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Acute Coronary Syndromes Flashcards

1
Q

Problems with supply

A

Epicardial Coronary artery obstruction

Microvascular obstruction

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2
Q

Epicardial Coronary artery obstruction

A
  1. Atherosclerosis
  2. Vaso-spasm
    - Printzmetal angina
  3. Embolus
  4. Extrinsic compression
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3
Q

Microvascular obstruction

A
  1. Atherosclerosis
  2. CT dz
  3. transplant vasculopathy
  4. Diabetic micro-angiopathy
  5. Micro-emboli-Kawasaki’s
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4
Q

Problems with demand

A 
Increased Demand
• Hypertension-high afterload
• Aortic valve stenosis-fixed afterload
• Peri-op-high catecholamines
• Anemia
• Tachycardia
• Hyperthyroidism
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5
Q

Stable Ischemic Heart Disease: Presentation

A
  • Exertional chest pain (or equivalent) that is chronic
  • May be asymptomatic
  • predictable angina pectoris
  • Typically seen in the outpatient clinic setting
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6
Q

Stable Ischemic Heart Disease: Pathophysiology

A
  • Obstructive(collaterals) or non-obstructive coronary artery plaque
  • Intact fibrous cap
  • Minimal platelet activation, inflammation or thrombus

•Other conditions: aorticstenosis, HOCM

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7
Q

Stable Ischemic Heart Disease: Clinical Integrated Assessment

A 
Symptoms
Prognostic Tests
Diagnostic Tests
Functional Capacity 
Risk Factors
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8
Q

Stable Ischemic Heart Disease: Angina Pectoris

A

Pain or discomfort in the chest caused by insufficient blood supply to the heart muscle

  • Typically brought on by exertion or emotional stress
  • Typically lasts 1-15minutes
  • Relieved by rest
  • Relieved by nitroglycerin
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9
Q

Stable Ischemic Heart Disease: Making the Dx

A 
“Exertional and Predictable”
indigestion

• Heaviness 
• Tightness 
• Squeezing 
• Burning can be misconstrued as
• Choking
• Radiating to the arms

Associated Symptoms 
• Weakness of the arms 
• Shortness of breath
• Dizziness
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10
Q

Populations with silent myocardial ischemia

*Examples of anginal equivalents

A

10-40% of patients will be silent

Women, Diabetes, elderly

*fatigue, weakness, shortness of breath

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11
Q

Stable Ischemic Heart Disease: Risk Factors

A
  • Tobacco use
  • Diabetes mellitus
  • Dyslipidemia
  • Family history of CAD
  • Hypertension
  • Peripheral artery disease
  • Renal Failure
  • Inflammatory Diseases (RA, SLE, Psoriasis)
  • Obesity
  • Sedentary Lifestyle
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12
Q

Stable Ischemic Heart Disease: Diagnosis and Prognosis

A

Don’t need to know details just know that there are a lot of ways to do this

• Stress Testing

  • Exercise/Pharmacologic
  • ECG
  • *Nuclear SPECT imaging
  • *Echo stress test
  • MRI

• Ventricular Function

  • Echocardiogram
  • Nuclear Imaging
  • MRI/CT/CardiacCatheterization
  • worse prognosis for those with low EF

• Coronary anatomy & physiology

  • CT Angiography
  • Cardiac Catheterization
  • –Intravascular Ultrasound
  • – Fractional Flow Reserve
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13
Q

Stable Ischemic Heart Disease: Exercise Stress Test (EKG)

A
  • Limited sensitivity & specificity(70%)
  • typically useful as a prognosis indicator when pre-test is intermediate: 50 year old male with 1 or 2 risk factors; not useful in say a morbidly obese person or a marathon runner
  • Sensitivity/Specificity worse in women than men
  • Diagnostic value of the test depends on“pre-test” probability of having coronary artery disease

EKG has ST depression for ischemia pattern

  • combine with imaging to improve sensitivity and specificity
  • nuclear scintigraphy (blood flow)
  • echo (contractility)
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14
Q

Stress Echo

A

Real-time US study to determine wall motion (contractility) of individual regions of LV before and after exercise

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15
Q

Nuclear Stress imaging

A

IV radio tracer: thallium or technitium conjugated to organic compound (Sestamibi)

-taken up by myocardium in proportion to blood flow

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16
Q

What can be used in lieu of exercise to stress the heart?

