Ischemic Heart Disease - Gibson

Front 1

What is the definition of ischemic heart disease?

Back 1

-imbalance between supply and demand of the heart for oxygen

*the MC type of heart disease in US

Front 2

What are the 3 causes of ischemic heart disease?

Back 2

1. Decrease in blood supply to myocardium
2. Decreased delivery and availability
3. Increased demand for oxygen

Front 3

What are 5 examples of decrease in blood supply to the myocardium?

Back 3

1. Arthrosclerosis (MC, >90%)
2. Coronary thrombosis
3. Coronary artery spasm
4. Coronary endarteritis
5. Shock w/ hypotensin

Front 4

What are 4 examples of decreased delivery and availability?

Back 4

1. Anemia (esp IDA)
2. Hypoxia in advance lung disease
3. CO poisoning
4. Cyanid poisoning

Front 5

What are 5 examples of increased demand for O2 in ischemic heart disease?

Back 5

1. Hypertension w/ valvular stenosis or insufficiency
2. Hyperthyroidism
3. Fever
4. Thiamine deficiency
5. Catecholamines

Front 6

Risk Factors (RF) of arthrosclerosis:

Back 6

1. Hypertension
2. Hyperlipidemia
3. Diabetes mellitus
4. Cigarettes (w/in last 5 yrs)
5. Family hx
6. Age, M>45, F>55
7. Metabolic syndrome

Front 7

What is important to note for MI pts?

Back 7

-about half do NOT have classic risk factors for CAD

Front 8

How is hyperlipidemia a RF of arthrosclerosis?

Back 8

-is directly related to high level LDL and inversely related to HDL levels

Front 9

Non-lipid factors in atherogenesis:

Hyper-homocysteinemia

Back 9

-AA of methionine metab
-toxic to endo cells INCREASING LDL OXIDATION
-inhibs anticoag of endos and promotes aggregation of platelets
-nutritional deficiencies, genetics, and homocysinuria

Front 10

Non-lipid factors in atherogenesis:

Lipoprotein associated phospholipase A2 (Lp-PLA2)

Back 10

-enzyme produced by inflamm cells and a/w LDL
-acts after oxidation of LDL to produce substance that contribute significantly to the inflamm process involved in atherosclerosis

Front 11

Non-lipid factors in atherogenesis:

CRP

Back 11

-acute phase reactant from liver in response to inflam cytokines
-***increased levels of plasma CRP, therefore may serve as a marker for atherosclerotic progression

Front 12

Non-lipid factors in atherogenesis:

Fibrinogen

Back 12

-also an acute phase reactant
-evidence suggests that inc levels of fibrinogen are strong independent predictor of future CV events in asymptomatic pts

Front 13

Non-lipid factors in atherogenesis:

Infection****

Back 13

-chlamydia pneumoniae may survive in macrophages and potentially could upregulate the production of inflam mediators w/in the plaque
-poss connection between infx and infarction

Front 14

What is the definition of CAD?

Back 14

-any vascular disorder that narrows or occludes a coronary artery

Front 15

What are the first 4 steps in the sequence of events of a MI?

Back 15

1. narrowing of coronary artery
2. decrease blood flow to myocardium
3. imbalance btwn metabolic needs and supply
4. Persistent ischemia --> hypoxia

Front 16

What are the last 4 steps in the sequence of events of a MI?

Back 16

5. Hypoxia determines anaerobic glycolysis
6. Lactic acid production
7. If blood flow returns, myocytes suffer reversible damage
8. if not, myoctyes may have suffered irreversible damage

Front 17

***Endothelial Cell (EC) injury and atherosclerosis

Back 17

-this is the most accepted explanation that atherosclerosis is a chronic inflammatory response of the arterial wall to EC injury

Front 18

What are the major factors of endothelial injury?

Back 18

-hyperlipidemia and hemodynamic disturbances***

Front 19

What is the hallmark lesion of arthrosclerosis?

Back 19

-fibro-fatty atheroma which is produced by the activation and interaction of ECs, SMCs, and lymphocytes which produce SMC prolif, collagen and other extracellular material

Front 20

What is the overall steps in the pathology of inflammation in arthrosclerosis?

Back 20

1. Chronic Endothelial injury
2. Endothelial dysfunction leading to increased permeability to lipids
3. Macrophages ingest intimal lipid accumulation become foam cells
4. Fatty streak formation
5. Conversion to fibro-fatty atheroma

Front 21

****What happens when the endothelium is damaged?

Back 21

-no longer serves as a barrier and LDL cholesterol passes into the subintima, accumulates and is modified (oxidized) by free radicals
-Cytokines/chemokines attract monocytes and T lymphos--> macros

Front 22

***When monocytes become macrophages at the subendothelial space what happens next?

Back 22

-macros ingest intimal lipid accumulation --> Foam cells
-Foam cells secrete PDGF, IL-1, TGF, TNF which activate SM cells to migrate and proliferate
-SMCs emigrate from the media to the intima

Front 23

In the conversion from a fatty acid streak to fibro fatty Atheroma what is happening?

