coronary artery disease Flashcards

1
Q

The endothelial cells lining the coronary arteries have
two major roles:

A
  1. Regulate vascular tone: vasodilation (e.g., nitric
    oxide) and vasoconstriction (e.g., endothelin, angiotensin-converting enzyme [ACE])
  2. Prevent intravascular thrombosis: (e.g., prostacyclin, plasminogen)
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2
Q

Factors that can impair endothelial function:

A
  1. Hemodynamic (e.g., shear stress, hypertension
    [HTN])
  2. Chemical (e.g., low-density lipoprotein [LDL],
    modified LDL, homocysteine)
  3. Biologic (e.g., viruses, bacteria, immune complexes)
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3
Q

how does atherosclerotic plaque form

A
  • Begins with disruption of endothelial cell integrity
  • Leukocytes, mostly macrophages, are then attracted to the site of disruption, where they collect lipids and coalesce to form a fatty streak
  • Fatty streaks mostly consist of lipid-laden macrophages containing cholesterol ester droplets (atheroma)
  • Chemoattractants (e.g., platelet-derived growth factor) then cause smooth muscle cells to migrate to the
    atheroma, where they produce collagen and fibrous tissue that contribute to plaque formation, covered by a layer of connective tissue called the fibrous cap
  • Most acute coronary syndromes (ACSs) occur when the
    fibrous cap ruptures, leading to thrombus formation
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4
Q

cardiology scale for ACS event

A
  1. stable angina
  2. unstable angina
  3. Nstemi
  4. stemi
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5
Q

Plaque characteristics, not size,
determine its vulnerability to rupture

A

a large, fibrotic plaque with a thick cap is more stable and less prone to
rupture than a small plaque with a soft lipid core and a thin fibrous cap.

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6
Q
  1. Reproducible angina symptoms (chest pain or pressure) of at least 2 months
  2. Precipitated by exertion or emotional stress.
  3. Relived by rest of nitroglycerin
A

angina pectoris

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6
Q

it is important to recognize that classic symptoms may be absent, and some demographic groups (women and patients with diabetes mellitus) may have atypical symptoms, including exertional dyspnea (if it presents any other way)

A

atypical angina

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7
Q

Presence of angina during strenuous, rapid, or prolonged ordinary activity
(walking or climbing the stairs).

A

Angina only with strenuous exertion class 1

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8
Q

tightness, heaviness, or gripping in the chest,

A

typical angina
white guy angina

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9
Q

Mild myocardial ischemia with no symptoms.

A

asymptomatic angina class 0

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10
Q

Slight limitation of ordinary activities when they are performed rapidly, after
meals, in cold, in wind, under emotional stress, during the first few hours
after waking up, but also walking uphill, climbing more than one flight of
ordinary stairs at a normal pace and in normal conditions

A

Angina with moderate exertion class 2

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11
Q

Having difficulties walking one or two blocks or climbing one flight of stairs at
normal pace and conditions.

A

angina with mild exertion class 3

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12
Q

No exertion needed to trigger angina

A

angina at rest class 4

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13
Q
  • The fundamental problem is an imbalance between myocardial oxygen supply and
    demand.
  • Insufficient coronary blood flow occurs when a plaque leads to arterial stenosis
  • Anginal symptoms occur during periods of exercise or stress when increased myocardial
    oxygen demand (e.g., from an increase in heart rate, contractility, afterload, or wall
    stress) is not met because of impaired coronary blood flow.
  • There is endothelial dysfunction preventing adequate vasodilation during exercise, which
    can occur in the absence of severe luminal narrowing
A

stable angina

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14
Q

independent risk factor for plaques

A

diabetes

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15
Q

strong risk factors for CAD
(2 or more, they have it)

A

1.Older age
2.Male
3.Postmenopausal females
4.Hyperlipidemia (high LDL low
HDL)
5.Cigarette smoking
6.Hypertension
7.Diabetes mellitus
8.Obesity or sedentary lifestyle
9.Family history of early CAD

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16
Q

how to diagnose stable angina

A

ECG
Approximately 50% of patients with chronic stable angina have a normal resting ECG
* Pathologic Q waves ( Old MI) and conduction system abnormalities (e.g., LBBB, left anterior fascicular block) increase the likelihood of having CAD

stress test
* Stress testing can help risk-stratify patients:
* The sensitivity of an exercise treadmill test is
approximately 70%, the specificity is approximately
80%
* Stress tests add little diagnostic information for
patients with either high or low pretest
probabilities for CAD
* Stress tests are most useful for diagnosing CAD in
patients with intermediate pretest probability

