-term lifestyle changes to maintain healthy behavior via independent continuation of the exercise program
    • cardiovascular risk reduction learned during phase II
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74
Q

What are the indications for Cardiac Rehabilitation?

A
  • ACS
    • in the preceeding 12 months
  • Chronic Angina
  • Chronic HF** (Class IIa)
  • Post-CABG
  • Post-PCI
  • PAD
  • LVAD
  • Valve replacement/repair
  • Heart/Heart-lung transplant

*****Remainder are Class I

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75
Q

What is the hospital readmission benefit associated with Cardiac Rehab during the year after a cardiac event?

A

20-30% reduction

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76
Q

Describe the findings and diagnosis:

  • 55 year old male with severe MR (due to leaflet prolapse) undergoes MV repair with annuloplasty ring –> VF immediatley after requiring defibrillation
A
  • Lateral wall STEMI following MV repair
  • Iatrogenic coronary occlusion
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77
Q

What is the next best step after iatrogenic coronary occlusion?

A

coronary angiography

  • can help to determine the mechanism of coronary occlusion
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78
Q

Describe iatrogenic coronary occlusion following MV repair/replacement

A
  • LCx and PDA are in close proximity to the MV annulus ( ~1mm)
  • Mechanisms of occlusion:
    • direct injury/distortion from suturing
    • coronary embolization
      • bone, suture material, silicone, thrombus, air
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79
Q

What are some medical therapies that may be useful in microvascular angina (MVA)?

A

Tobacco cessation

  • Nicotine replacement
  • Varenicline (Chantix)
  • Bupropion
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80
Q

Describe the findings and diagnosis:

A
  • EKG:
    • ST depressions ► 2mm in anterior precoridal leads (V1-V4)
  • Posterior MI - LCx occlsuion (left dominant)
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81
Q

What is the best way to assess for posterior MI?

A

Posterior leads

  • performed with the lead on the same horizontal plane as V6
    • V7 - posterior axillary line
    • V8 - beneath the scapular angle
    • V9 - on the paravertebral line
  • ST-elevation > 0.5 mm in any of V7-V9 is considered diagnostic of infarction
    • required diagnosis is lower due to increased distance from the myocardium
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82
Q

What is the accurary of posterior leads in detecting posterior MI?

What is the most sensitive lead?

A
  • > 91% of patients with LCx occlusion
  • Highest sensitivity –> V8 (100% in one series)
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83
Q

What is the recommendation for statin therapy:

  • CAC score = 1-99
A

Reasonable to initiate statin therapy for patients ► 55 years of age

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84
Q

What is the diagnosis?

  • Harsh systolic murmur at left sternal border
  • Palpable thrill
  • Loud pulmonic component of S2
  • S3 Gallop
A

Ventricular septal rupture

  • occurring 1-5 days after acute MI
  • managed conservatively (no revascularization)
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85
Q

What method of determining ASCVD risk offers the highest discriminatory value for future ASCVD events?

A

Coronary Artery Calcium Score (CAC)

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86
Q

What does the risk assessment for primary prevention of atherosclerotic cardiovascular disease (ASCVD) involve?

A
  • Estimation of ASCVD risk
  • Use of risk enhancers to personalize risk assessment
  • Selective use of CAC in some:
    • borderline risk adults
    • intermediate risk adults
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87
Q

When can CAC be utlized to reclassify (“de-risking”) patients?

A
  • Intermediate risk ( ► 7.5% to < 20% 10-year ASCVD risk)
  • Borderline risk (5% to < 7.5% 10-year ASCVD risk)

****CAC = 0 –> statin therapy can be witheld

  • reassessment of risk and possibly CAC score in another 5-10 years
  • as long as high-risk conditions are not present
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88
Q

What CAC score should prompty initiation of statin therapy?

A

CAC ► 100

or

► 75% percentile

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89
Q

What ASCVD score should prompt initiation of pharmacologic therapy for stage 1 HTN (SBP 130-139 mmHg)?

A

ASCVD ► 10%

  • both pharmacologic and nonpharmacologic therapies should be initiated
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90
Q

What is the diagnosis based on histological changes:

  • necrotic myocardium and fibrous tissue
A

LV aneurysm

  • as a complication of transmural myocardial infarction
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91
Q

What is the diagnosis based on histological changes:

  • lipomatous or fibrolipomatous replacement of the myocardium
A

ARVC

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92
Q

What is the diagnosis based on histological changes:

  • necrotic myocardium with eosinophilic and lymphocytic infiltration
  • mural thrombus
A

Hypereosinophilic syndrome

  • HES or Loeffler’s syndrome
  • Typical Echo findings include:
    • thrombotic and fibrotic obliteration of the ventricular apices
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93
Q

What is the diagnosis based on histological changes:

  • lymphocytic infiltration with fibrosis and noncaseating granulomas
A

Cardiac Sarcoidosis

  • Echo:
    • areas of wall thinning
    • aneurysm
    • focal areas of edema, akinesis, dyskinesis
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94
Q

What is the diagnosis based on histological changes:

  • myofibril disarray
A

Hypertrophic cardiomyopathy (HCM)

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95
Q

What is the next best step?

  • 50 year old, asymptomatic male
  • CAC score = 300
A

Moderate-high intensity statin therapy

  • revascularization does not confer mortality benefit in asymptomatic patients
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96
Q

What are the key factors when determining reperfusion strategy for STEMI?

A
  • Time from onset of symptoms
  • Risk level of STEMI
  • Risk of bleeding
  • Availability and time required for transporting the patient to a skilled PCI facility
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97
Q

Which patients benefit maximally from BB therapy following STEMI?

A
  • Impaired LV function
  • HF (clinical)
  • Ventricular arrhythmias
  • Non-revascularized
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98
Q

What BB’s should be utilized in STEMI associated with cocaine use?

A
  • Carvedilol
  • Labetalol
    • alpha- and beta-blocking effects
    • decrease systemic BP without increasing coronary vascular resistance
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99
Q

When should an Echo be repeated in post-STEMI patients with reduced LV function?

A

> 40 days post-MI

  • addresses the potential need for ICD therapy
  • allows for recovery from myocardial stunning
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100
Q

What is the most powerful predictor of death in MI patients?

A

Heart Failure

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101
Q

What medications should be started following STEMI?