Back 23

SMCs engulf lipids too --> more foam cells-->eventually erupt
-SMCs secrete collagen, elastin, and proteoglycans
-Foam cells also release tissue factor which is highly thrombogenic
-CT covers lipid debris and engenders fibrosis

Front 24

***How does the mature fibro-fatty atheroma appear?

Back 24

-a core of lipid and lipid debris surrounded by SMC and collagen
-the prominent CT formation intruding on the intimal surface is the fibrous cap
-atheroma causes vessel lumen narrowing with ischemia

Front 25

Angina Pectoris

Back 25

-chest discomfort or pain that occurs in recurrent episodes

Front 26

What is Stable Angina?

Back 26

-by chronic coronary obstruct
1. gradual narrow/harden of vessels --> cannot dilate, for inc demand
2. PREDICTABLE
3. 3-5 minutes and relieved by rest
4. plaque is stable w/ fibrous cap
5. also rapid heart beat, gallops

Front 27

What is unstable angina?

Back 27

-severe pain w/ longer duration than stable angina
1. attacks occur at risk
2. Serious predictor of progression to ischemic heart disease

Front 28

What is Variant (Prinzmetal) angina?

Back 28

-uncommon pattern of angina
1. can occur at rest adn is due to CA spasm w/ or w/out CAD
2. a/w use of certain drugs, emotional stress, exposure to severe cold and cigarettes

Front 29

What is MI?

Back 29

-necrosis of myocardial cells resulting from ischemia
-can result from vasospasm, obstruction of narrowed lumen by emoblus, and MC it involves an acute change in an unstable plaque

Front 30

What is an acute plaque change?

Back 30

-atherosclerotic plaque that is rich in lip
-a/w inflam and w/ a thin fibrous cap
-unstable and vulnerable to acute rupture and thrombus formation that leads to coronary flow obstruct

Front 31

What is a vulnerable plaque?***

Back 31

-thin, friable fibrous cap separating substantial thrombogenic lipid core from blood
-lumen could be well preserved (more inflam cells involved)

Front 32

What is a "Stable" plaque?

Back 32

-not as many, not as likely to sever off as an emboli
-same risk of factors for MI as arthrosclerosis
-leading cause of death in US

Front 33

***What is the breakdown of time for necrosis of myocardium?

Back 33

1. 18-24 hrs = infarction are is pale and cyanotic
2. 24 hrs - 3 days = the affected area is pale w/ dark molting
3. 3-7 days = yellow/brown color (MYOMAYLACIA)
4. 6 weeks = fibrous scar formed

Front 34

***What is the breakdown of time for microscopic changes during an MI?

Back 34

1. 1-12 hrs - vascular degen
2. 12-72 hrs - coag necrosis w/ PMNs
3. 3-7 days - dead cells removed
4. 7-10 days - granulation tissue --> becomes a scar

Front 35

What are the 3 types of infarct patterns?

Back 35

1. Transmural - complete persistent obstruct of CA
2. Regional subendocardial - re-estab of blood flow after obstruction
3. Circumferential subendocardial

Front 36

What are the surgical treatments for MI?***

Back 36

1. Angioplasty - mechanical opening of vessels
2. Revascularization - bypass -CABG
-vascular replacement and/or shunt around occluded vessels

Front 37

What are diagnostic techniques for MI?***

Back 37

1. Abnormal ECG
2. Serum markers
a) Inc in plasma enzymes (creatine kinase - elevated but not specific, MB fraction)
b. Cardiac specific troponins
c. leukocytes
d. possible increase in blood sugar

Front 38

What is the arterial side of the vascular tree called vs the venous side?

Back 38

-high-pressure system
-low pressure system

Front 39

What are the 3 components of a normal artery?

Back 39

1. Intima
2. Media (SMC and elastic tissue)
3. adventitia (loose CT, and sometimes vasa vasorum

Front 40

Large elastic arteries?

Back 40

-sustain large surges in pulse P and using the stored kinetic energy of systole rebound during diastole

Front 41

Medium muscular arteries>

Back 41

-to various organs
-muscular arteries easily maintain blood flow by contraction and dilation

Front 42

Arterioles

Back 42

-primary determinants of the systemic blood pressure

Front 43

Types of Arteries and Associated diseases:

Large/Elastic

Back 43

-Aorta
-made of elastin/SMCs
-Atherosclerosis

Front 44

Types of Arteries and Associated diseases:

Medium/Muscular

Back 44

-Coronaries, Renal
-made of SMCs, little elastin
-Atherosclerosis and arteriosclerosis

Front 45

Types of Arteries and Associated diseases:

Small/Arterioles

Back 45

-Parenchymal
-SMCs
-Hypertension