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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
What are three complications that can occur with acute anteroapical MI's?
* Dynamic LVOT obstruction * LV aneurysm * LV thrombus
26
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.
* **Dynamic LVOTO with systolic anterior mitral leaflet motion** * **Normal saline** * **​**treatment is centered around reducing the obstruction: * decrease inotropy * increase preload * increase afterload
27
What are causes of mitral regurgitation in post-AMI patients?
* LV dilatation * Ischemic papillary muscle dysfunction * Severe regional wall motion abnormality adjacent to a papillary muscle * Papillary muscle rupture
28
What is the AMI mortality associated with papillary muscle rupture?
5% of AMI deaths
29
Describe blood supply of the papillary muscles
* Anterolateral papillary muscle * dual blood supply * LAD * CFx * Posteromedial papillary muscle * RCA --\> PDA
30
Describe acute papillary muscle rupture? * Incidence and timing * Presentation * Diagnosis * Treatment
* 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
31
What is the pattern of LGE on cMRI: * Stress Cardiomyopathy
**No LGE** * no myocardial scarring and therefore no LGE
32
What is the pattern of LGE on cMRI: * Myocarditis
Mid myocardial LGE
33
What is the pattern of LGE on cMRI: * Cardiac amyloidosis
Diffuse, subendocardial LGE
34
EKG Definition: * ST and/or T wave abnormalities suggesting myocardial ischemia
* \> 1 mm of horizontal or downsloping ST-T segment depression and/or * T wave inversion ► 2 mm
35
Describe acute free wall rupture? * Incidence and timing * Presentation * Diagnosis * Treatment
* 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
36
Describe ventricular septal rupture? * Incidence and timing * Presentation * Diagnosis * Treatment
* 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
37
What leads to formation of pseudoaneurysm?
* Anterior MI --\> free wall rupture * **Organizing thrombus and hematoma, together with pericardium --\> sealing a rupture of the LV**
38
What is the classic RVMI presentation?
**Hypotension + Clear Lungs** * relative bradycardia * may be a clue to enhanced vagal tone * can also be seen in this setting
39
What is the differential diagnosis: * post ACS patient with recurrent chest pain * revascularized with PCI
* 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
40
What is the differential diagnosis: * post ACS patient with recurrent chest pain * revascularized with thrombolytics
failed reperfusion and recurrent coronary occlusion
41
What is the first step in patients with: * recent ACS with PCI * post-ACS exertional chest pain
Optimize antianginal therapy
42
Describe the findings:
* 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
43
Define "no-reflow"
* characterized by suboptimal myocardial perfusion despite restoration of lumen patency in the infarct related artery * angiographically is associated with TIMI flow « 2
44
What is one test that should be performed post-ACS?
**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
45
What test carries the highest negative predictive value for myocardial infarction?
**Troponin I**
46
What are the treatment stategies for NST-ACS as determined by risk stratification scores?
* Invasive * Immediate (within 2 hours) * Early (within 24 hours) * Delayed (25-72 hours) * Ischemia guided strategy * noninvasive strategy first
47
In the setting of NST-ACS, what are the indications for an: * Immediate Invasive ( « 2 hours) treatment strategy
* 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
48
In the setting of NST-ACS, what are the indications for an: * Early Invasive ( \< 24 hours) treatment strategy
* 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
49
In the setting of NST-ACS, what are the indications for an: * Delayed Invasive ( 25-72 hours) treatment strategy
* 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%
50
In the setting of NST-ACS, what are the indications for an: * Ischemia guided treatment strategy
* Low risk score * TIMI 0-1 * Grace \< 109 * Low-risk, troponin negative, female patients * Absence of high risk features + patient or physician preference
51
What is the effect of TTS on mortality?
Higher long-term mortality * higher compared with general age-matched population * outcomes resemble those of patients with ACS
52
What are TTS features which are associated with unfavorable long-term prognosis?
* Older age * Physical stressors * Atypical ballooning
53
What is the recurrence rate of TTS?
10-20% recurrence rate
54
What are potential cardiovascular complications associated with TTS?
* MR * LVOT obstruction * Cardiogenic shock
55
What is the recovery time for TTS?
hours - weeks
56
What are the treatment recommendations for antiplatelet therapy in SIHD?
**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
57
What trial compared ASA and Clopidogrel in patients with ASCVD?