A
  • ASA
  • P2Y12 inhibitor
  • Statin therapy
  • BB
    • LV dysfunction (if no CHF present)
    • should be started after HF resolves
  • ACE/ARB
    • LVEF « 40% and/or heart failure
    • reduces the risk of hospitalization and death
    • < 24 hours
  • Aldosterone antagonists (Spironolactone or Eplerenone)
    • LVEF « 40%
    • 3-14 days after STEMI
    • Do not have renal dysfunction or hyperkalemia
      • Cr < 2.5 (men) and < 2 (women)
      • K < 5
    • Receiving therapeutic doses of ACE
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102
Q

Describe the steps in the progression of a coronary plaque

A
  • Intimal thickening
  • Intimal Xanthoma
  • Pathologic intimal thickening
  • Fibrous Cap Atheroma
  • Thin-Cap Fibroatheroma
  • Rupture
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103
Q

What is the sequence of platelet effects that take place after rupture of a fibrous cap (coronary plaque)?

A
  • Fibrous cap ruptures –> procoagulant substances exposed to blood pool
  • Platelets:
    • Adhesion
    • Activation
    • Aggregation
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104
Q

What percentage of patients with normal, resting EKG who undergo ETT will require further risk stratificaiton?

A

25-40%

  • will have intermediate-risk treadmill tests and require further risk stratification
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105
Q

What is the importance of a normal resting EKG in regards to ETT?

A
  • 92-98% of patients with normal resting EKG –> normal LV function
    • when measured by a variety of methods
  • Higher specificity in patients:
    • normal resting EKG vs. ST-T abnormalities
106
Q

What are the major differences in the Mayo study:

  • clinical-ETT model
  • clinical-ETT imaging model
A
  • 3% of patients correctly reclassified
    • most were shifting patients from intermediate –> low risk
  • Imaging model
    • failed to identify more patients with LM or 3V-CAD
    • not any more accurate for predicting clinical events
  • Cost analysis
    • $20,000 cost reduction for each reclassification
107
Q

Define “stunned myocardium”

A
  • state of delayed recovery of regional LV dysfunction
  • after a transient period of ischemia that has been followed by reperfusion
  • Episodes –> myocardial stunning can be:
    • brief or long
    • single or multiple
    • never severe enough to lead to myocardial necrosis
108
Q

Define “hibernating myocardium”

A
  • adaptive rather than injurious response of the myocardium
  • due to repetitive:
    • ischemia and
    • chronic hypoperfusion
    • without acute injury
  • ​Viable, but dysfunctional myocardium
109
Q

Describe differences in treatment:

  • stunned myocardium
  • hibernating myocardium
A
  • Stunned myocardium
    • interventions aimed at decreasing frequency, severity or duration of ischemic episodes
    • improved contractile function
  • Hibernating myocardium
    • interventions that favorably alter supply-demand relationship:
      • improved blood flow
      • reduction in demand
    • improved contractile function
    • Large areas –> improved survival with revascularization
110
Q

Describe the response of hibernating myocardium in a dobutamine stress test

A

Bimodal response

  • Rest –> Hypokinesis
  • Low-dose –> Improves
  • High-dose –> Akinetic (due to ischemic response)
111
Q

What are the 4 broad categories of risk stratification that should be considered for pre-operative evaluation?

A
  • Clinical evaluation and assessment of comorbidities
  • Functional capacity/noninvasive evaluation for ischemia
  • Ventricular function
  • Coronary anatomy
112
Q

Describe the image

A
113
Q

What is the mechanism of ASA (for antiplatelet therapy)?

A
  • irreversible acetylation of the platelet COX-1 enzyme
  • inhibition of platelet activation and subsequent platelet aggregation
    • inhibits generation of TxA2 and TxA2 induced platelet aggregation
  • may also have additional pleiotropic effects that contibute to anithrombotic properties
114
Q

Describe the pharmacokinetic properties of ASA

A
  • T 1/2 = 5-7 days (20 min - 6 hours –> plasma T 1/2)
    • irreversibly and non-selectively binds COX-1 for the life span of platelets
115
Q

What is the most common side effect of ASA therapy?

A

GI intolerance (5-40%)

116
Q

What is the recommended antiplatelet therapy if ASA cannot be tolerated?

A

Clopidogrel

117
Q

Why should NSAIDS be avoided with ASA use?

What strategies should be used if they are necessary therapy?

A
  • NSAIDS (particularly Ibuprofen) can compete for binding sites at COX-1
  • Delay administration of NSAIDS or Ibuprofen:
    • 30 minutes after immediate release ASA
      • or
    • 8 hours before
118
Q

What levels indicate ASA resistance?

A

COX-1 activity < 10%

119
Q

What are the P2Y12 receptor blockers?

A
  • Clopidogrel
  • Prasugrel (Effient)
  • Ticagrelor (Brilinta)
  • Cangrelor (IV)
120
Q

Describe the activation of P2Y12 inhibitors

A
121
Q

What P2Y12 inhibitor was discontinued as a result of adverse side effects?

A

Ticlopidine

  • rash, nausea, neutropenia and thrombocytopenia
  • Clopidogrel gained favor in the early 1990’s –> incorporated into large clinical trials
122
Q

What did the CURE study demonstrate?

A
  • CURE (Clopidogrel in Unstable Angina to Prevent Recurrent Events) - 2001
  • Clopidogrel (300mg loading dose followed by 75mg daily) and ASA (75-325 mg/d) in pateints (n = 12,562) with NSTE ACS was associated with:
    • 20% reduction in the primary combined endpoint of 12-month CV mortality, nonfatal MI, and stroke compared with ASA monotherapy
    • 1% absolue risk increase in major bleeding
123
Q

What did the PCI-CURE trial demonstrate?

A
  • PCI-CURE (Effects of Pretreatment With Clopidogrel and Aspirin Followed by Long-Term Therapy in Patients Undergoing Percutaneous Coronary Intervention)
    • study subset analysis of the CURE study
    • pretreatment with clopidogrel for a median of 6 days before PCI was associated with:
      • 31% reduction in the primary composite endpoint
124
Q

What did the ARMYDA-2 study demonstrate?

A
  • ARMYDA-2 (Antiplatelet therapy for Reduction of MYocardial Damage during Angioplasty)
  • 600 mg loading dose of clopidogrel compared with 300 mg administered 6 hours prior to PCI was associated with:
    • significant reduction in death, MI, or target vessel revascularization in patients undergoing elective PCI (12% vs. 4%, p = 0.041)
125
Q

What is the mutation associated with reduced Clopidogrel activity?

What has this been proven to cause?

A
  • single nucleotide polymorphisms of the gene encoding CYP450 2C19
  • loss-of-function (LoF) allele (CYP2C19*2, *3, *4, *5) lead to:
    • recurrent ischemic event occurence
    • particularly stent thrombosis
    • primarily in patients treated with PCI as demonstrated in genetic substudies of large-scale clinical studies and meta-analyses

***FDA advised health care providers to consider use of other antiplatelet medications or alternatie dosing strategies in poor metabolizers of clopidogrel (those having two LoF CYPC19 alleles)

126
Q

What should be done in poor metabolizers (resistance) of Clopidogrel?

