Chapter 13 Flashcards

1
Q

T or F CAD is the second largest cause of death in adults

A

False, its the first, and is the most common cause of premature deaths in adults before the age of 65.

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2
Q

what are the 4 major determinants of prognosis in patients with CAD?

A
  1. coronary obstruction- # of vessels and severity of obstruction.
  2. L ventricular function- ability to pump blood over body
  3. presence of ischemia - frequency and severity of episodes
  4. risk factor analysis - age, gender, clinical hx (labs, co-morbids),
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3
Q

Define the Left Main coronary artery (LMCA) system

A
  1. uppoer portion of L aortic sinus, and passes behind R V outflow.
    - contaisn Left circumflex arter (LCx) at right andles and con’t into LAD.
    - Most important system
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4
Q

What is the purpose of the LAD?

A

artery supplies the anterior and septal walls of the L V, passing down the anterior interventrical groove toward the cardiac apex.
- LAD + branches are usually considered most important system after LMCA

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5
Q

What is the purpose for the L circumflex artery?

A

travels the AV groove, and responsible for blood suply to the Lateral ventricular wall.

  • can terminate in one or more large obtuse marginal (OM) branches, or can continue as a large artery in the AV groove.
  • in 10-15% of cases it gives rise to the posterior descending artery, which provides circulation to the inferior and posterior walls of the LV.
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6
Q

Define the Right coronary artery (RCA)

A

located in R sinus of Valsalva. and courses upways from plane of the Aortic Valve and travels in the R AV goove to reach posterior LV wall.
- 85% of cases, posterior descending artery arises from RCA before it reaches the ‘crus’ of the heart.
After ficing rise to posterior descending artery, the RCA becomes intramuocardial at the crux and gives rise to the AV node artery.

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7
Q

what is the crux?

A

junction of the interatrial and interventricular septa.

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8
Q

Which parts of the coronary circualtion are visualized via angiography?

A

major branches and their second, third, and perhaps fourth order brances.

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9
Q

The term “dominance” often is used to describe what?

A
the anatomic configuration of the blood supply to the posterior descending artery. 
R dominance (posterior descending artery emerging from RCA) occurs in 85% of cases
L domiance( LCx provides the posterior descending circulation) 15% of cases.
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10
Q

What are the 3 layers of teh coronary arterial wall?

A
  1. intima - inner layer connecting with blood.
  2. media- smooth muscle cells and connective tissues responsible for the vasodilatory properties
  3. adventitia. - outer layer made of up fibroelastic tissues without smooth muscle cells. it houses nutrient vessels of the vascular wall and never fibers. gives vascular wall stability by connecting the artery to its surrounding tissues.
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11
Q

What is the lumen?

A

the open space thorugh which blood flows between cell layers.

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12
Q

What is the most important structure in the itima layer of teh coronary artery?

A

endothelium- its a layer of endothelial cells lining the whole vascular wall. it protects agaisnt atherosclerosis and acts as a selective barrier to prevent plasma lipid ACCUMULATION within the vessel wall. It also has been shown to prevent blood clot formation and arterial spasm.

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13
Q

Astherosclerosis affects mainly the medium-sized coronary arteries on the epicardial (outer) surface of the heart. There are several types of lesions, please name 3.

A
  1. initial lesion- fatty streak- yellow slightly raised lesions that are accumulations of lipidladen cells (foam cells)
  2. more advanced lesions- atheroma- rounded raise lesions whiter, that cause some degree of vascular lumen narrowing. compossed of fibrotic cap and a cretotic core containing cellular debris, lipids, cholesterol crystals, calcific deposits and blood-borne material.
  3. lesion associated with coronary events- complicated plaque, ruptures or dissured plaques arose from the thin fibrotic cap or d/t fissure from subsequent exposure of teh interval contituents of teh atherosclerotic plaue into the flowing blood. They have high thrombogenic properties
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14
Q

In spontaneous atherosclerosis, what is the tenet cause of endothelial injury?

A

result of disturbance of the pattern of blood flow in certain parts of the coronary arterial tree.

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15
Q

What are typical CAD risk factors?

A

HTN, hypercholesterolemia as well as circulating vasoactive amines, immune complexes, infection, chemical irritants in tobacco smoke, and potentiate chronic endothelial injury.,

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16
Q

There are 3 types of vascular injuries. Describe them

A
  1. early form of injury. causes functional alteration of endothelial cells without morphological changes. leads to increase permeability to plasma lipids and monocutes, and change in EDFR reponse to stimuli.
  2. more sever injury with endothelial denudation and intima injury caused by release of toxic products by macrophages. Macrophages+platelets+endothelium causes release of various growth factrs which leads to simultaneous migration and proliferation of smooth muscle cells, forming fibrous capsuls over lipid ledions.
    type 3- accelerated version of atherosclerotic process appears to account for premature CAD in those undergoing heart surgery. Its usually critical initiating event.
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17
Q

T or F: fissuring or rupture of complicated atherosclerotic plaque with subsequent occlusive thrombi plays a fundamental role in developement of the acute ischemic syndromes?