**CAPRIE TRIAL (2003)** * Clopidogrel provided superior secondary prevention of atherosclerotic vascular events by a small margin
58
What are contraindications to ASA use?
* ASA allergy * NSAID allergy * Samter's syndrome * asthma * rhinitis * nasal polyps
59
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
**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
60
Describe the findings and diagnosis:
* **Posterior MI - LCx occlusion** * EKG * ST elevations in II, III and I, V5, V6 * ST depressions in V1-V3
61
Differentiate between STEMI in RCA and LCx
**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
62
What is the presentation and EKG findings in LMCA occlsuion?
* Often Fatal * Subtotal occlusions / EKG: * global ST depressions * Variable ST-elevations: V1 and aVR
63
Describe EKG findings: * LAD occlusion
* ST-elevation: V1-V3 * ST-depressions: II, III, aVF
64
Describe typical EKG findings: * Conus branch occlusion
Arrhythmias without significant ST changes * depending on size of the branch
65
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?
* **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**
66
What are atypical EKG presentations that may prompt emergent coronary angiography?
* BBB * positive Sgarbossa criteria * Ventricularly paced rhythm * Isolated posterior MI * LMCA or MVCAD
67
Describe atypical EKG findings that would prompt emergent angiography: * Bundle branch block (LBBB) * V-paced rhythm
* 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
68
Describe atypical EKG findings that would prompt emergent angiography: * Posterior MI (isolated)
* ST-depression (isolated) ► 0.5mm in V1-V3 * ST-elevation ► 0.5mm in V7-V9 (posterior leads)
69
Describe atypical EKG findings that would prompt emergent angiography: * LMCA or MVCAD
ST-depression ► 1 mm in ► 8 surface leads and ST-elevation in aVR and / or V1 \*\*\*\*Suggests LMCA, LM-equivalent or severe MVCAD
70
How many phases of Cardiac Rehabilitaiton are there?
**4 phases** * Phase I - Inpatient phase * Phase II - Outpatient phase * Phase III/IV - Maintenance phase
71
Describe CR - Phase I
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
72
Describe CR - Phase II
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.
73
Describe CR - Phase III / IV
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
74
What are the indications for Cardiac Rehabilitation?
* 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
75
What is the hospital readmission benefit associated with Cardiac Rehab during the year after a cardiac event?
**20-30% reduction**
76
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
* Lateral wall STEMI following MV repair * **Iatrogenic coronary occlusion**
77
What is the next best step after iatrogenic coronary occlusion?
**coronary angiography** * can help to determine the mechanism of coronary occlusion
78
Describe iatrogenic coronary occlusion following MV repair/replacement
* 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
79
What are some medical therapies that may be useful in microvascular angina (MVA)?
**Tobacco cessation** * Nicotine replacement * Varenicline (Chantix) * Bupropion
80
Describe the findings and diagnosis:
* EKG: * ST depressions ► 2mm in anterior precoridal leads (V1-V4) * **Posterior MI - LCx occlsuion (left dominant)**
81
What is the best way to assess for posterior MI?
**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
82
What is the accurary of posterior leads in detecting posterior MI? What is the most sensitive lead?
* **\> 91% of patients with LCx occlusion** * **Highest sensitivity --\> V8** (100% in one series)
83
What is the recommendation for statin therapy: * CAC score = 1-99
Reasonable to initiate statin therapy for patients **► 55 years of age**
84
What is the diagnosis? * Harsh systolic murmur at left sternal border * Palpable thrill * Loud pulmonic component of S2 * S3 Gallop
**Ventricular septal rupture** * occurring 1-5 days after acute MI * managed conservatively (no revascularization)
85
What method of determining ASCVD risk offers the highest discriminatory value for future ASCVD events?
**Coronary Artery Calcium Score (CAC)**
86
What does the risk assessment for primary prevention of atherosclerotic cardiovascular disease (ASCVD) involve?
* Estimation of ASCVD risk * Use of risk enhancers to personalize risk assessment * Selective use of CAC in some: * borderline risk adults * intermediate risk adults
87
When can CAC be utlized to reclassify ("de-risking") patients?
* 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
88
What CAC score should prompty initiation of statin therapy?
**CAC ► 100** or **► 75% percentile**
89
What ASCVD score should prompt initiation of pharmacologic therapy for stage 1 HTN (SBP 130-139 mmHg)?