A

change to more potent P2Y12 inhibitors (Prasugrel, Ticagrelor)

  • increased dosing is an inferior strategy to overcome resistance
127
Q

When can platelet reactivity testing be considered?

A
  • history of stent thrombosis
  • prior to undergoing high-risk PCI

***not currently recommended by the guidelines

128
Q

What did the TRITON-TIMI 38 Trial show?

A
  • TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel-Thrombolysis in Myocardial Infarction 38)
    • Prasugrel (60mg/10mg daily) plus ASA was associated with:
      • 19% reduction in primary composite endpoints of CV death, nonfatal MI, and nonfatal stroke at a median 14.5-month follow up compared with Clopidogrel/ASA in patients with NSTEMI/STEMI undergoing planned PCI
      • Increased TIMI major bleeding (life threatening and fatal bleeding)
129
Q

Describe Prasugrel:

  • Class / MOA
  • Active substance
  • Loading / Maintenance
  • Pharmacokinetics
  • Reversal agent
A
  • Class / MOA
    • Irreversibly and directly binds to P2Y12 receptors
    • Reduces platelet aggregation (and activation)
  • Active substance:
    • Pro-drug with 2 step activation process:
      • hydrolyzed by intestinal and plasma esterases
      • oxidized by hepatic CYP3A4 AND CYP2B6 –> R-138727 (active metabolite)
  • Loading / Maintenance
    • LD 60mg (60-70% inhibition) / MD 10mg daily
    • Plasma concentration of active metabolite 30 min after LD
  • Pharmacokinetics
    • T 1/2: 7 hour (plasma)
    • Duration of effect:​ 5-10 days (life of platelet)
    • Onset of action - 30 minutes
  • Reversal agent
    • not reversible, platelets?
130
Q

What are contraindications to Prasugrel?

A
  • Active pathological bleeding
  • History of TIA / CVA
  • ≥ 75 years of age
  • Patients undergoing urgent CABG
131
Q

Describe Ticagrelor

  • Class
  • MOA
  • Active substance
  • Loading/maintenance dose
  • Pharmacokinetics
A
  • Class/MOA
    • Reversibly binding, direct-acting P2Y12 inhibitor
    • Reduces platelet aggregation (and activation)
  • Active substance
    • both drug and metabolite are active
  • Loading/maintenance
    • LD 180mg / MD 90mg BID
      • maximum plasma concentrations achieved 1-3 hours after LD
  • Pharmacokinetics
    • Onset of action - 30 minutes
    • T 1/2 - 7-9 hours
    • Duration of effect - 3-5 days
  • Reversal agent
    • Platelets
132
Q

What did the PLATO trial demonstrate?

A
  • PLATO (Ticagrelor versus Clopidogrel in Patients with Acute Coronary Syndromes) Tiral:
  • ACS patients in whom invasive strategy was planned, Ticagreolor (180mg LD / 90mg BID) versus Clopidogrel (300-600 mg LD / 75mg daily) was associated with:
    • significant reduction in the primary efficacy endpoint of CV death, MI, or stroke
    • Significant reduction in mortality associated with ticagrelor therapy

****benefit less apparent in North American population –> thought to be secondary to high-dose ASA ( > 75mg daily)

133
Q

What are the major side effects of Ticagrelor?

A
  • Dyspnea
    • 15% of patients within the first week of treatment
    • thought to be secondary to decreased adenosine clearance and/or effects on sensory neuron’s
  • Bradycardia
134
Q

What is Vorapaxar?

A
  • PAR-1 inhibitor, selective, reversibly binding
  • developed to prevent thrombin-induced platelet aggregation
  • approved for use to be added to aspirin and/or clopidogrel to reduce the risk of MI, stroke, CV death, revascularization in patients without a history of CVA / TIA
135
Q

What pharmacologic agents directly block the binding of fibrinogen?

A

GP IIb/IIIa receptor inhibitors

  • more effective in inhibiting platelet aggregation than any oral antiplatelet strategy
136
Q

Describe the effects of Abciximab (Reopro):

  • Type
  • Platelet binding t 1/2
  • Plasma t 1/2
  • Drug-to-receptor ratio
  • % dose in bolus
  • Renal adjustment
  • Platelet aggregation recovery
  • Reversibility with platelet infusion
A
137
Q

Describe the effects of Eptifibatide:

  • Type
  • Platelet binding t 1/2
  • Plasma t 1/2
  • Drug-to-receptor ratio
  • % dose in bolus
  • Renal adjustment
  • Platelet aggregation recovery
  • Reversibility with platelet infusion
A
138
Q

Describe the effects of Tirofaban (Aggrastat):

  • Type
  • Platelet binding t 1/2
  • Plasma t 1/2
  • Drug-to-receptor ratio
  • % dose in bolus
  • Renal adjustment
  • Platelet aggregation recovery
  • Reversibility with platelet infusion
A
139
Q

What are the 3 GP IIb/IIIa receptor inhibitors approved for use in the US?

A
  • Abciximab
  • Eptifibatide
  • Tirofiban
140
Q

Which of the GP IIb/IIIa receptor inhibitors can be reversed?

What is the reversal agent?

A
  • Abciximab
    • very low drug/receptor ratio
  • Platelets
141
Q

How does Abciximab differ from other GP IIb/IIIa receptor inhibitors?

A
  • Monoclonal antibody fragment
  • Reversible with platelets
    • very low drug/receptor ratio (1.5-2 / 1)
  • Effect can last for days
    • platelet aggregation recovery –> 48 hours
    • shortest plasma half life, longest biologic half life
  • Safe in kidney disease
    • no dose adjustment for renal impairment
142
Q

What is the indications and dosing for Abciximab?

What % of dose is given as bolus?

A
  • PCI
    • Bolus: 0.25 mg/kg
    • Infusion: 0.125 μg/min (maximum 10 μg/min) for 12h
  • UA (not responding to medical therapy with PCI planned < 24h)
    • Bolus: 0.25 mg/kg
    • Infusion: 10 μg/min for 18-24h until 1h after PCI

****90% of Abciximab dose given as bolus

143
Q

What GP IIb/IIIa receptor inhibitors require adjustment for renal insufficiency?

When?

A
  • Eptifibatide
    • CrCl < 50 mL/min
  • Tirofaban (Aggrastat)
    • CrCl < 60 mL/min
144
Q

Which anticoagulant acts as an indirect inhibitor of thrombin?

How does it work?