A

yes,

plaque distributiom, thrombosis and scarring can be also important in the progression of atherosclerosis in Asxs individuals or those with stable angina.

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18
Q

What are some current approaches to stabilizing or retarding the progression of atherosclesosis, or even causing its regression?

A
  1. reducing risk factors such as lipid levels.
  2. use of antithrombotic therapy- since thrombus formation is an important factor in the initiation of an acute cardiac event and progression of the disease.
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19
Q

Define Myocardial ischemia

A

occurs when myocardial O2 supply cannot meet the myocardial oxygen demand in a region of the ventricle.

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20
Q

Define Myocardial infarction

A

It is the irreversible myocardial cell injury and death that occurs following prolonged ischemia.

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21
Q

When does muscle necrosis occur?

A

when an ischemic episode is prolonged beyond 30-40 mins.

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22
Q

Coronary artery size is controlled by a number of factors that influence coronary artery smooth muscle activation. What are they (3)?

A
  1. neural regulation
  2. locally-produced chemicals, such as adenosine.
  3. endothelium-derivered relaxing factors (EDRF) such as nitrous oxide and the prostaglandins.
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23
Q

What does the EDRF do for the coronary blood flow?

A

optimizes it in response to a variety of stimuli and also exerts potent anti-aggregant effects on platelets at the release site.

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24
Q

What controls Myocardial oxygen demand?

A
  1. heart rate
  2. contractility of the myocardium
  3. LV wall tension.
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25
Q

What happens when a epicardial coronary artery is briefly occluded?

A
  1. there is a change in myocardial metabolism (detected by PET scannig) > changes in myocardial function
  2. diastolic dysfunction appears > systolic dysfunction with contractile disturbances. - detected by radionuclide or MUGA scan or cardiac catherization. At the same time, reversible regional myocardial perfusion defects appear, detectable with radionuclide imaging.
  3. relatively late in the myocardial ischemia stages, EKG abN and CP appears.
  • these findings are potentially reversible with restoration of blood flow.
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26
Q

What happens after prolonged disruptions in the myocardial supply and demand balance,?

A

potential to result in myocardial injury and cell death (MI- infarctions).

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27
Q

T or F: hybernation myocardium can persist for months without cell death.

A

True

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28
Q

Define an exercise stress test

A
  1. most frequently performed test for dx and assessment of CAD.
  2. done with treadmill usuing standardized protocols, where the pt starts with low workloads and increases to high ones, wth BP, and pulse monitored through an EKG.
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29
Q

What are the EKG signs of myocardial ischemia?

What are the important stress testing parameters?

A
horizonal or ST segment depressions or >1mm. 0.08 seconds after the J point. 
---------------
exercise duration
ST segment changes with exercise
blood pressure reponse 
sxs with exercise
EF, with resting and exercise
Thallium/ SPECT defects
ECHO wall motion abN
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30
Q

What are some possible reasons for a false positive stress test?

A
  1. Electrolyte disturbances
  2. digoxin therapy
  3. ventricular hypertrophy
  4. mitral valve prolapse
  5. conduction abnormalities
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31
Q

What has been done to improve the dx accuracy of stress tests?

A

use of supplementary radionuclide and ECHO/Doppler imaging during test.

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32
Q

what is the most widely applied radionuclide for myocardial perfusion imaging?

A

thallium.

its related to regional blood flow and myocardial viability.
reversible defects on thallium scans generally reflect ischemic myocardium, whereas non-reversible defects often indicate scarring from previous MI.

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33
Q

Which exercise tests have the highest sensistivity and the highest specificity. Order them in best to worse

A

sensitivity:
SPECT> exercise ECHO> exercise EKG
specificity
exercise ECHO > exercise EKG > SPECT

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34
Q

ECHO/doppler studies or gated-blood pool scanning using radioisotopes as contrast agents can be done during exercise and compared with resting studies. What would you see if myocardial ischemia is detected?

A
  1. decrease in LV EF during exercise

2. development of regional wall motion abnormalities not present at rest.

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35
Q

Define the PET test

A

very accurate test for identifing how much the heart has been damaged by infarction and how much is still viable.

