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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
Medical Therapy vs PCI
PCI did not reduce risk of death, MI, or other major event compared to medical therapy alone
26
Optimal Medical Therapy
1. Smoking Cessation 2. Total Dietary Fat / Saturated Fat 40 mg/dL 6. Triglyceride (secondary goal) 27.5 Goal: 10% relative weight loss 9. Blood Pressure
27
CABG vs. PCI
- similar CV events | * more revascularization for PCI
28
Acute Coronary Syndromes: Types and General Pathology
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
Acute Coronary Syndromes Diagnostic tests
1. EKG | 2. Serum biomarkers: troponin I and T (hallmark of MI)
30
Why do plaques rupture?
``` • Mechanical factors (shear stress) • Endogenous factors (catecholamines) • Inflammation • Exogenous Factors (smoking) ```
31
Why do coronary arteries thrombose?
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
Platelet Activation
``` “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
Why is an acutely occluded artery not always a STEMI?
1. Pre-formed collaterals 2. Electrically silent area of myocardium affected “Circumflex artery”
34
Acute coronary syndrome: angina pectoris
occurs at rest lasts >10 minutes severe, new onset crescendo pattern
35
ACS: Emergency Assessment
``` • 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
TIMI Risk Score Criteria
Death, MI, Severe ischemia requiring revascularization
37
TIMI Risk Scores
``` 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
Unstable Angina/NSTEM Tx: Treating Symptoms
NTG + morphine
39
Unstable Angina/NSTEM Tx: Preventing Events: | Death, MI, stroke, revasc.
``` Anti-platelet therapy Anti-thrombin therapy Statins Beta-blockers ACE-Inhibitors Revascularization Lifestyle measures - exercise - diet/wt reduction - smoking cessation ```
40
Unstable Angina/NSTEM Tx: ACS and Antiplatelet Therapy: 2 types
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
Unstable Angina/NSTEM Tx: Anti-thrombins
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
Unstable Angina/NSTEM Tx: Beta Blockers
Improved Survival Reduction in MI Reduction in Stroke Reduction in HF Reduction in Arrhythmia
43
Unstable Angina/NSTEM Tx: 1. fibrinolytic therapy 2. PCI/CABG
1. No benefit, only harm | 2. Indicated if high risk features; reduction in ischemic events
44
Unstable Angina/NSTEM Tx:Lifestyle Measures
* Exercise * Diet * Weight reduction * Smoking Cessation * Stress reduction CARDIAC REHABILITATION
45
Focus for... 1. Stable Ischemic Heart Disease 2. Unstable Angina/NSTEMI:
1.Symptom Management Preventing CV Events Selective Revascularization 2. Preventing CV Events Greater role for Revascularization (But no fibrinolytics)
46
Wave Front of Ischemic Death
1. Necrosis 2. Microvascular Injury Interstitial Hemorrhage 3. Cessation of Microvascular Perfusion
47
histopathology: 22 h after chest pain onset
``` • Wavy fibers • Fibers separated by spaces • “Contraction bands” Ca2+ dependent-hypercontractile state -->contractile necrosis • Neutrophil infiltration ``` slide 76
48
histopathology: 7 days post MI
``` • Vacuoles within myocytes • Mononuclear cell and macrophage infiltration • Small vessel proliferation • Fibroblast proliferation ``` Slide 77
49
histopathology: 14 days post MI
Fibrosis-->patchy scar Slide 78
50
Management of STEMI
* PROMPT Reperfusion * ASA (aspirin) * Thienopyridine (ie. clopidogrel) * Cardiac Care Unit Care * Statin * Beta-blocker * ACE-Inhibitor * Cardiac Rehab * Secondary Prevention
51
STEMI Reperfusion Therapy: | 1. Fibrinolytic Therapy
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
STEMI Reperfusion Therapy: Indications for PCI & timeframe
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
Gusto IIb 30 day mortality if DTB: a) 91 min
a) 1% b) 3.7% c) 4.0% d) 6.4%
54
Summary of STEMI 1. Goal of therapy? 2. What interventions improve survival?
1. Goal of therapy for STEMI is prompt reperfusion
55
Complications following MI
* Congestive heart failure * Arrhythmias * Cardiogenic Shock * Post-MI Pericarditis
56
Post MI Ventricular Remodeling
“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
Pathophysiologic ans Biochemical Events Post MI
``` 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
Why is the antero-apical region most vulnerable for infarct expansion?
* Thinnest area of myocardium * Greatest curvature * Greatest deforming forces * Site of thrombus due to stasis * Site of rupture
59
Ventricular Arrhythmias
Post MI ventricular fibrillation and ventricular tachycardia are common •VF or VT after 48 hours predicts increased risk of sudden death
60
Cardiogenic Shock
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
Post MI Pericarditis 1. Definition 2. Peri-infarction Pericarditis 3. Late Pericarditis (Dressler's)
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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