A
  • Heparin
  • Activation of antithrombin III –>
    • inactivates factors IIa (thrombin), IXa and Xa
145
Q

What is the mechanism of hypotension?

  • Sildenafil
  • Nitroglycerin
A

Excess cGMP-mediated vasodilation

146
Q

What are the four Class I options for initial anticoagulation in NSTE-ACS?

A
  • Heparin
  • Enoxaparin
  • Fondaparinux
  • Bivalirudin
147
Q

What is the reversal agent for UFH?

A

IV Protamine sulfate

  • 10 mg per 1,000 U of UFH
148
Q

What is the reversal agent for enoxaparin?

A

Protamine Sulfate

  • partially reversible (approximately 50%)
  • 1mg protamine / 1mg enoxaparin
    • only if last dose < 8 hours
    • max dose: 50mg
149
Q

Describe the details of Heparin:

  • Target
  • Half-life
  • Risk of HIT
  • Protein binding
  • Reversal agent
  • Excretion
A
  • Target
    • Factor Xa = Factor IIa
  • Half-life:
    • 1.5 hours
  • Risk of HIT
    • Yes
  • Protein binding
    • Yes
  • Reversal agent
    • Protamine Sulfate
  • Excretion
    • Reticuloendothelial, renal
150
Q

Describe the features of enoxaparin:

  • Target
  • Half-life
  • Risk of HIT
  • Protein binding
  • Reversal agent
  • Excretion
A
  • Target
    • Faxtor Xa > Factor IIa
  • Half-life
    • 4-7 hours
  • Risk of HIT
    • Yes, low
  • Protein binding
    • Low
  • Reversal agent
    • Protamine sulfate (partial ~ 50%)
  • Excretion
    • Renal
151
Q

What is used to monitor the therapeutic index of Heparin?

A

ACT (activated clotting time)

  • time required for a blood sample to form a clot in response to activator of the intrinsic pathway
  • Normal 70-120s

or

aPTT (activated partial thromboplastin time)

  • typically goal is 1.5-2 times control for patients being maintained on UFH
152
Q

What interaction can cause anaphylaxis in a patient on UFH?

How can you avoid this?

A
  • Long-acting insulins and Protamine sulfate
  • SC test dose should be administered prior to administration
153
Q

What is the incidence of thrombocytopenia with Heparin use?

A
  • Mild thrombocytopenia - 10-20% of patients
  • Significant rhombocytopenia (platelets < 100,000) - 1-5% of patients
    • typically occuring several days after therapy
  • HIT - < 0.2% of patients
154
Q

Define “chronic stable angina”

A
  • angina that has been stable in frequency and severity for ► 2 months
  • with episodes that are provoked by exertion or stress of similiar intensity
155
Q

Describe the difference in risk:

  • SIHD with no major event
  • SIHD with prior major event (MI, CVA, PAD event)
A

Increased 4-year CV death, MI, or stroke (18.3% vs. 12.2%)

  • REACH Registry (Reduction of Atherothrombosis for Continued Health)
156
Q

Describe the effects of polyvascular disease on CV death, MI, stroke or hospitalization?

A

Dependent on the number of vascular beds involved

  • One –> 12.6%
  • Two –> 21.1%
  • Three –> 26.3%
157
Q

Describe the classificaiton/types of chest pain

A
158
Q

What trial demonstrated benefit for CAD/primary prevention with use of CCTA?

A

SCOT-HEART Trial (2018)

  • Scottish CT of the HEART trial
    • 4,000 low-intermediate risk patients with chest pain suggestive of CAD
  • nonsignificant increase in cardiac catheterization
  • 40% relative reduction in MI after 5-years of follow up
    • due to intensified medical therapy and lifestyle modificaitons
159
Q

What are the components of the Duke Treadmill Score?

A
  • Exercise duration (N = minutes exercised)
  • Maximal ST depression ( -n x 5)
  • Presence and severity of angina
    • non-limiting = ( -n x 4)
    • limiting = (-n x 8)
160
Q

Describe risk associated with the DTS

A

Exercise time (minutes) - ST depression x5 - Angina (non-limiting x4 vs. limiting x8) = DTS

  • Low ► 5
  • Intermediate 4 to -10
  • High « -11
161
Q

In addition to the DTS, what are other metrics that offer insight into the overall CV status and help to identify high-risk patients?

A
  • Abnormal BP response
  • Abnormal HR recovery pattern
  • Prolonged ST-depression
    • > 8 minutes into recovery
162
Q

In what scenarios is myocardial imaging appropriate in patients with SIHD?

A
  • Clarify equivocal, boderline, or discordant prior stress test where myocardial ischemia remains a concern
  • Intermediate or high DTS
  • New or worsneing symptoms in a patient with known atherosclerosis
  • Evaluate the physiologic consequence of coronary stenosis or anatomic abnormality of uncertain significance
163
Q

When is repeat MPI appropriate in:

  • asymptomatic, stable patient
  • history of abnormal coronary angiography or abnormal stress test
A

stress test > 2 years prior (may be appropriate)

164
Q

What is the most common pathophysiologic mechanism for a NSTEMI?

A

Disruption of the fibrous cap (plaque rupture or erosion)

  • stimulates thrombogenisis
165
Q

What are the high risk features ( ► 3% annual mortality rate) in noninvasive testing?

A
  • MPI:
    • Large perfusion defect
      • > 12% of myocardium
      • particularly if anterior
    • Multiple perfusion defects of moderate size
    • Large, fixed perfusion defect with:
      • LV dilatation or
      • Increased Lung uptake
    • Moderate perfusion defect with:
      • LV dilatation or
      • Increased Lung uptake
    • Severely reduced LV function at rest ( LVEF « 35%)
    • Severe reduction in CFR ( < 1.5)
  • ETT
    • High-risk DTS ( score « -11)
    • Severe exercise-induced LV dysfunction (exercise LVEF « 35%)
  • Stress Echo:
    • Echo wall-motion abnormality (involving > 2 segments) developing
      • at a low dose-Dobutamine ( « 10 mg/kg/min) or
      • low HR ( « 120 bpm)
    • Evidence of extensive ischemia
166
Q

What are the recommendations regarding initiation of ACE/ARB following STEMI?

A
  • Anterior STEMI
  • Heart Failure
  • LVEF « 40%

****Class I recommendations

167
Q

What are the recommendations and benefits for ACE/ARB use in STEMI patients?

A

Early initiation (within 24 hours) and continued long term treatment –>

significant reduction in mortality and recurrent CV events

  • ​benefit seen in those with/without LV dysfunction
168
Q

Which patients with STEMI will be least likely to benefit from ACE therapy?