**ASCVD ► 10%** * both pharmacologic and nonpharmacologic therapies should be initiated
90
What is the diagnosis based on histological changes: * necrotic myocardium and fibrous tissue
**LV aneurysm** * as a complication of transmural myocardial infarction
91
What is the diagnosis based on histological changes: * lipomatous or fibrolipomatous replacement of the myocardium
ARVC
92
What is the diagnosis based on histological changes: * necrotic myocardium with eosinophilic and lymphocytic infiltration * mural thrombus
Hypereosinophilic syndrome * HES or Loeffler's syndrome * Typical Echo findings include: * thrombotic and fibrotic obliteration of the ventricular apices
93
What is the diagnosis based on histological changes: * lymphocytic infiltration with fibrosis and noncaseating granulomas
Cardiac Sarcoidosis * Echo: * areas of wall thinning * aneurysm * focal areas of edema, akinesis, dyskinesis
94
What is the diagnosis based on histological changes: * myofibril disarray
Hypertrophic cardiomyopathy (HCM)
95
What is the next best step? * 50 year old, asymptomatic male * CAC score = 300
**Moderate-high intensity statin therapy** * revascularization does not confer mortality benefit in asymptomatic patients
96
What are the key factors when determining reperfusion strategy for STEMI?
* 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
97
Which patients benefit maximally from BB therapy following STEMI?
* Impaired LV function * HF (clinical) * Ventricular arrhythmias * Non-revascularized
98
What BB's should be utilized in STEMI associated with cocaine use?
* Carvedilol * Labetalol * alpha- and beta-blocking effects * decrease systemic BP without increasing coronary vascular resistance
99
When should an Echo be repeated in post-STEMI patients with reduced LV function?
**\> 40 days post-MI** * addresses the potential need for ICD therapy * allows for recovery from myocardial stunning
100
What is the most powerful predictor of death in MI patients?
**Heart Failure**
101
What medications should be started following STEMI?
* 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
102
Describe the steps in the progression of a coronary plaque
* Intimal thickening * Intimal Xanthoma * Pathologic intimal thickening * Fibrous Cap Atheroma * Thin-Cap Fibroatheroma * Rupture
103
What is the sequence of platelet effects that take place after rupture of a fibrous cap (coronary plaque)?
* Fibrous cap ruptures --\> procoagulant substances exposed to blood pool * Platelets: * **Adhesion** * **Activation** * **Aggregation**
104
What percentage of patients with normal, resting EKG who undergo ETT will require further risk stratificaiton?
25-40% * will have intermediate-risk treadmill tests and require further risk stratification
105
What is the importance of a normal resting EKG in regards to ETT?
* **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
What are the major differences in the Mayo study: * clinical-ETT model * clinical-ETT imaging model
* **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
Define "stunned myocardium"
* 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
Define "hibernating myocardium"
* adaptive rather than injurious response of the myocardium * due to repetitive: * ischemia and * chronic hypoperfusion * without acute injury * **​Viable, but dysfunctional myocardium**
109
Describe differences in treatment: * stunned myocardium * hibernating myocardium
* 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
Describe the response of hibernating myocardium in a dobutamine stress test
**Bimodal response** * Rest --\> Hypokinesis * Low-dose --\> Improves * High-dose --\> Akinetic (due to ischemic response)
111
What are the 4 broad categories of risk stratification that should be considered for pre-operative evaluation?
* Clinical evaluation and assessment of comorbidities * Functional capacity/noninvasive evaluation for ischemia * Ventricular function * Coronary anatomy
112
Describe the image
113
What is the mechanism of ASA (for antiplatelet therapy)?
* **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
Describe the pharmacokinetic properties of ASA
* 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
What is the most common side effect of ASA therapy?
GI intolerance (5-40%)
116
What is the recommended antiplatelet therapy if ASA cannot be tolerated?
Clopidogrel
117
Why should NSAIDS be avoided with ASA use? What strategies should be used if they are necessary therapy?
* 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
What levels indicate ASA resistance?
COX-1 activity \< 10%
119
What are the P2Y12 receptor blockers?
* Clopidogrel * Prasugrel (Effient) * Ticagrelor (Brilinta) * Cangrelor (IV)
120
Describe the activation of P2Y12 inhibitors
121
What P2Y12 inhibitor was discontinued as a result of adverse side effects?