A

Coronary vasodilators: adenosine and dipyridamole

hypercontractility agents: dobutamine

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17
Q

Invasive Coronary Angiography/Invasive cardiac catetherization

A

“gold standard” for diagnosing atherosclerotic coronary artery disease and assessing its severity

  • simple test with low risk
  • often outpatient
  • catheters advanced from a percutaneous (“needle stick”) puncture in femoral artery to the heart and are used to inject a radio-opaque contrast into the right and left coronary arteries
  • The flow of contrast through the arteries is recorded using X-ray cinematography

***Left ventricular function-assessed by measuring intra-cardiac pressures and by injecting contrast into LV to determine its size, shape and contractility

***However demonstrates only the lume; not sensitive to detect early, preclinical atherosclerosis where positive remodeling preserves the luminal dimensions, often despite extensive atherosclerosis

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18
Q

IV Ultrasound

A

invasive technique

arteries via a miniaturized ultrasonic piezo-electric crystal mounted in an angioplasty-type wire

very sensitive to detect the full extent of atherosclerosis in coronary arteries

***commonly employed clinically to measure vessel size and assess plaque burden

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19
Q

Fractional Flow Reserve

A

Invasive

cath lab to define the “functional” significance of a lesion

coronary guidewire mounted with a miniature pressure transducer is placed across the lesion

Maximum hyperemia via adenosine administration

FFR=(distal coronary pressure)/(proximal)
*during max hyperemia

FFR

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20
Q

Coronary CT angiography

A

newer, noninvasive approach to visualizing the coronary arteries

ID’s obstructive plaques, but can also detect non-obstructive calcifications in the coronary artery, which is diagnostic of the presence of coronary artery atherosclerosis

promising noninvasive technique; the lower spatial resolution, imaging related artifacts, higher radiation dose, and healthcare reimbursement issues have prevented universal adoption of this method

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21
Q

Stable Ischemic Heart Disease: treatment

A

Focus is on treating symptoms and preventing events (Death, MI, stroke, revasc.)

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22
Q

Stable Ischemic Heart Disease: Treating Symptoms

A
  1. Nitrates-vasodilator
  2. Calcium channel blockers
    - vasodilator and decrease HR (decreasing demand)
  3. Beta Blockers
    - Decrease HR
  4. Revascularization:
    PCI (stents/angioplasty) CABG
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23
Q

Stable Ischemic Heart Disease: Preventing Events

A
  1. Lifestyle measures
    - exercise
    - diet/wt reduction
    - smoking cessation
  2. Anti-platelet meds
    a) Aspirin
    - 50% reduction in mortality for previous MI
    b) clopidogrel and prasrugrel
  3. Statins
  4. ACE-Inhibitors
  5. Thieonopyridine
  6. If considered to be very high risk (ie. stress testing)
    then may consider
    PCI (stents/angioplasty) and CABG
    -PCI really only provides relief and does not decrease total rates of MI or death
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24
Q

CABG vs. Medical Therapy

A

Survival related to 2 main things: LV function and severity of CAD

Improved survival only for those with Left Main CAD or Severe 3 vessel disease + reduced LV fxn

*no benefit to low risk patients

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25
Q

Medical Therapy vs PCI

A

PCI did not reduce risk of death, MI, or other major event compared to medical therapy alone

26
Q

Optimal Medical Therapy

A
  1. Smoking Cessation
  2. Total Dietary Fat / Saturated Fat
    40 mg/dL
  3. Triglyceride (secondary goal) 27.5
    Goal: 10% relative weight loss
  4. Blood Pressure
27
Q

CABG vs. PCI

A
  • similar CV events

* more revascularization for PCI

28
Q

Acute Coronary Syndromes: Types and General Pathology

A
  1. Unstable Angina (UA)
  2. NSTEMI
  3. STEMI
Pathology: 
•Obstructive coronary artery plaque
• Plaque rupture or erosion
-thin fibrous cap w/large lipid pool 
• Platelet activation, inflammation, thrombus
29
Q

Acute Coronary Syndromes Diagnostic tests

A
  1. EKG

2. Serum biomarkers: troponin I and T (hallmark of MI)

30
Q

Why do plaques rupture?