A

preserved LV function

+

adequate revascularization

+

absence of DM or HF

169
Q

What is the classical clinical triad of an RV infarct?

A
  • Hypotension
  • JVD
  • Normal lung examination
170
Q

What are medications that should be avoided in an RV infarct?

A

Reduce RV preload –> should be avoided

  • Diuretics
  • Nitrates
  • Opiates
171
Q

What are some ways to improve RV contractility in an RV infarct?

A

Dopamine or Dobutamine

172
Q

What are the preferred treatments for microvascular angina?

A

traditional antianginal drugs

  • Alpha-Beta Blockers
  • CCB’s
  • novel therapies
    • potassium channel openers
    • metabolic agents
    • rho-kinase inhibitors
    • ACE
    • Ivabradine
    • Statins
    • Phosphodieterase inhibitors
173
Q

What is an anti-anginal therapy that can be used to reduce myocardial oxygen consumption independent of systemic hemodynamic effects?

A

Ranolazine

  • antianginal effects are independent of significant changes to the HR-BP product
  • does not alter myocardial blood flow
174
Q

What are the characteristics that indicate an increased vulnerability to plaque rupture?

A
  • Fewer smooth muscle cells
  • Intraplaque hemorrhage
  • Thinner fibrous caps
  • Large, necrotic lipid cores
  • Neoangiogenesis
  • Macrophage infiltration (increased)
  • Presence and degree of inflammation
175
Q

When should fibrinolytics be administered in the setting of STEMI (in non-PCI capable facility)?

A

non-PCI capable hospitals

+

anticipated FMC time at PCI-capable hospital > 120 minutes

176
Q

When fibrinolysis has been chose as the primary perfusion strategy, when should it be adminstered?

A
  • < 30 minutes of arrival
  • < 10 minutes from STEMI diagnosis

*****Transfer to PCI-capable facility ASAP after bolus lytics administration

177
Q

When do Troponin levels peak after the onset of symptoms?

A

12-24 hours

178
Q

What are the recommendations regarding anticoagulation in fibrinolytic adminstration?

A
  • should receive anticoagulant therapy
    • ► 48 hours
    • preferably for the duration of the index hospitalization
    • up to 8 days
    • or until revascularization is peformed
179
Q

What are the recommended anticoagulant options in STEMI with fibrinolytic adminstration?

A
  • Heparin
  • Enoxaparin
    • ExTRACT-TIMI 25 (Enoxaparin and Thrombolysis Reperfusion for AMI Treatment)
  • Fondaparinux
    • OASIS-6 (Organization for the Assessment of Strategies for Ischemic Syndromes 6)
180
Q

Describe the pathophysiology of HF after AMI:

  • Sympathetic nervous system
  • Parasympathetic nervous system
  • RAAS system
A
  • Increase Sympathetic activity
    • increase in circulating norepinephrine
    • increased B1-adrenergic activity
  • Decreased parasympathetic activity
    • through acetylcholine signaling
  • RAAS activation
    • increased renin levels
    • increased angiotensin II levels
181
Q

What accounts for nearly 25% of the ACS cases in women < 50 years old?

A

Spontaneous coronary artery dissection (SCAD)

182
Q

Describe the findings:

A

LV Pseudoaneurysm

  • CT findings:
    • inferior wall pseudoaneurysm
  • results from transmural MI –> ventricular free wall rupture
  • contained by localized pericardial adhesions
  • inferior wall is more likely to be affected
    • late presentation with ST-elevation in inferior leads
183
Q

When is Ivabridine indicated in heart failure?

A

Reduces HF hospitalization’s (Class IIa)

  • Symptomatic (NYHA II-III) + stable chronic HFrEF (LVEF <<35%)
  • Already receiving GDMT - including BB at maximally tolerated dose
  • NSR with HR >> 70 bpm
184
Q

What is the 5-year survival for DTS findings:

  • Low
  • Intermediate
  • High
A
  • Low ( > 5) –> 97%
  • Intermediate ( 4 to -10) –> 90%
  • High ( < -11 ) –> 65%
185
Q

What TIMI risk score in UA/NSTEMI should prompt early-invasive management strategy?

A

TIMI score > 2

  • early-invasive management strategy = coronary angiography < 48 hours
186
Q

What should risk stratification after the initial reperfusion strategy include?

  • Assessment
  • Studies
A
  • Assessment
    • success of reperfusion (epicardial and microvascular)
    • detection of HF or mechanical complications
    • evaluation of LV function
    • selective assessment of ischemia
    • susceptibility of serious ventricular arrhythmias
  • Studies (to consider)
    • EKG
    • Echo
    • Stress testing
    • Stress nuclear imaging
    • CMR
    • Coronary angiography and ventriculography
    • Dynamic use of risks scores that incorporate the clinical course of complications of MI
187
Q

What is the most appropriate diagnostic test?

  • 58 year old woman with several weeks of substernal chest pressure brought on by emotional stress, lasting < 5 minutes
  • PMH: HTN, HLD, CKD, Asthma, recent ankle fracture
  • Meds: Amlodipine, Atorvastatin, Albuterol
  • PE: scattered wheezing with O2 sat 94% on RA
  • EKG: NSR
  • Labs: Cr 2.2
A

Dobutamine stress echo

  • ETT contraindicated to recent ankle fracture
  • Active wheezing –> Regadenoson and Adenosine are contraindicated
  • CCTA –> contraindicated due to elevated creatinine
  • MRI –> increased risk of nephrogenic systemic fibrosis
188
Q

What are the initial anticoagulation treatment strategies in NST-ACS (in addition to antiplatelet therapy)?

A
  • Enoxaparin
    • continued for the duration of hospitalization ( « 8 days) or
    • until PCI is performed
  • Bivalirudin
    • only in patients managed with an early invasive strategy (< 48 hours) and continued until diagnostic angiography complete
  • Fondaparinux
    • continued for the duration of hospitalization ( « 8 days) or
    • until PCI is performed
      • with UFH or Bivalirudin administered during PCI due to risk of catheter thrombosis
  • UFH
    • continued for 48 hours or
    • until PCI performed
189
Q

What are the recommendations regarding anticoagulation in patients undergoing CABG?

A
  • UFH –> up to time of CABG
  • Bivalirudin –> « 3 hours prior to CABG –> with continuance of UFH
  • Enoxaparin –> « 12-24 hours
  • Fondaparinux –> « 24 hours
190
Q

What does the Killip classification describe?

