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SMP - Cardiopulmonary Exam 1 > CC 6 - Atherosclerosis, Hypertension, and Million Hearts > Flashcards

CC 6 - Atherosclerosis, Hypertension, and Million Hearts Flashcards

1
Q

Definition of stenosis?

A

Luminal narrowing of the artery

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2
Q

What is another word for stenosis?

A

Lesion

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3
Q

What is a plaque?

A

Atherosclerotic deposition within the intima or adventitia of vessels

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4
Q

What does PCI stand for? What does it mean?

A

Percutaneous Coronary Intervention

Interventions to put in balloons and stents inside vessels

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5
Q

What does ACS stand for? Definition?

A

Acute Coronary Syndrome = any condition brought on by a sudden reduction or blockage of blood flow to the heart

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6
Q

What does STEMI stand for?

A

ST Elevation Myocardial Infarction

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7
Q

What does NSTEMI stand for?

A

Non-ST Elevation Myocardial Infarction

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8
Q

Is a lesion always visible on an angiogram?

A

NOPE, flow does not exclude the possibility of a narrowing present

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9
Q

What are the 3 types of ACS? What do we call type 2 and 3 together?

A
  1. STEMI
  2. NSTEMI
  3. Unstable angina

2 + 3 = Non-ST Elevation Acute Coronary Syndrome

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10
Q

What does PMH stand for?

A

Past Medical History

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11
Q

What does NSR stand for?

A

Normal Sinus Rhythm (on EKG)

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12
Q

At what point does atherosclerosis become symptomatic?

A

When plaque stenosis exceeds 70% of the vessel lumen

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13
Q

What fraction of all deaths in the US and Europe are due to vascular disease? What are these exactly due to?

A

Half of all deaths:

  • 2/3rds: atherosclerosis and thrombosis of the coronary arteries
  • 1/3rd: thrombosis and hemorrhage in other arteries (e.g. stroke)
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14
Q

What is the most common first symptom of coronary artery disease?

A

Unexpected myocardial infarction OR sudden death (first symptom for 50% of people)

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15
Q

How many people have a myocardial infarction each year?

A

1,450,000 (1 every 25 seconds)

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16
Q

How many people have a stroke each year?

A

800,000

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17
Q

What fraction of people die from CVD each year?

A

1 in 3

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18
Q

What are most acute coronary syndromes caused by?

A

Rupture of lesions less than 50% stenosed (2/3rds due to this)

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19
Q

Why has CVD incidence fallen over the years?

A
  1. Less tobacco
  2. Better BP control
  3. Better lipid control
  4. Other unknown factors
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20
Q

Where does the word atherosclerosis come from?

A

Greek:

  • Athero = gruel or porridge
  • Sclerosis = hardening
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21
Q

What is the definition of atherosclerosis?

A

Progressive pathological condition characterized by the accumulation of lipids, cells, and fibrous elements in the large arteries (but also smaller vessels)

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22
Q

What other diseases does atherosclerosis underlie?

A
  1. CAD
  2. Cerebrovascular disease
  3. Diseases of the aorta and peripheral arterial circulation
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23
Q

Why is the intima of the arterial wall so important?

A

If it is damaged it exposes a lot of tissue factors and pro-coagulable factors causing blood clots

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24
Q

Under basal conditions, in what state does the endothelium maintain the vessels?

A

Relatively dilated state

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25
Q

What happens during an exercise stress test?

A

During exercise the arteries to the skeletal muscles and to the heart should widen due to shear stress and metabolic regulation, so if someone has atherosclerosis as you increase the blood demand, the fixed stenosis will prevent adequate blood flow causing ischemia which will cause certain EKG patterns or specific results on other imaging tests

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26
Q

List the 5 normal characteristics of endothelial cells?

A
  1. Impermeable to large molecules
  2. Anti-inflammatory
  3. Resist leukocyte adhesion
  4. Promote vasodilation
  5. Resist thrombosis
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27
Q

How does atherosclerosis affect the normal characteristics of endothelial cells?