A 
• Mechanical factors (shear stress)
• Endogenous factors (catecholamines)
• Inflammation
• Exogenous Factors
(smoking)
31
Q

Why do coronary arteries thrombose?

A

After rupture, lipid core is exposed:

• Activation of intrinsic clotting
- Tissue Factor

• Platelet activation

  • Collagen
  • von Willebrand Factor
  • catecholamines
  • smoking

• Endothelial dysfunction

  • reduction in NO
  • reduction in prostacyclin
  • vasoconstriction
32
Q

Platelet Activation

A 
“Triggers”
Just be aware that there are a lot and they mainly deal with platelet aggregation
• Catecholamines
• Cigarette smoking 
• Collagen
• Tissue Factor
• vWF

“Feed-back”-vicious cycle
• Adenosine Diphosphate
• Serotonin
• Thromboxane A2

*platelets activate extrinsic clotting path

33
Q

Why is an acutely occluded artery not always a STEMI?

A
  1. Pre-formed collaterals
  2. Electrically silent area of myocardium affected
    “Circumflex artery”
34
Q

Acute coronary syndrome: angina pectoris

A

occurs at rest lasts >10 minutes

severe, new onset crescendo pattern

35
Q

ACS: Emergency Assessment

A 
• Characterize discomfort onset, character, severity
• Identify risk factors
• Physical Examination 
– signs of instability 
-Rule out other causes of chest pain
• Cardiac Biomarkers (Troponin, CK-MB) 
• ECG (ST depression or ST elevation)
• Rule out other causes of chest pain
36
Q

TIMI Risk Score Criteria

A

Death, MI, Severe ischemia requiring revascularization

37
Q

TIMI Risk Scores

A 
0/1 — 4.7 percent 
2— 8.3 percent
3— 13.2 percent
4— 19.9 percent 
5— 26.2 percent 
6— 40.9 percent
38
Q

Unstable Angina/NSTEM Tx: Treating Symptoms

A

NTG + morphine

39
Q

Unstable Angina/NSTEM Tx: Preventing Events:

Death, MI, stroke, revasc.

A 
Anti-platelet therapy 
Anti-thrombin therapy 
Statins
Beta-blockers 
ACE-Inhibitors Revascularization 
Lifestyle measures
- exercise
- diet/wt reduction
- smoking cessation
40
Q

Unstable Angina/NSTEM Tx: ACS and Antiplatelet Therapy: 2 types

A
  1. ASA/Aspirin
    • irreversibly blocks the catalytic site of (COX-1) in platelets
    • COX-1 is required for the metabolism of arachidonic acid to PGH2 which processed to thromboxane A2, a powerful promoter of platelet aggregation
    
    2.P2Y12 Receptor Blockers
    *Don’t worry about details, just know they inhibit platelet aggregation
    • Irreversibly inhibits the low-affinity ADP receptor (P2Y12) on the platelet membrane.
    • Inhibits the activation of the GpIIb-IIIa (directly inhibiting fibrinogen cross-linking)
41
Q

Unstable Angina/NSTEM Tx: Anti-thrombins

A

Goal: prevent formation of thrombin

Be aware but don’t worry:
Unfractionated Heparin
Low Molecular Weight Heparin: Enoxaparin Direct thrombin Inhibitor: Bivalirudin Factor Xa Inhibitor: Fondaparinux

42
Q

Unstable Angina/NSTEM Tx: Beta Blockers

A

Improved Survival Reduction in MI
Reduction in Stroke Reduction in HF
Reduction in Arrhythmia

43
Q

Unstable Angina/NSTEM Tx:

  1. fibrinolytic therapy
  2. PCI/CABG
A
  1. No benefit, only harm

2. Indicated if high risk features; reduction in ischemic events

44
Q

Unstable Angina/NSTEM Tx:Lifestyle Measures

A
  • Exercise
  • Diet
  • Weight reduction
  • Smoking Cessation
  • Stress reduction