**Ticlopidine** * rash, nausea, neutropenia and thrombocytopenia * Clopidogrel gained favor in the early 1990's --\> incorporated into large clinical trials
122
What did the CURE study demonstrate?
* 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
What did the PCI-CURE trial demonstrate?
* 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
What did the ARMYDA-2 study demonstrate?
* 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
What is the mutation associated with reduced Clopidogrel activity? What has this been proven to cause?
* **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
What should be done in poor metabolizers (resistance) of Clopidogrel?
**change to more potent P2Y12 inhibitors (Prasugrel, Ticagrelor)** * increased dosing is an inferior strategy to overcome resistance
127
When can platelet reactivity testing be considered?
* history of stent thrombosis * prior to undergoing high-risk PCI \*\*\*not currently recommended by the guidelines
128
What did the TRITON-TIMI 38 Trial show?
* 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
Describe Prasugrel: * Class / MOA * Active substance * Loading / Maintenance * Pharmacokinetics * Reversal agent
* 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
What are contraindications to Prasugrel?
* Active pathological bleeding * History of TIA / CVA * ≥ 75 years of age * Patients undergoing urgent CABG
131
Describe Ticagrelor * Class * MOA * Active substance * Loading/maintenance dose * Pharmacokinetics
* 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
What did the PLATO trial demonstrate?
* 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
What are the major side effects of Ticagrelor?
* **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
What is Vorapaxar?
* 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
What pharmacologic agents directly block the binding of fibrinogen?
**GP IIb/IIIa receptor inhibitors** * more effective in inhibiting platelet aggregation than any oral antiplatelet strategy
136
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
137
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
138
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
139
What are the 3 GP IIb/IIIa receptor inhibitors approved for use in the US?
* Abciximab * Eptifibatide * Tirofiban
140
Which of the GP IIb/IIIa receptor inhibitors can be reversed? What is the reversal agent?
* Abciximab * very low drug/receptor ratio * Platelets
141
How does Abciximab differ from other GP IIb/IIIa receptor inhibitors?
* **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
What is the indications and dosing for Abciximab? What % of dose is given as bolus?
* 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
What GP IIb/IIIa receptor inhibitors require adjustment for renal insufficiency? When?
* Eptifibatide * CrCl \< 50 mL/min * Tirofaban (Aggrastat) * CrCl \< 60 mL/min
144
Which anticoagulant acts as an indirect inhibitor of thrombin? How does it work?
* **Heparin** * Activation of antithrombin III --\> * inactivates factors IIa (thrombin), IXa and Xa
145
What is the mechanism of hypotension? * Sildenafil * Nitroglycerin
**Excess cGMP-mediated vasodilation**
146
What are the four Class I options for initial anticoagulation in NSTE-ACS?
* Heparin * Enoxaparin * Fondaparinux * Bivalirudin
147
What is the reversal agent for UFH?
**IV Protamine sulfate** * 10 mg per 1,000 U of UFH
148
What is the reversal agent for enoxaparin?
**Protamine Sulfate** * partially reversible (approximately 50%) * 1mg protamine / 1mg enoxaparin * only if last dose \< 8 hours * max dose: 50mg
149
Describe the details of Heparin: * Target * Half-life * Risk of HIT * Protein binding * Reversal agent * Excretion
* 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
Describe the features of enoxaparin: * Target * Half-life * Risk of HIT * Protein binding * Reversal agent * Excretion
* 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
What is used to monitor the therapeutic index of Heparin?
**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
What interaction can cause anaphylaxis in a patient on UFH? How can you avoid this?
* **Long-acting insulins and Protamine sulfate** * SC test dose should be administered prior to administration
153
What is the incidence of thrombocytopenia with Heparin use?
* 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
Define "chronic stable angina"
* 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
Describe the difference in risk: * SIHD with no major event * SIHD with prior major event (MI, CVA, PAD event)
**Increased 4-year CV death, MI, or stroke (18.3% vs. 12.2%)** * REACH Registry (Reduction of Atherothrombosis for Continued Health)
156
Describe the effects of polyvascular disease on CV death, MI, stroke or hospitalization?