A
  1. Increased permeability
  2. Increased expression of inflammatory cytokines which allow cells flowing through the vessel to dock on the endothelial cell wall
  3. Increased leukocyte adhesion molecules, so do not resist their adhesion as well
  4. Decreases vasodilatory molecules so do not promote vasodilation as well
  5. Decreased antithrombotic molecules so do not resist thrombosis as well
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28
Q

How does atherosclerosis affect the smooth muscle cells of vessels?

A
  1. Increased inflammatory cytokines
  2. Increased extracellular matrix synthesis
  3. Increased migration and proliferation into subintima
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29
Q

Which cells of the blood vessels maintain the extracellular matrix?

A

Smooth muscle cells

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30
Q

Where does a lot of the endothelium dysfunction occur in the CV system with atherosclerosis? Why?

A

Regions of vessel bifurcation because of turbulent flow

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31
Q

What are 8 interventions that improve endothelium function in atherosclerotic patients?

A
  1. Smoking cessation
  2. HT control
  3. Cholesterol lowering/statin drugs
  4. Exercise
  5. ACE inhibitors
  6. Estrogen
  7. Antioxidants
  8. Reduction of inflammation
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32
Q

What is the earliest abnormality caused by atherosclerosis? Causes?

A

Damage to the vascular endothelium causing vascular endothelial dysfunction

Causes: smoking, HT, hyperlipidemia, diabetes, obesity, aging, lack of exercise…

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33
Q

Describe the progression of atherosclerosis.

A

Vascular endothelial dysfuntion => increased expression of adhesion molecules on the endothelial cells + decreased ability to release NO and other substances that prevent adhesion of macromolecules => monocytes and lipids accumulate at the site of injury => monocytes cross endothelium and enter the intima => monocytes differentiate into macrophages => macrophages ingest and oxidize the lipoproteins via scavenger receptors => macrophages have a foam-like appearance = foam cells forming a lipid core => foam cells aggregate on blood vessel and eventually pop leaving cholesterol crystal which cause fatty streaks => with time fatty streaks grow larger and attract macrophages by secreting chemo and cytokines which secrete substances that cause inflammation and cause the fibrous (collagen and elastin) and smooth muscle cells to proliferate to form fibrous plaques aka atheromas => vicious cycle leading to the development of vulnerable or stabilized plaques

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34
Q

What kind of lipids accumulate on a damaged endothelium?

A

LDLs = low density lipoproteins

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35
Q

When do LDLs get oxidized during atherosclerosis? What does this cause?

A

When it gets under the subendothelial matrix => macrophages and monocytes recognize them

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36
Q

At what age do macrophages start accumulating in the vessel walls?

A

Infancy

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37
Q

At what age do fatty streaks appear in the vessel walls?

A

During early adolescence (as early as 9 yo)

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38
Q

At what age do lesions appear in the vessel walls?

A

Around 20

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39
Q

What is an atheroma?

A

Accumulation of degenerative material in the tunica intima of artery walls consisting of macrophage cells containing lipids, calcium, and a variable amount of fibrous connective tissue

40
Q

Can you recover from an early atheroma?

A

Yes with therapy and better lifestyle it can undergo a healing process

41
Q

Describe the healing process of an atheroma.

A

Atheroma becomes a stabilized plaque with smooth muscle cell proliferation which has a thick fibrous cap and a small lipid core (unlikely to rupture) => lumen is preserved

42
Q

Describe the development of vulnerable plaques from atheromas. What happens to these plaques?

A

Atheromas can develop into vulnerable plaques, which are more likely to rupture as they have a large lipid core with a thin fibrous cap and increased inflammatory content => macrophages produce matrix metallo-proteinases (MMPs), which are enzymes that eat the excess fibrous tissue causing rupture => once they rupture, platelets adhere causing thrombosis, leading to either:

  1. Nonocclusive thrombus with unstable angina or non Q-wave MI (non STEMI) => healed ruptured plaque with a very narrow lumen and a very fibrous tunica intima => angina
  2. Occlusive thrombus with Q-wave acute myocardial infarction (STEMI), coronary death, stroke, or critical leg ischemia
43
Q

What is the Glagov phenomenon? What do we call this? What does this explain?

A

As atherosclerotic lesions develop within coronary arteries, the artery increases in diameter through outward growth of the vessel in the region of the atherosclerotic lesion to maintain the arterial lumen = positive remodeling

Explains why most acute coronary syndromes are caused by the rupture of lesions less than 50% stenosed

44
Q

What is the role of platelets in atherosclerosis?