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17
Q
  • Typically occur during physical exertion and
    gradually resolve with exercise cessation
  • Symptoms can also occur in conditions that
    increase oxygen demand (e.g., anemia, fever,
    sepsis, thyrotoxicosis
  • Substernal chest pressure or burning (less common
    to have sharp pain)
  • Pain may radiate to the upper extremities (left arm
    more often than right arm), neck, jaw, or face
  • Associated symptoms include dyspnea,
    diaphoresis, palpitations, and lightheadedness
  • Women, diabetics, and the elderly are more likely
    to have atypical symptoms
A

symptoms of stable angina

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18
Q

different types of stress tests

A
  • exercise
    -meds that mimic exercise (dobutamine, adenosine)
  • nuclear imaging (thallium 201, technetium 99)
  • echocardiography (stressing and doing echo)
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19
Q
  • Noninvasive and quantitative assessment of
    coronary artery calcification
  • Higher coronary artery calcium scores are
    associated with increased risk of MI and death
A

Calcium score screening CT:

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19
Q

allows for direct coronary artery visualization of a beating heart with little motion artifact
* Most accurate noninvasive modality in ruling out CAD with a very high negative predictive value
(>95%)
* Less accurate in differentiating degrees of coronary artery stenosis greater than 50%; the positive
predictive value varies between 60 and 90

with dye

A

Coronary CT
angiography (CCTA):

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20
Q
  • Considered the gold standard for diagnosing CAD
  • Refer for cardiac catheterization if:
    1. Need to confirm or exclude CAD
    2. Medical therapy fails to relieve anginal
    symptoms
    3. History and noninvasive testing suggest high-risk
    coronary anatomy
A

cardiac angiography

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21
Q

Treatment of Chronic CAD Decrease modifiable risk factors:
before Cath lab

A
  • Address modifiable risk factors (e.g., lipid lowering, cigarette cessation)
  • Treat Sleep Apnea
  • Weight loss
  • Correct illnesses that can precipitate or exacerbate angina (e.g., anemia, infection, thyroid disease)
22
Q

Treatment of Chronic CAD (stable angina): Anti-anginal (pain)

A

(First-line therapy) both:

  • β-Blockers
    Reduce myocardial oxygen (O2) demand by decreasing heart rate, BP, and contractility
  • Nitrates
    Major effect stems from venodilation, which
    decreases cardiac preload, thereby decreasing wall stress and O2 demand
    Very good at relieving angina and improving exercise tolerance but does not affect mortality
22
Q

Treatment of
Chronic CAD:
Anti Thrombosis

A

Aspirin
* Reduces risk of MI and death
* All patients with CAD should be on aspirin unless there
is a clear contraindication
Clopidogrel
* Platelet P2Y12 receptor inhibitor.
* If Allergic to ASA
* Neither prasugrel nor ticagrelor has been studied in the
context of stable angina, and their role in managing this
condition remains to be established.

23
Q

Treatment of
Chronic CAD:
Antihypertensive
Reduce BP <130/80

A

Beta Blockers:
* Increase dose till resting HR 55-60/minute
Calcium Channel Blockers:
* If BP not controlled or still symptomatic add long acting
CCB (Amlodipine)
ACE inhibitors
* Clear decrease in mortality and morbidity rates in
patients with left ventricular (LV) dysfunction (ejection
fraction [EF] <40%)

24
Q

Treatment of
Chronic CAD:
Lipid Lowering

A
  • High Intensity Statin
  • If LDL still > 70 consider Ezetimibe
  • PCSK9 inhibitors
24
Q

Treatment of
Chronic CAD:
Revascularization

A

The major indication for revascularization in
chronic CAD is for relief of angina symptoms in
patients on optimal medical management

  • In patients with stable CAD, PCI is quite effective in reducing angina, but it does not reduce the risk of death or MI

It has 2 components:
* 1-Percutaneous transluminal coronary angioplasty (PTCA), in which a balloon is used to split the atheromatous plaque and stretch the
artery.
* 2-Stent deployment, which provides a metal scaffold to help maintain artery patency