Dependent on the number of vascular beds involved * One --\> 12.6% * Two --\> 21.1% * Three --\> 26.3%
157
Describe the classificaiton/types of chest pain
158
What trial demonstrated benefit for CAD/primary prevention with use of CCTA?
**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
What are the components of the Duke Treadmill Score?
* 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
Describe risk associated with the DTS
Exercise time (minutes) - ST depression x5 - Angina (non-limiting x4 vs. limiting x8) = DTS * Low ► 5 * Intermediate 4 to -10 * High « -11
161
In addition to the DTS, what are other metrics that offer insight into the overall CV status and help to identify high-risk patients?
* Abnormal BP response * Abnormal HR recovery pattern * Prolonged ST-depression * \> 8 minutes into recovery
162
In what scenarios is myocardial imaging appropriate in patients with SIHD?
* 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
When is repeat MPI appropriate in: * asymptomatic, stable patient * history of abnormal coronary angiography or abnormal stress test
stress test \> 2 years prior (may be appropriate)
164
What is the most common pathophysiologic mechanism for a NSTEMI?
**Disruption of the fibrous cap (plaque rupture or erosion)** * stimulates thrombogenisis
165
What are the high risk features ( ► 3% annual mortality rate) in noninvasive testing?
* **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
What are the recommendations regarding initiation of ACE/ARB following STEMI?
* Anterior STEMI * Heart Failure * LVEF « 40% \*\*\*\*Class I recommendations
167
What are the recommendations and benefits for ACE/ARB use in STEMI patients?
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
Which patients with STEMI will be least likely to benefit from ACE therapy?
preserved LV function + adequate revascularization + absence of DM or HF
169
What is the classical clinical triad of an RV infarct?
* Hypotension * JVD * Normal lung examination
170
What are medications that should be avoided in an RV infarct?
Reduce RV preload --\> should be avoided * Diuretics * Nitrates * Opiates
171
What are some ways to improve RV contractility in an RV infarct?
Dopamine or Dobutamine
172
What are the preferred treatments for microvascular angina?
traditional antianginal drugs * Alpha-**Beta Blockers** * CCB's * novel therapies * potassium channel openers * metabolic agents * rho-kinase inhibitors * ACE * Ivabradine * Statins * Phosphodieterase inhibitors
173
What is an anti-anginal therapy that can be used to reduce myocardial oxygen consumption independent of systemic hemodynamic effects?
**Ranolazine** * antianginal effects are independent of significant changes to the HR-BP product * does not alter myocardial blood flow
174
What are the characteristics that indicate an increased vulnerability to plaque rupture?
* Fewer smooth muscle cells * **Intraplaque hemorrhage** * Thinner fibrous caps * Large, necrotic lipid cores * Neoangiogenesis * Macrophage infiltration (increased) * Presence and degree of inflammation
175
When should fibrinolytics be administered in the setting of STEMI (in non-PCI capable facility)?
non-PCI capable hospitals + anticipated FMC time at PCI-capable hospital **\> 120 minutes**
176
When fibrinolysis has been chose as the primary perfusion strategy, when should it be adminstered?
* **\< 30 minutes of arrival** * **\< 10 minutes from STEMI diagnosis** \*\*\*\*\*Transfer to PCI-capable facility ASAP after bolus lytics administration
177
When do Troponin levels peak after the onset of symptoms?
**12-24 hours**
178
What are the recommendations regarding anticoagulation in fibrinolytic adminstration?
* should receive anticoagulant therapy * ► 48 hours * preferably for the duration of the index hospitalization * up to 8 days * or until revascularization is peformed
179
What are the recommended anticoagulant options in STEMI with fibrinolytic adminstration?
* 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
Describe the pathophysiology of HF after AMI: * Sympathetic nervous system * Parasympathetic nervous system * RAAS system
* 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
What accounts for nearly 25% of the ACS cases in women \< 50 years old?
**Spontaneous coronary artery dissection (SCAD)**
182
Describe the findings:
**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
When is Ivabridine indicated in heart failure?
**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
What is the 5-year survival for DTS findings: * Low * Intermediate * High
* Low ( \> 5) --\> **97%** * Intermediate ( 4 to -10) --\> **90%** * High ( \< -11 ) --\> **65%**
185
What TIMI risk score in UA/NSTEMI should prompt early-invasive management strategy?