A

describes a spectrum of heart failure signs and symptoms in the setting of AMI

  • higher Killip class correlates with increased mortailty in patients presenting with STEMI
191
Q

Describe Killip classifications

A
  • Class I
    • no clinical signs of heart failure
  • Class II
    • Rales (crackles) in the lungs, an S3, and elevated JVP
  • Class III
    • acute pulmonary edema
  • Class IV
    • Cardiogenic shock or hypotension (SBP < 90 mmHg) and
    • evidence of peripheral vasoconstriction
192
Q

What is the incidence of high-grade AV block (2nd degree Mobitz II or 3rd degree) in ACS?

A
  • 7% in fibrinolytic era
  • 1-3% in primary PCI era
193
Q

Describe the difference in AV block in ACS:

  • Inferior wall
  • Anterior wall
A
  • Inferior wall
    • more common
    • more likely to recover
    • AV node supplied by RCA in most patients
  • Anterior wall
    • usually associated with large infarct
    • unlikely to recover
194
Q

What are the steps in treatment of high-grade AV block occuring in the setting of PCI/reperfusion?

A
  • Assess for reversible causes
  • Atropine (class IIa)
  • Severe symptoms/hemodynamically unstable
    • Pacing
  • MI with Block
    • Yes –> Aminophylline (class IIb)
    • No –> Beta-agonsists (class IIb)
    • Pacing
195
Q

When is pacing indicated in patients with high-degree AV block following PCI/reperfusion?

A

Symptoms related to ventricular rate emerge

  • pacing is generally not indicated as often transient
196
Q

Define Bezold-Jarisch reflex

A
  • occurs in setting of AMI (particularly inferior MI) –> reperfusion (of complete occlusion)
  • Presentation (vagally-mediated):
    • Bradycardia
    • Hypotension
    • Vasodilatation
  • Mechanism:
    • stimulation of cardiac sensory receptors, particularly concentrated in the inferior wall of the LV –>
    • with nonmyelinated vagal fibers that increase parasympathetic activity and lower sympathetic activity
197
Q

What is the treatment for Bezold-Jarisch reflex?

A
  • Atropine
    • antagonizes both bradycardia and reflex cholinergic vasodilation
  • IV fluids
  • Refractory:
    • Isoproterenol or
    • TV pacing
    • IABP
      • only if refractory hypotension after IVF’s
198
Q

Describe the findings:

A

SCAD

  • spiral dissection in the LAD
  • diffuse smooth narrowing of the LM due to intramural hematoma and compression of the true lumen
199
Q

When are ARNI’s indicated in HF?

A

Reduces Morbidity and Mortality

  • Chonic, symptomatic, NYHA II or III HFrEF who tolerate an ACE/ARB
200
Q

What are common associations with SCAD?

A
  • Premonopausal women
  • Pregnancy / Multiparity
  • Hormonal therapy
  • Fibromuscular dysplasia
  • Systemic Inflammatory conditions
  • Connective tissue disorders
201
Q

Describe the findings:

  • 72 year old woman 3 days following acute STEMI with LAD stent and residual 80% RCA lesion who develops acute chest pain
  • VS: HR 110 bpm, BP 80/40 mmHg, JVP 14 cm H2O
  • PE: clear lungs, extremities cool without edema
  • RHC: RA 18, PA 40/20, PCWP 20 with V waves to 22, TDCO 1.6, PA sat 47%
A

LV free wall rupture –> Surgery (definitive treatment)

  • acute chest pain + hemodynamic collapse following acute MI
202
Q

What are early EKG indicators of high risk in STEMI?

A

Large territory at risk (those that reflect)

  • Extreme magnitude of ST-elevation
  • Posterior extension
    • ST-depressions in anterior leads in patients with inferior MI
    • Indicates either posterior extension or concomitant LAD ischemia
    • ST-elevation in V4R –> RV infarct
  • Involvement of conduction system
203
Q

What CAD disease patterns demonstrate survival improvement with CABG?

A
  • LM disease (significant)
  • Severe 3V-CAD involving the proximal LAD
204
Q

What is unique in regards to ST-elevation pattern in high-lateral MI?

A

ST-elevation in aVL is rarely pronounced

  • beause QRS voltage in aVL is usually very low
  • ST voltage cannot exceed QRS voltage
205
Q

When is PCI noninferior to CABG in LM disease?

A

Low Syntax score anatomy ( < 22 or < 32?)

206
Q

What trials identified noninferiority for PCI vs. CABG in LM disease?

A
  • EXCEL (2016)
  • NOBLE (2017)
207
Q

What is the effect of acetylcholine in coronary microvascular disease?

A

impaired endothelial-dependent activity

208
Q

What are two medications that can increase coronary blood flow?

A
  • Acetylcholine –> NO
    • Endothelial dependent (CFRe)
  • Adenosine
    • Nonendothelial dependent (CFRne)
209
Q

What is required to make a diagnosis of PCI-related MI (type 4a)?

A
  • Elevated biomarkers
    • > 99th percentile URL in patients with normal baseline values ( « 99th percentile URL) or
    • rise of cTn values > 20% of the baseline value when it is above the 99th percentile URL but it is stable or falling

and

  • Evidence of new myocardial ischemia
    • EKG
    • Imaging
210
Q

Describe the findings and diagnosis:

A

LV aneurysm

  • post-anterior wall MI
  • No evidence of LV thrombus or pseudoaneurysm
  • GDMT: Spironolactone in patients with LVEF < 40%
211
Q

What are the major physiologic effects of cocaine?

A
  • MI, Stroke, Arrhythmias, Cardiomyopathy, Aortic dissection, Pulmonary Hypertension
  • Impaired calcium binding
  • Impaired CBF, cerebral vasoconstriction
  • Increase in myocardial O2 demand
  • Increased endothelin-1, reduced NO, alpha-stimulation
  • Catecholamine surge
  • Vessel wall injury
  • Prothrombotic state
  • Deranged myocardial currents, catecholamine surge, ischemia, hyperthermia
212
Q

What is Trousseau’s syndrome?

A
  • sign of malignancy - often precedes diagnosis
  • hypercoaguability of malignancy in combination with episodes of vessel inflammation due to blood clot (thrombophlebitis)
  • often recurrent or appearing in different locations over time (thrombophlebitis migrans or migratory thrombophlebitis)
213
Q

What is one major benefit of DES vs. BMS?

A

decreases target-vessel revascularization

  • HORIZONS-AMI (5.8% vs. 8.7%; HR 0.65; 95% CI, 0.48-0.89; p < 0.006) at 12 month follow up.
  • Further supported by meta-analysis of 13 randomized trials
214
Q

Describe Dressler’s Syndrome

A
  • occurs as the result of an immune response to pericardial injury –> resulting in inflammation of the pericardium and sometimes adjacent myocardium
  • occurs 1-8 weeks after infarction
    • time required for development of antibodies
215
Q

Define target-vessel revascularization

A

any repeat PCI of the target lesion or bypass surgery of the target vessel performed for restenosis or other complication of the target lesion

216
Q

What is the treatment for postinfarction pericarditis (Dressler’s Syndrome)?