24
Q

Revascularization
of chronic CAD-
Coronary artery
bypass grafting
(CABG):

A
  • Recommended for patients with extensive CAD, patients with left main or three-vessel CAD.
  • Revascularization with CABG results in decreased recurrence of angina, lower rates of MI, and fewer repeat revascularization procedures compared with PCI.
  • Long-term (10-year) follow-up demonstrated a survival advantage with CABG compared with
    medical therapy alone among patients with multivessel CAD and severe left ventricular dysfunction.
25
Q
  • Unstable angina (UA),
  • Non–ST-segment elevation MI (NSTEMI),
  • ST-segment elevation MI (STEMI)
A

Acute
Coronary
Syndrome
(ACS)

25
Q
  • Clinically like UA, but distinguished by evidence of myocardial necrosis (i.e., an elevation in serum cardiac enzymes)
  • ECG does not show ST-segment elevation
  • positive labs
A

Non ST
segment
Elevated
Myocardial
Infarction
(NSTEMI):

26
Q
  1. Angina at rest (usually prolonged more than 20 minutes),
  2. New-onset exertional angina (i.e., angina with only mild exertion),
  3. Preexisting angina that has increased in frequency or duration or that is now brought on with less exertion than before.
  4. Post MI angina
A

unstable angina

27
Q
  • Presence of elevated cardiac enzymes
  • ECG criteria that include greater than 1-mm ST- segment elevation in two or more contiguous limb
    leads, or greater than 2-mm ST-segment elevation in two or more contiguous precordial leads
  • ST-segment elevation suggests total occlusion of the infarcted artery by thrombus; in contrast, most patients presenting with UA or NSTEMI do not have a totally occluded infarct artery
A

ST segment
Elevated
Myocardial
Infarction
(STEMI):

28
Q

ST elevation

A

STEMI

29
Q

ST depression

A

NSTEMI

30
Q
  • Larger, fibrotic plaques with thicker caps are less
    prone to rupture than smaller plaques, which have
    softer atherogenic lipid cores and thinner caps
  • Inflammation can lead to plaque instability and
    rupture
  • Other factors can contribute to plaque
    vulnerability, including shear stress and enzymatic
    degradation, which both weaken the plaque cap
A

the vulnerable plaque

31
Q

T inversion

A

NSTEMI

31
Q

occurs when a vulnerable plaque ruptures,
leading to platelet activation and aggregation,
resulting in the formation of intracoronary
thrombus

A

ACS

32
Q
  • Following plaque rupture, thrombotic factors from
    within the lipid core are exposed to the
    bloodstream
  • Activated platelets then adhere to the vessel wall
    when platelet glycoprotein binds to the von
    Willebrand factor
  • Tissue factor is also released from the lipid core,
    activating the coagulation cascade and leading to
    thrombin formation, the most potent platelet
    activator
  • Platelets stick to one another during the final
    common pathway of platelet activation, when
    platelets expose glycoprotein IIb/IIIa receptors that
    bind to fibrinogen
A

formation of thrombus

32
Q
  • Variable ECG findings, including
    having no abnormalities,
  • ST-segment depression,
  • T-wave inversions
  • Nonspecific ST-segment and T-
    wave changes
A

UA and NSTEMI

33
Q
  • Characterized by greater than 1-
    mm ST-segment elevation in two
    or more contiguous limb leads,
    or
  • Greater than 2-mm ST-segment
    elevation in two or more
    contiguous precordial leads
A

STEMI

34
Q

Diagnosis &
Evaluation:
Cardiac
Enzymes (labs for ACS)

A

cardiac panel:

  • Troponin T and I: highest sensitivity and specificity for detecting MI; appear within 4 hours; peak at
    24 to 48 hours and decline slowly; remain detectable for up to 7 to 10 days
  • Creatine phosphokinase myocardial band (CPK-MB): first measurable in the bloodstream at 6 to 10 hours; peaks at 24 hours; baseline by 48 to 72 hours
  • Lactate dehydrogenase: obsolete; increases at 24 to 48 hours and remains elevated for 10 days
  • Myoglobin: one of the earliest enzymes released in the circulation during MI (2 to 3 hours), returns to normal within 24 hours; very low specificity
35
Q