TIMI score \> 2 * early-invasive management strategy = coronary angiography \< 48 hours
186
What should risk stratification after the initial reperfusion strategy include? * Assessment * Studies
* 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
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
**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
What are the initial anticoagulation treatment strategies in NST-ACS (in addition to antiplatelet therapy)?
* 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
What are the recommendations regarding anticoagulation in patients undergoing CABG?
* UFH --\> **up to time of CABG** * Bivalirudin --\> **« 3 hours prior to CABG --\> with continuance of UFH** * Enoxaparin --\> **« 12-24 hours** * Fondaparinux --\> **« 24 hours**
190
What does the Killip classification describe?
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
Describe Killip classifications
* 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
What is the incidence of high-grade AV block (2nd degree Mobitz II or 3rd degree) in ACS?
* 7% in fibrinolytic era * 1-3% in primary PCI era
193
Describe the difference in AV block in ACS: * Inferior wall * Anterior wall
* 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
What are the steps in treatment of high-grade AV block occuring in the setting of PCI/reperfusion?
* 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
When is pacing indicated in patients with high-degree AV block following PCI/reperfusion?
Symptoms related to ventricular rate emerge * pacing is generally not indicated as often transient
196
Define Bezold-Jarisch reflex
* 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
What is the treatment for Bezold-Jarisch reflex?
* **Atropine** * antagonizes both bradycardia and reflex cholinergic vasodilation * IV fluids * Refractory: * Isoproterenol or * TV pacing * IABP * only if refractory hypotension after IVF's
198
Describe the findings:
**SCAD** * spiral dissection in the LAD * diffuse smooth narrowing of the LM due to intramural hematoma and compression of the true lumen
199
When are ARNI's indicated in HF?
**Reduces Morbidity and Mortality** * Chonic, symptomatic, NYHA II or III HFrEF who tolerate an ACE/ARB
200
What are common associations with SCAD?
* Premonopausal women * Pregnancy / Multiparity * Hormonal therapy * **Fibromuscular dysplasia** * Systemic Inflammatory conditions * Connective tissue disorders
201
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%
**LV free wall rupture --\> Surgery (definitive treatment)** * acute chest pain + hemodynamic collapse following acute MI
202
What are early EKG indicators of high risk in STEMI?
**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
What CAD disease patterns demonstrate survival improvement with CABG?
* LM disease (significant) * Severe 3V-CAD involving the proximal LAD
204
What is unique in regards to ST-elevation pattern in high-lateral MI?
ST-elevation in aVL is rarely pronounced * beause QRS voltage in aVL is usually very low * ST voltage cannot exceed QRS voltage
205
When is PCI noninferior to CABG in LM disease?
**Low Syntax score anatomy ( \< 22 or \< 32?)**
206
What trials identified noninferiority for PCI vs. CABG in LM disease?
* EXCEL (2016) * NOBLE (2017)
207
What is the effect of acetylcholine in coronary microvascular disease?
**impaired endothelial-dependent activity**
208
What are two medications that can increase coronary blood flow?
* **Acetylcholine --\> NO** * Endothelial dependent (CFRe) * **Adenosine** * Nonendothelial dependent (CFRne)
209
What is required to make a diagnosis of PCI-related MI (type 4a)?
* 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
Describe the findings and diagnosis:
**LV aneurysm** * post-anterior wall MI * No evidence of LV thrombus or pseudoaneurysm * GDMT: **Spironolactone** in patients with LVEF \< 40%
211
What are the major physiologic effects of cocaine?
* 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
What is Trousseau's syndrome?
* 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
What is one major benefit of DES vs. BMS?
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
Describe Dressler's Syndrome
* 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
Define target-vessel revascularization
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
What is the treatment for postinfarction pericarditis (Dressler's Syndrome)?
* **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
Define Type II MI
* 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
What are the most important (heavily weighted) independent predictors of mortality in the TIMI (STEMI) classification system?
* 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
What are screening/follow up recommendations in those with SCAD?
**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
Why is troponin elevated in decompensated heart failure?
increased myocardial wall stress
221
Describe the findings:
**Remote inferior MI** * fragmented EKG morphologies in the inferior leads * Lead II: Rr' * Lead III: rSR' * Lead aVF: fragmented QRS
222
What have similar specificity and sensitivity when compared with pathologic Q waves for diagnosing remote MI?
**Fragmented QRS complexes**
223
Why does QRS fragmentation occur in remote MI?