A

The normal endothelium prevents their adherence, but when the damage of the endothelium exposes collagen which causes adhesion, activation, aggregation, and secretion of platelets => thrombotic/clotting process

45
Q

What do the platelets bind to on the endothelium? What chain reaction does this cause?

A

Von Willebrand factor binds platelet with glycoprotein Ib => platelet releases ADP, serotonin (causes vasospasms), and thromboxane => fibrinogen is cleaved to fibrin by glycoprotein IIb/IIIa which forms a mesh to trap more platelets => blood clot formation

46
Q

How do antioxidants help prevent the development of atherosclerosis?

A

They inhibit LDL oxidization in the subendothelium matrix

47
Q

What are the 9 genetic risk factors for atherosclerosis?

A
  1. Elevated LDL cholesterol
  2. Low HDL cholesterol
  3. Elevated lipoprotein a (Lp(a))
  4. Hypertension
  5. Elevated homocysteine
  6. Family history
  7. Diabetes, metabolic syndrome and obesity
  8. Elevated hemostatic factors
  9. Inflammation
48
Q

Discuss the issues with therapies targeted at decreasing HDL levels.

A

Drugs to lower LDL levels and raise HDL levels increased mortality

49
Q

What are the 4 environmental risk factors for atherosclerosis?

A
  1. Atherogenic diet
  2. Smoking
  3. Inactivity
  4. Infectious agents (?)
50
Q

What is a restenosis? When does it happen? Examples?

A

Reoccurance of stenosis in the arterial wall after injury leading to restricted blood flow

E.g. happens after percutaneous transluminal coronary angioplasty (PTCA)

51
Q

What is the 2 stage physiological response to damage to the blood vessel by angioplasty causing restenosis? When does each stage happen? Clinical manifestation for each? What do we call this if a stent has been placed?

A
  1. Stage 1 (immediately after tissue trauma): thrombus forms at the site of damage and further hinders flow, and is accompanied by an inflammatory immune response (in-stent thrombosis presents as MI)
  2. Stage 2 (3-6 months after procedure): neointimal hyperplasia due to the proliferation of smooth muscle cells in the intima AND patient returns with progressive symptoms or shortness of breath (in-stent restenosis presents as stable angina)
52
Q

Treatment for restenosis?

A
  1. PTCA (angioplasty) with stent (within the previous stent)

2. CABG (coronary artery bypass surgery)

53
Q

Why has the incidence of restenosis decreased?

A

Since the use of drug eluting stents

54
Q

Can an atheroma reform within a stent?

A

YUP

55
Q

Is the process of restenosis the same as atherosclerosis?

A

NOPE, completely different

56
Q

What is instent thrombosis?

A

Stent is placed in vessel => strut fails to be re-endothelialized => thrombus forms => thrombus propagates if anti-platelet therapy is inadequate => occlusion of the vessel

57
Q

Is the process of instent thrombosis the same as atherosclerosis?

A

NOPE, completely different

58
Q

What are some nutritional changes that can be done to reduce atherosclerosis development?

A

Cut sodium and trans fats

59
Q

What are the 2 types of HT? Describe each. Which is the most common?

A
  1. ***Primary = high blood pressure with no identifiable cause or origin
  2. Secondary = high blood pressure with an identifiable cause or origin
60
Q

2 other names for primary HT?

A

Essential HT = idiopathic HT

61
Q

Prehypertension: systolic and diastolic P?

A

120-139/80-89

62
Q

Stage 1 hypertension: systolic and diastolic P?

A

140-159/90-99

63
Q

Stage 2 hypertension: systolic and diastolic P?

A

160+/100+

64
Q

HT diagnosis?

A

2 measurements greater than 140/90

65
Q

Is having a high diastolic pressure worse than having a high systolic pressure?

A

NOPE

66
Q

What % of American adults have HT?

A

29%

67
Q

Describe HT incidence across genders and races.

A

Men: 43% of AAs and 31% of whites

Women: 46% of AAs and 31% of whites

68
Q

What % of HT patients have their BP under control?

A

50%

69
Q

Describe the pathogenesis of essential HT.