Unstable Angina
and Non–ST-
Segment
Elevation MI:
Risk stratification

A
  • As a rule, it is most appropriate to treat low-risk
    patients conservatively (i.e., noninvasive testing,
    medical management).
  • More aggressive treatment (e.g., catheterization,
    PCI) is the best choice for intermediate-risk and
    high-risk patients
36
Q

TIMI Risk Score (don’t memorize)
- know if high score = high mortality

A
  1. Age >65 years
  2. Three or more coronary artery risk factors
  3. Prior coronary stenosis ≥50%
  4. Two or more anginal events in past 24 hours
  5. Aspirin use in past 7 days
  6. ST-segment changes
  7. Positive cardiac markers
    TIMI risk score, predicts 14-day death, recurrent MI, and urgent revascularization rates
36
Q
  • Findings include abrupt, severe, “tearing” chest
    pain that radiates to the back or abdomen,
    unequal pulses and BP in the upper extremities, or
    a new murmur of aortic regurgitation
  • ECG can reveal ST-segment elevations if the
    dissection involves one or more of the coronary
    arteries (typically affects the right coronary artery
    first)
  • Thrombolytics and anticoagulants are
    contraindicated
A

aortic dissection

36
Q
  • Findings include chest pain that may be pleuritic or
    is relieved by sitting up; pericardial friction rub may
    be present
  • ECG may reveal diffuse ST-segment elevation and
    PR interval depression
  • Thrombolytics and anticoagulants are
    contraindicated
A

acute pericarditis

37
Q
  • Clinical clues include risk factors for PE (e.g.,sedentary or immobile patient status, history of deep venous thrombosis, leg trauma, or oral contraceptive use);
  • Symptoms include sudden-onset chest pain and dyspnea
  • ECG may show only sinus tachycardia, but classic findings include an S wave in lead I, Q wave in lead III, and T-wave inversion in lead III; can also present with new right bundle branch block or right axis deviation
A

pulmonary embolism

37
Q

anti angina Management of UA & NSTEMI: (pain)

A
  • Nitrates
  • B-Blockers
  • Morphine
38
Q

Management
of STEMI

A
  • Rapid recognition of a STEMI and immediate
    initiation of reperfusion therapy are crucial.
  • The faster normal flow can be restored in the
    occluded artery, the better the prognosis
38
Q

Anti clot anti angina Management of UA & NSTEMI: (save lives)

A
  • Anti-platelets*: aspirin
  • Anti-coagulants*: heparin
  • Statins
  • ACE-I/ARB if EF <40%
  • Percutaneous coronary
    intervention
39
Q

Management of STEMI:
Anti-angina:

A
  • Nitrates
  • B-Blockers
  • Morphine
40
Q

Management of STEMI: anti clot:

A
  • Anti-platelets
  • Anti-coagulants
  • Statins
  • ACE-I/ARB if EF <40%
  • Thrombolytic
  • Revascularization (PCI & CABG)
41
Q
  • Major advantages over thrombolytics:
  • Higher reperfusion rates (greater than 90% success
    rate of opening the occluded artery)
  • Decreased incidence of stroke
  • More effective than thrombolytics in patients with
    acute decompensated heart failure, cardiogenic
    shock, and prior bypass surgery
  • Major disadvantages:
  • Not available in all hospitals, and it may take too
    much time to get the patient to the appropriate
    facility
A

Management
of STEMI:
PCI

42
Q

preferred method of
treating STEMI

A
  • PPCI is the preferred method of
    treating STEMI
  • The goal time from first medical contact
    until PPCI is 90 minutes or less.
  • When the patient presents to a PCI-
    capable hospital or can be transferred
    from an index hospital to a PCI-capable
    center quickly (time from first medical
    contact to PPCI of ≤120 minutes)
43
Q

when is thrombolytic therapy most effective

A
  • Approximately 60% successful
  • Most effective when given in the first 6 hours, but
    can be given up to 12 hours after onset of chest
    pain
  • After 12 hours, the risk/benefit is unfavorable
    because the benefit decreases and the risk of
    myocardial rupture increases
44
Q

absolute contraindications of Management of STEMI: Thrombolytic
therapy

A

1.Any history of intracranial bleed
2.Known cerebral vascular lesion (e.g., AVM)
3.Known malignant intracranial
neoplasm
4.Ischemic stroke within 3 months
5.Suspected aortic dissection
6.Active bleeding or bleeding diathesis (excluding menses)
7.Closed-head or facial trauma within 3 months