  • tracer is injected then detection then radiactive decay is measured by use of a scanner./
  • high resolution and detaiol.
  • limited ability and $$
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36
Q

Define how a CAT scan is used for cardiac diagnosis

A

rapid CT systems low for less blurry images then regular Ct scans of the heart. 64 slices per second. This results in two important cardiac testing modalities- the Coronary calcium scan and the CT angiogram

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37
Q

When is an ultrafast CT scanner, also known as EBCT used?

A

they take xray images so quiclkly they can freeze the motion of the heart and snap pics between beats with no blurriness.
pics in a 1/10 of a secon.

EBCT - can detect very early signs of atherosclerosis by detecting flkes of Ca in coronary arteries- which are though to be associated with plaque.

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38
Q

How is a CT angiogram used in the study of CAD

A

rapid sequence imaging which reveals coronary artery anatomy non-invasively.

  • can detect small non-obstructive atherosclerotic plaque as well as flow-limiting larger stenotic coronary lesions.
  • dense Ca particles in aterial walls reduce image quality and there is high radiation exposure
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39
Q

How are MRI’s used in the study of CAD?

A
  • produces cross-sectional images of anatomy by placing individuals in a stong magnetic field and bombarding them with radio wave
  • allows for heart and large vessel visualization; good for Aortic aneurysm, lesions in aorta, congenital heart abN, chest tumors, pericardial disease and myocardial scar.
40
Q

How are Coronary angiographies used in the study of CAD?

A

its the technique in which a specialised catheter is passed into the coronary artery and radiographic contrast material is injected into the artery while a special x-ray or video is take.
This identifies the presence, site, extent and severity of coronary obstruction.
this is done to assess the severity of coronary stensosi.

41
Q

How is the severity of coronary stenosis measured?

A

recorded as a reduction in the lumen diameter expresed as a percentage. Anything greater than a 50-70% reduction in diameter is a lesion that can produce ischemia.

42
Q

A complete cardiac catherization study usually includes ventriculography with injection of contrast medium directly into the L ventricle. Why is this done?

A

to assess LV size and function, the presence and degree of regional wall motion abnormalities and the presence and severity of MR.

This used to be the gold standard but has been supplanted by newer radionuclide and echo/doppler techniques.

43
Q

The location of an obstruciton will be described in a relation to the origin of that coronary artery. What does this mean?

A

proximal lesion = stenosis is close to the origine of the artery
mid lesions= further along, after significant branching has occured.
distal lesions = occur near the terminal portions of the imaged artery.

44
Q

What does “myocardium at risk” mean?

A

the prognosis in CAD that is directly related to the amount of damage that could occur., should a coronary lesion undergo sudden and total occlusion.
it is based on a scoring system

45
Q

What is the myocardium at risk scoring system

A
  1. prognosis is related to the number of coronary arteries with sig stenosis.
  2. leisons in Left main artery are worse
  3. proximal lesions = ^ risk than mid or distal lesions
  4. LAD lesions = larger risk,
  5. LCx and RCA stenoses depends on the dominance fo the system as well as severity and location.
46
Q

Define the sxs of patient with stable angina pectoris

A

CP with effort, exercise or during situation where myocardial O2 demand is increased
- occurs in prediactable manner and is relived by rest or sublingual nitroglycering.

47
Q

The severity of stable angina is classified according to the degree of physical activity required to bring on chest discomfort.

A
  1. no angina with ordinary physcial acitvity.
  2. angina with walking more than 2 blocks or 1 flight of stairs at normal pase.
  3. angina working 1-2 blocks on normal level at normal pacce
  4. inability to perform any physical activity without angina
48
Q

What is revascularization therapy ?

A

coronary angioplasty or bypass grafting.

this offers high probably for relief or improvement of sxs.

can also increase survival rate in those with anatomical factors such as L main stensosi or 3-vessel CAD with reduced ventricular functionFJ <35%.

49
Q

Define Variant Angina Pectoris (Prinzmetal’s Angina)

A

unusual syndrome of cardiac pain that occurs almost exclusively at rest, usually not precipitated by physical exertion or emotional stress and is associated with ECG ST segment elevation. It;’s associated with

  1. acute MI
  2. severe cardiac arrhythmias,
  3. sudden death
50
Q

What causes variant angina pectoris?

A

d/t coronary artery spasms. which is a transient, abrupt, marked reduction in the diameter of an epicardial coronary artery resulting in myocardial ischemia. This can be reverse with nitro and can occur in normal and diseased arteries.
- sxs of angina at rest.

51
Q

How is variant angina pectoris diagnosed?

A
  1. sxs of angina at rest
  2. dx’ed in the development of ST segment elevations with pain.