A

Not completely understood, but what we know:

  1. Increased SNS activity with enhanced beta-adrenergic responsiveness
  2. Increased angiotensin II and aldosterone activity
70
Q

Describe the genetic risk factor of essential HT.

A

HT twice as common in patients who have or more HT parents

71
Q

What are the 7 risk factors for HT?

A
  1. African American (more common and more severe)
  2. HT in parents
  3. Salt intake
  4. Excess alcohol intake
  5. Obesity
  6. Dyslipidemia
  7. Certain personality traits (hostile/impatient)
72
Q

Does BP vary during the day?

A

YUP!

73
Q

How high can systolic pressure be in athletes?

A

400 mmHg

74
Q

What are 10 causes of secondary HT?

A
  1. Primary renal disease — both acute and chronic renal disease, particularly with glomerular or vascular disorders
  2. Oral agents: oral contraceptives, chronic non-steroidal antiinflammatory agents, many antidepressants 3. Chronic alcohol intake and alcohol abuse
  3. Pheochromocytoma
  4. Primary hyperaldosteronism
  5. Renovascular disease (narrowing of the arteries of the kidneys)
  6. Cushing’s syndrome
  7. Other endocrine disorders — both hypothyroidism, hyperthyroidism, and hyperparathyroidism
  8. Sleep apnea (especially with patients with COPD)
  9. Coarctation of the aorta
75
Q

When is a hypertensive patient at risk of developing serious complications?

A

When BP rises above 110/75 mmHg

76
Q

What are complications of HT?

A
  1. CVD
  2. Heart failure
  3. LV hypertrophy
  4. Stroke
  5. Intracerebral hemorrhage
  6. Chronic kidney disease and end-stage renal disease
77
Q

What is the increase in CVD risk associated with HT importantly affected by?

A

Presence or absence of other risk factors

78
Q

What is the most common and most important risk factor for stroke and intracerebral hemorrhage?

A

HT

79
Q

What is LV hypertrophy associated with?

A
  1. Heart failure
  2. Ventricular arrhythmias
  3. Death following myocardial infarction
  4. Sudden cardiac death
80
Q

What are some ethnicity disparities with end stage renal disease?

A

AAs are 4 times more likely to have it and need dialysis than whites and are only 70% as likely to be referred for evaluation for transplant than whites

81
Q

LV hypertrophy risk in AAs compared to whites?

A

3 times more likely

82
Q

What is the goal of the Million Hearts initiative? Describe it.

A

National initiative co-led by CDC and CMS and supported by many other orgs.

Goal = prevent 1 million heart attacks and strokes in 5 years

83
Q

What is the greatest contributor to racial disparities in life expectancy in the US?

A

Heart disease and strokes

84
Q

How many strokes and heart attacks each year? How many die?

A

2 million +

800,000 die

85
Q

How much $ does heart disease and strokes cost each year?

A

$444 B in healthcare costs and lost productivity: $1 for every $6 spent

86
Q

What is the leading cause of preventable death in people above the age of 65?

A

Heart disease and strokes

87
Q

What are the key components of Million Hearts?

A
  1. Clinical prevention to optimize care

2. Community prevention

88
Q

What are the ABCS?

A

Main routine prevention aspects for CVD:

  1. Aspirin
  2. BP
  3. Cholesterol
  4. Smoking
89
Q

What % of people at increased risk for CVD are taking aspirin?

A

46%

90
Q

What % of people with HT have adequately controlled BP?

A

46%

91
Q

What % of people with high cholesterol are effectively managed?

A

33%

92
Q

What % of people who try to quit smoking get help?

A

23%

93
Q

What % of Americans exceed the recommended sodium intake?

A

90%

94
Q

What is an unstable angina?

A

Condition in which your heart doesn’t get enough blood flow and oxygen leading to chest pain

95
Q

How can you prevent first stage from happening after damage to blood vessels by angioplasty?

A

Anti-platelet therapy

96
Q

How many deaths due to CVD per 100,000 patient years?

A

250

97
Q

What drives the progression of a plaque from stable to vulnerable in early atheroma?

A

The plaque ratio of macrophages (aka the more macrophages, the more unstable)

SMP - Cardiopulmonary Exam 1 (28 decks)

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