CARDIAC REHABILITATION

45
Q

Focus for…

  1. Stable Ischemic Heart Disease
  2. Unstable Angina/NSTEMI:
A

1.Symptom Management
Preventing CV Events Selective Revascularization

  1. Preventing CV Events Greater role for Revascularization
    (But no fibrinolytics)
46
Q

Wave Front of Ischemic Death

A
  1. Necrosis
  2. Microvascular Injury Interstitial Hemorrhage
  3. Cessation of Microvascular Perfusion
47
Q

histopathology: 22 h after chest pain onset

A 
• Wavy fibers
• Fibers separated by spaces
• “Contraction bands”
Ca2+ dependent-hypercontractile state
-->contractile necrosis
• Neutrophil infiltration

slide 76

48
Q

histopathology: 7 days post MI

A 
• Vacuoles within myocytes
• Mononuclear cell and macrophage
infiltration
• Small vessel proliferation
• Fibroblast proliferation

Slide 77

49
Q

histopathology: 14 days post MI

A

Fibrosis–>patchy scar

Slide 78

50
Q

Management of STEMI

A
  • PROMPT Reperfusion
  • ASA (aspirin)
  • Thienopyridine (ie. clopidogrel)
  • Cardiac Care Unit Care
  • Statin
  • Beta-blocker
  • ACE-Inhibitor
  • Cardiac Rehab
  • Secondary Prevention
51
Q

STEMI Reperfusion Therapy:

1. Fibrinolytic Therapy

A

Fibrinolytic (also called Thrombolytic) Therapy

  • Amplifies activation of plasmin from plasminogen
  • plasmin hydrolyzes fibrin
ie.
streptokinase 
alteplase 
tenectaplase 
retavase
*****Problems****
• Failure to open infarct artery ~40%
• Intracranial hemorrhage 
1-2% because it causes systemic lysis
• Contraindications up to 40%
• Lytic outcomes consistently inferior
to timely PCI
52
Q

STEMI Reperfusion Therapy: Indications for PCI & timeframe

A

Indications:

  1. ST elevation of 1-2mm in two contiguous leads
  2. New onset Left Bundle Branch Block (controversial)
Timeframe: 
#1: Primary PCI – goal
53
Q

Gusto IIb
30 day mortality if DTB:
a) 91 min

A

a) 1%
b) 3.7%
c) 4.0%
d) 6.4%

54
Q

Summary of STEMI

  1. Goal of therapy?
  2. What interventions improve survival?
A
  1. Goal of therapy for STEMI is prompt reperfusion
55
Q

Complications following MI

A
  • Congestive heart failure
  • Arrhythmias
  • Cardiogenic Shock
  • Post-MI Pericarditis
56
Q

Post MI Ventricular Remodeling

A

“Time-dependent & dynamic structural alterations in the ventricle resulting from coronary occlusion and myocardial necrosis.”

*a lot of the meds given to MI patients are to prevent this remodeling

57
Q

Pathophysiologic ans Biochemical Events Post MI

A 
Myocyte death leads to: 
-inflammatory cascade
-activation of RAAS
-up-regulation of 
pro-inflammatory and pro-vasculatory things that contribute to remodeling
  • early remodeling: wall thinning/dilatation
  • myocyte hypertrophy
  • late remodeling: fibrosis

slide 95

58
Q

Why is the antero-apical region most vulnerable for infarct expansion?

A
  • Thinnest area of myocardium
  • Greatest curvature
  • Greatest deforming forces
  • Site of thrombus due to stasis
  • Site of rupture
59
Q

Ventricular Arrhythmias

A

Post MI ventricular fibrillation and ventricular tachycardia are common

•VF or VT after 48 hours predicts increased risk of sudden death

60
Q

Cardiogenic Shock

A

Definition: Decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume

  • Pump failure (massive infarction of >40% myocardium)
  • Myocardial rupture
  • papillary muscle – causes severe mitral regurgitation
  • ventricular septum – causes severe L to R shunt
  • free wall rupture – causes pericardial tamponade

• Prognosis is very poor:
up to 80% in hospital mortality

61
Q

Post MI Pericarditis

  1. Definition
  2. Peri-infarction Pericarditis
  3. Late Pericarditis (Dressler’s)
A

Not common anymore since we’re getting good at early reperfusion therapy

Definition:
• Inflammation of the parietal pericardium following transmural infarct
• Sharp, pleuritic, positional chest pain sharp-not like MI pain
• Pericardial friction rub

  1. Peri-infarction Pericarditis
    • Common
    • Symptoms

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