2/3 of people have severe proximal coronary atherosclerosis of at least on mahor vessel, and spasm usually occurs 1cm from the obstruction. The remaining have normal coronaries.

52
Q

What is Cardiac Syndrome X?

A

a syndrome of angina or like CP wiht a normal coronary angiogram.

  • survival here is usually excellent.
  • cause of syndrome unknown. Several studies have demonstrated and abN reduce capacity to increase coronary flow in response to increased Myocardinal oxygen demand. This affects the small resistance vessels, while the larger vessels appear normal.
53
Q

Define silent myocardial ischemia

A

episodes of asymptomatic ischemia with objective evidence of coronary insufficiency provided by exercise testing or holter monitoring.
- usually occur at low acitvity and HR, suggesting that changes in myocardial O2 supply and demand might be responsible for these Asxs changes.

54
Q

Silent myocardial ischemia is classified into 3 categories. Define them

A
  1. type 1- occurs in pt who are well and Asxs. Detection usually by EKG. mortality risk ^ 200-500% depending on other CAD factors
  2. type 2- pt who are Asxs after a proven acute MI. it is the presence of ischemia, rather then the presence or absence of sxs that is prognostically important.
  3. type 3- seen in pt with angina in whom episodes of both sxs and silent ischemia are detected.
55
Q

What is non-ST elevation syndrome in relation to acute coronary syndrome?

A

pt classified as having unstable agina without infarction as well as those with non-0Q wave infarctions

56
Q

What is ST elevation syndrome in ration to acute coronary syndrome?

A

classic EKG pattern for acute myocardial infarctions. Infarct Q waves on EKG can develop during or after the acute event.

57
Q

The early classification used for unstbale angina was based on a description of the symptoms and was included into what 3 sub groups? How has the descriptive classification changed now?

A
  1. new onset angina in person previously sxs-free
  2. cresendo angina and pain at rest occuring in someone with known stable angina
  3. acute coronary insufficiency, with episodes of CP at rest, 15 or more in duration, no related to any prevous precipitating factors.

now: has been extended to include the clinical background for its presentation, ie unstable angina after MR, post-bypass or post-angioplasty. This can cause a change in the tx.

58
Q

T or F:

Most individuals with unstable angina have multivessel CAD, and thrombi are commonly seen as a results

A

T.

59
Q

What happens to individuals suspected of unstable angina?

A

placed at rest.
Acute MI is ruled out by serial enzyme and EKG studies.
nitrates are used for the treatment. Ca channel and betta blockers have been shown to reduce ischemic episodes.
aspirin and heparin help reduce complications.
once sxs are controlled coronary angiography is usually perfomed.

60
Q

More than 50% of the deaths associated with MI occur when

A

within one hour of the event and are attributable to arrhythmias- Ventricular fibrillation.

61
Q

How is MI diagnosed?

A

clinical presentation characterized by proloonged and severe CP.
note 25-30% of MIs are probably silent or unrecognbized. I
laboratory findings:
1. ECG or serum enzyme evidence (CPK and MB) as well as myoglobin and cardiac-specific troponins (T and I)

62
Q

What is the most sensitive and specific biomarker?

A

Troponins,
note they are not detected in the peripheral circulation under normal circumsatances, thus even minor elevations are though to indicate myocardial necrosis.

63
Q

What can imaging with Tc99m-labeled pyrophosphate show?

A

it localizes the injured region and provides a window of detection for myocardial damage that extends to approx 7 days.

64
Q

How can stress thalium scanning and MRI scan assist in the confirmation of an MI dx in selective individuals when ECG and enzyme studies are clear

A

non-reversble perfusion detects cold spots on stress thallium scanning as well as “delayed enhancement” on MRIs

65
Q

What are the EKG changes for those with hx of ischemia, injury and cellular death?

A

T wave changes, ST segment elevation and appearance of T waves (respectively)

66
Q

How can the sensitivity of an EKG be increased?

A

with the use of serial tracings. (95% sensitive)

67
Q

A definite dx of old MI on EKG depends on what?

A

presence of pathological Q waves. The specitivity of abN Q waves for MI is high, but sensitivity is slow.
there are two kinds Q wave infarctions (replaced term transmural) and non-Q wave (replaced subendocardinal term)

68
Q

T or F: Compared with individuals with Q wave infarction, those who have a non-Q wave infarctions appear to have a larger infarction size and a increased early mortality.

A

F. they have small infarction size and a reduced early mortalitiy, however they appear to be at higher risk for reinfarction, continuing angina, and perhaps death later.