A
  • High-dose ASA (750-1000 mg every 6-8 hours)
    • ​gradual decrease over 3-4 weeks
  • Colchicine 0.6 mg BID
    • ​helps prevent recurrence
  • PPI
    • consider for GI protection on high dose ASA
217
Q

Define Type II MI

A
  • detection of a rise and/or fall of cardiac troponin values with at least one value above the 99th percentile URL, and
  • evidence of an imbalance between myocardial oxygen supply and
  • demand unrelated to acute coronary atherothrombosis and
  • at least one of the following:
    • symptoms of acute myocardial ischemia
    • new ischemic EKG changes
    • development of pathological Q waves
    • imaging evidence of new loss of viable myocardium in a pattern consistent with an ischemic etiology
218
Q

What are the most important (heavily weighted) independent predictors of mortality in the TIMI (STEMI) classification system?

A
  • 3 points
    • Age ► 75 years
    • SBP < 100 mmHg
  • 2 points
    • Age 65-74 years
    • HR > 100 bpm
    • Killip classs II-IV
  • 1 point
    • History of DM, HTN, or angina
    • Weight < 67 kg
    • Anterior STEMI or LBBB
    • Time to reperfusion therapy > 4 hours
219
Q

What are screening/follow up recommendations in those with SCAD?

A

Extracoronary vascular screening

  • strongly associated with SCAD and have potential to affect management and inform prognosis
  • FMD is a commonly associated condition:
    • CTA carotids
    • CTA renal arteries
220
Q

Why is troponin elevated in decompensated heart failure?

A

increased myocardial wall stress

221
Q

Describe the findings:

A

Remote inferior MI

  • fragmented EKG morphologies in the inferior leads
    • Lead II: Rr’
    • Lead III: rSR’
    • Lead aVF: fragmented QRS
222
Q

What have similar specificity and sensitivity when compared with pathologic Q waves for diagnosing remote MI?

A

Fragmented QRS complexes

223
Q

Why does QRS fragmentation occur in remote MI?

A
  • Prior MI typically –> necrosis and fibrosis of the myocardium
  • “islands” of viable myocardium interspersed in diseased myocardial tissue
  • areas of viable myocardium have slow activation due to partial depolarization and depressed action potential upstroke velocities
  • This results in heterogeneous activation of the ventricle
224
Q

What EKG changes are indicative of prior MI?

A
  • Any Q wave in leads V2-V3 > 0.02s or

QS complex in leads V2-V3

  • Q wave ► 0.03s and ► 0.1 mV deep or QS complex in leads I, II, aVL, aVF or V4-V6 in any two leads of a contiguous lead grouping (I, aVL; V1-V6; II, III, aVF)
  • R wave ► 0.04s in V1-V2 and R/S ► 1 with a concordant positive T wave in absence of conduction defect

******Only valid in absence of LVH and LBBB

225
Q

When is PCI supported:

  • IVUS of LM
A

MLA « 6.0 mm2

226
Q

When is PCI supported:

  • FFR
A

< 0.80

227
Q

When is PCI supported:

  • iFR
A

« 0.89

  • iFR lesions 0.9-0.93 should be investigated by FFR as well
228
Q

When is revascularization supported:

  • LM stenosis
A

► 50%

229
Q

When is PCI supported:

  • coronary stenosis
A

► 70%

230
Q

What is the benefit of a CAC = 0?

A

15-year warranty period ( < 1% annual mortality)

  • in low-intermediate risk individuals
231
Q

What are common EKG findings associated with LV aneurysm post-MI?

A

ST-elevation occuring 6 weeks after a transmural MI

232
Q

What is the most appropriate next step in care?

  • 62 year old woman presents for evaluation of HTN
  • PMH: HTN, prior tobacco abuse (quit 3 years prior)
  • Meds: Lisinopril, Chlorthalidone
  • PE: BP 128/68, HR 78 - nonsignificant
  • EKG: LVH with repolarization abnormalities and inferior Q waves that are new from EKG 5 years earlier
  • Echo: preserved LV function, LVH, akinesis of the distal half of the inferior wall
A

Exercise SPECT

  • silent or unrecognized MI may be incidentally be detected on routine EKG or imaging modalities
  • functional evaluation of CAD is appropriate
  • imaging should be added due to LVH with repolarization abnormalities
233
Q

Describe the type of chest pain:

  • intermittent, occurring over the past 3 months
  • squeezing chest pain, deep within his chest
  • exacerbated by stressful situation
  • alleviated with deep breathing and attempts at relaxation
A

Typical angina

234
Q

What major adverse effect is associated with aspiration thrombectomy?

A

Increased stroke

  • Larger-scale studies have since shown no benefit in the composite primary outcomes:
    • cardiovascular death
    • recurrent MI
    • stent thrombosis
    • TVR
235
Q

What echocardiographic feature is the strongest predictor of patient survival post-MI?

A

LV ejection fraction

236
Q

What is the next best step?

  • 56 year old woman post-elective laparoscopic cholecystectomy, asymptomatic
  • PMH: HTN, HLD, Tobacco abuse, Obesity
  • Post-op EKG: new TWI –> Repeat EKG: NSR
  • Serial Troponin: 0.12 > 0.11 > 0.14
  • Meds: ASA, Rosuvastatin, Lisinopril, Insulin
A

Pharmacologic MPI

  • troponin elevation + EKG changes in setting of noncardiac surgery
  • requires further risk stratification prior to discharge
237
Q

What are indications for oral anticoagulation following STEMI?

A
  • A-fib
  • Recent venothromboembolism
  • LV thrombus « 6 months
238
Q

What is the preferred P2Y12 inhibitor when “triple therapy” is necessary?

A

Clopidogrel

  • preferred P2Y12 inhibitor to minimize excess bleeding
239
Q

What are measures to reduce bleeding in patients with STEMI?

A
  • Radial rather than femoral access
  • Use of lower dose ASA
  • Bivalirudin use without GP IIb/IIa inhibitors instead of Heparin + GP IIb/IIa inhibitors
  • Shorter duration of DAPT therapy post-stenting with new-generation stents
240
Q

Why are Non-Vitamin K antagonist’s oral anticoagulants preferred in “triple therapy” use?

A

Reduced risk of bleeding

241
Q

What is the cut-off for NTG use in ACS in the setting of phosphodiesterase use?

A
  • Sildenafil or Vardenafil –> 24 hours
  • Tadalafil –> 48 hours
242
Q

What are contraindications to initiating BB therapy in ACS?