* 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
What EKG changes are indicative of prior MI?
* 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
When is PCI supported: * IVUS of LM
MLA « 6.0 mm2
226
When is PCI supported: * FFR
\< 0.80
227
When is PCI supported: * iFR
« 0.89 * iFR lesions 0.9-0.93 should be investigated by FFR as well
228
When is revascularization supported: * LM stenosis
► 50%
229
When is PCI supported: * coronary stenosis
► 70%
230
What is the benefit of a CAC = 0?
15-year warranty period ( **\< 1% annual mortality**) * in low-intermediate risk individuals
231
What are common EKG findings associated with LV aneurysm post-MI?
ST-elevation occuring 6 weeks after a transmural MI
232
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
**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
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
**Typical angina**
234
What major adverse effect is associated with aspiration thrombectomy?
**Increased stroke** * Larger-scale studies have since shown no benefit in the composite primary outcomes: * cardiovascular death * recurrent MI * stent thrombosis * TVR
235
What echocardiographic feature is the strongest predictor of patient survival post-MI?
**LV ejection fraction**
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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
**Pharmacologic MPI** * troponin elevation + EKG changes in setting of noncardiac surgery * requires further risk stratification prior to discharge
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What are indications for oral anticoagulation following STEMI?
* A-fib * Recent venothromboembolism * LV thrombus « 6 months
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What is the preferred P2Y12 inhibitor when "triple therapy" is necessary?
**Clopidogrel** * preferred P2Y12 inhibitor to minimize excess bleeding
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What are measures to reduce bleeding in patients with STEMI?
* 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
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Why are Non-Vitamin K antagonist's oral anticoagulants preferred in "triple therapy" use?
Reduced risk of bleeding
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What is the cut-off for NTG use in ACS in the setting of phosphodiesterase use?
* Sildenafil or Vardenafil --\> **24 hours** * Tadalafil --\> **48 hours**
242
What are contraindications to initiating BB therapy in ACS?
* 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
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What hormone is classically elevated in stress cardiomyopathy?
**Epinephrine** * pathophysiologic mechanism * cathecholamine excess * derangement of myocardial glucose and fatty acid metabolism * microcirculatory dysfunction * coronary vasospasm * estrogen deficiency
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EKG Definition: * Anterolateral MI, age recent or probably acute
* 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
What are causes of LAD on EKG?
* COPD * Hyperkalemia * Inferior MI * LAFB * axis must be \> -45 degrees * LBBB * LVH * Ostium primum ASD
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When utilizing the GRACE score for STEMI, what is the strongest predictory of mortality?
**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
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What is the diagnosis based on the respone: * decreased coronary artery diameter in response to intracoronary acetylcholine
endothelial macrovascular dysfunction
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What is the diagnosis based on the response: * decreased coronary artery diameter in response to intracoronary nitroglycerin
nonendothelial macrovascular dysfunction
249
What is the strongest prognostic exercise test variable in an exercise-treadmill test?
**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
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What is a measurable diagnostic value for coronary microvascular dysfunction?
**CFR \< 2.5 in response to intracoronary adenosine** * indicates endothelial microvascular dysfunction
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What is the most common pathophysiologic mechanism for a NSTEMI?
**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
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What is the best treatment strategy: * asymptomatic * delayed presentation STEMI ( \> 24 hours)
**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
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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)
**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
In PAH, what is a prominent pathway in vasoconstriction?
**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
What are the treatment recommendations for VA/SCA due to coronary artery spasm?
* 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**
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When is PCI recommended in patients with delayed STEMI ( \> 24 hours)?
* 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)
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When is PCI recommended in patients with delayed STEMI ( 12-24 hours)?
* CHF (severe, congestive) * hemodynamic instability * electrical instability * Evidence of severe ischemia
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What is one lab that should be checked and corrected prior to urgent intervention in NSTEMI?
**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
What is the differential diagnosis for inverted P-waves in I and aVL?
* 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**
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What lab is most useful in the decision to start lipid-lowering therapies in patients with borderline ASCVD?
**Hs-CRP** * hs-CRP ► 2 * considered a risk-enhancing factor for ASCVD risk stratification
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What labs can aid in the decision to start lipid-lowering therapies in patients with borderline ASCVD?
* 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)
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Medical (69 decks)

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