A
  • HF (acute)
  • Low-output state
  • Cardiogenic shock (increased risk)
  • Contraindications to BB:
    • PR interval > 0.24s
    • 2nd or 3rd degree AV block without PPM
    • Asthma (active)
    • Reactive airway disease
243
Q

What hormone is classically elevated in stress cardiomyopathy?

A

Epinephrine

  • pathophysiologic mechanism
    • cathecholamine excess
    • derangement of myocardial glucose and fatty acid metabolism
    • microcirculatory dysfunction
    • coronary vasospasm
    • estrogen deficiency
244
Q

EKG Definition:

  • Anterolateral MI, age recent or probably acute
A
  • Anterolateral Leads - V3-V6
    • Pathological Q waves must be ► 30 ms wide and 0.1 mV deep in amplitude or
    • QS complexes
  • Evidence of acute or evolving myocardial injury
    • ST elevation in two contiguous leads ► 2mm - men or 1.5mm - women in V3 and 1mm in V4-V6
245
Q

What are causes of LAD on EKG?

A
  • COPD
  • Hyperkalemia
  • Inferior MI
  • LAFB
    • axis must be > -45 degrees
  • LBBB
  • LVH
  • Ostium primum ASD
246
Q

When utilizing the GRACE score for STEMI, what is the strongest predictory of mortality?

A

Age

  • GRACE risk factor / max score
    • AGE - 100 points
    • Killip class - 59 points
    • SBP - 58 points
    • HR - 58 points
    • Cardiac arrest at admission - 39 points
    • Creatinine - 28 points
    • ST-segment deviation - 28 points
    • Elevated enzymes - 14 points
247
Q

What is the diagnosis based on the respone:

  • decreased coronary artery diameter in response to intracoronary acetylcholine
A

endothelial macrovascular dysfunction

248
Q

What is the diagnosis based on the response:

  • decreased coronary artery diameter in response to intracoronary nitroglycerin
A

nonendothelial macrovascular dysfunction

249
Q

What is the strongest prognostic exercise test variable in an exercise-treadmill test?

A

Exercise duration

  • poor capacity –>
    • high risk for LM / 3vCAD
    • high clinical event rate
  • Exercise stage 1 or 2 + positive EKG
    • 60% –> 3vCAD
    • 25% –> LM
  • Exercise stage 3 or 4 + negative EKG
    • 10% –> 3vCAD
    • 4% –> LM
250
Q

What is a measurable diagnostic value for coronary microvascular dysfunction?

A

CFR < 2.5 in response to intracoronary adenosine

  • indicates endothelial microvascular dysfunction
251
Q

What is the most common pathophysiologic mechanism for a NSTEMI?

A

Disruption of the fibrous cap (plaque rupture or erosion)

  • stimulates thrombogenesis
  • most ACS result from disruption of a fibrous cap atheroma or superficial plaque erosion
252
Q

What is the best treatment strategy:

  • asymptomatic
  • delayed presentation STEMI ( > 24 hours)
A

Exercise/Pharmacologic MPI

  • PCI of totally occluded infarct artery > 24 hours after STEMI is not recommended in asymptomatic patients with one- or two-vessel disease if they are (OAT trial 2013):
    • hemodynamically stable
    • electrically stable
    • no evidence of severe ischemia
253
Q

What is the most likely cause of the EKG findings:

  • 68 year old male presents with chest pain radiating to his back x 2 hours
  • PMH: HTN
  • Meds: Lisinopril, Metoprolol, Chlorthalidone
  • VS: HR 96 bpm, BP 160/100 (R arm) and 110/78 (L arm)
A

Coronary artery dissection

  • back pain + differential BP in each arm –> aortic dissection with retrograde extension into the coronaries
  • may compromise coronary flow by an expanding false lumen compressing the proximal coronary artery (thus external compression is an incorrect choice)
254
Q

In PAH, what is a prominent pathway in vasoconstriction?

A

Increase in ET1

  • potent vasoconstrictor and smooth muscle mitogen
  • Treatments (endothelin-receptor antagonists): bosentan, ambrisentan, macitentant

***The pulmonary circulation has a nubmer of vasoactive pathways, which control the balance between vasoconstriction and vasodilatation, as well as affecting proliferation and anti-proliferation.

255
Q

What are the treatment recommendations for VA/SCA due to coronary artery spasm?

A
  • Ventricular arrhythmia
    • maximally tolerated doses (Class I)
      • CCB
      • smoking cessation
  • SCA (resuscitated) + medical therapy ineffective or not tolerated
    • ICD (if survival ► 1 year) - IIa
  • SCA (resuscitated) from coronary artery spasm
    • ICD (if survival ► 1 year) + medical therapy - IIb
256
Q

When is PCI recommended in patients with delayed STEMI ( > 24 hours)?

A
  • hemodynamic instability
  • electrical instability
  • Evidence of severe ischemia

*******PCI of totally occluded infarct artery > 24 hours after STEMI is not recommended in asymptomatic patients with one- or two-vessel disease if they do not demonstrate any of the above symptoms (OAT trial 2013)

257
Q

When is PCI recommended in patients with delayed STEMI ( 12-24 hours)?

A
  • CHF (severe, congestive)
  • hemodynamic instability
  • electrical instability
  • Evidence of severe ischemia
258
Q

What is one lab that should be checked and corrected prior to urgent intervention in NSTEMI?

A

Hemoglobin –> RBC transfusion

  • although use of nitrates and UFH are first-line therapies in ACS
  • correcting anemia, which can be a common cause of myocardial oxygen-supply-demand mismatch, should be evaluated
259
Q

What is the differential diagnosis for inverted P-waves in I and aVL?

A
  • Ectopic atrial rhythm
  • Dextrocardia
  • Limb lead reversal

****Ectopic atrial rhythm –> expect a normal axis

****Limb Lead Reversal –> normal R-wave progression across the precordium

****Dextrocardia –> Reverse R-wave progression

260
Q

What lab is most useful in the decision to start lipid-lowering therapies in patients with borderline ASCVD?

A

Hs-CRP

  • hs-CRP ► 2
    • considered a risk-enhancing factor for ASCVD risk stratification
261
Q

What labs can aid in the decision to start lipid-lowering therapies in patients with borderline ASCVD?

A
  • hs-CRP ( ► 2)
  • TG (► 175)
  • Lipoprotein a ( > 50 mg/dL or > 125 nmol/L)
  • Apolipoprotein B (► 130 mg/dL)
    • indication would be TG > 200
    • equivalent would be LDL 160
  • ABI ( < 0.9)
262
Q
A

Medical (69 decks)

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