Those with Q-waces have high risk of coronary thrombus at early angiography compared to non-Q wave.

69
Q

How is MI treated?

A

administration of thrombolyctic agents, and coronary angiography/other surgery

70
Q

How is the Reperfusion of the infarct-related artery performed?

A

catheter-based strategy.

71
Q

How is an (percutaneous coronary inversion) PCI preformed?

A

includes angioplasty and stent insertion.

  • used in tx of those with acute ST elevation MI
  • if administered promptly it is superior to thrombolytic therapy
72
Q

Within the post-MI population, up to 1/3 of individuals have coronary anatomy. How is this treated?

A

coronary artery bypass graft surgery improves prognosis.

73
Q

how is post-Mi risk assessed?

A
clinical findings (Age, previous MI, presence of Heart failure and ventricular arrhythmias) and non invasive studies.
There is also review of LV function, those with EJ >50% have greater pronosis.
74
Q

How are high risk post-MI groups associated?

A

low exercise capacity,
failure to have systolic BP rise,
ischemic ST segment depression at low workload,

*with or without angina.

75
Q

What is Sudden Cardiac death (SCD)

A
  • major cause of death in those with CAD
  • defined as death from cardiac disease within one hour of the onset of sxs in someone who was no expected to die.
  • usually d/t arrhythmias occuring in presence of chornic coronary or structural heart disease.
76
Q

Fatal arrhythmia events are complex but usually include a triggering acute event superimposed on an arrhythmogenic substrate. What is the anatomic substrate for SCD?

A

frequently a chornically abN myocardium harboring various degrees of fibrosis.
- usualy caused by CAD, but other triggers include acute MI, hemodynamic factors, electrolyte abnormalities, automonic influences and drug interactions.

77
Q

What the the most common arrhythmias that cause SDC?

A

ventricular tachycardia and fibrillation.

78
Q

management of survivors of an SCD episode includes an evaluation of what 3 systems?

A
  1. coronary anatomy by angiography
  2. LV function
  3. electrophysiologic testing (EPS)
79
Q

all acute ischemia and electrolyte abnormalities need to be addressed to remove the arrhythmogenic substrate. When no effective medical regimen is identified- what tx are used?

A
  1. radiofrequency ablation
  2. surgical suppression of the arrhythmia
  3. implantation of an automatic internal cardiac defib (AICD).
80
Q

Medical therapy for angina pectoris includes nitrates, beta-blockers, and calcium channel clockers. Describe their use and dosing schedules.

A

nitrates: most useful, can be taken oraly, subligually, topically and intraveniously. Good for acute angina relief and can be used to prevent ischemic pain.
2. beta-blockers: initial therapy for stable angina, d/t low cost and cardioprotective properties. usually well trolerated and effective at reducing angina frequency.
3. Ca+ channel blockers: good for chronic tx of stable angina pectoris, they’re also useful in vasospastic angina nd angina suspected pt. oral and IV fortm in short or fast-acting.

** combination therapy is used to enhance the effects or minimized the side effects.

81
Q

T or F, therapy with anticoagulants has been shown to have a role in the treatment of stable angina pectoris

A

False,

however aspirin, when used as an antiplatelet agen, can reduce teh risk of possible MI and SCD in stable angina patients.

82
Q

Define Percutaneous transluminal coronary angiopolasty (PTCA)

A

alternative method to tx CAD
ballon-tipped catheter is inserted percutaneously into teh coronary circulation, its then inflated at high pressure at the site of stenosis to fracture the plaque..
- limitation related to significant restenosis rate and need for repeat revascularization precursors.

83
Q

Define coronary stenting

A

devices with metal structural suports infused with anti-coagulant medication that are inserted at sites of atherosclerosis narrowing. once in place it provides structural suypport and improved arterial flow.
- better than the ballon PTCA method.

84
Q

Define IMA (internal mammary artery) bypass graft

A

a superior conduit to CABG.

85
Q

When would CABG more likely be used?

A

in those with angina pectoris unrelieved by medical therapy and are not ameanable to PTCA.

where Left main artery has a stenosis of >50% failed PTCA, and tripple vessel coronary disease, specially when large amounts of myocardium is at risk.

individuals with single-vessel CAD can be CABG candidates ie those with very proximal LAD lesion beofre the first septal perforator, just beyond main L artery, not ameanable to PTCA.

86
Q

Define the difference between PTCA and CABG treatments

A

successful PTCA is less traumatic, less costly, and requires shorter hospital stays. BUT PTCA of multiple- vessels can cause incomplete revascularization.

the degree of LV dysfunction is the factor to predict preoperative and long-term mortality.

CABG prolongs survival but does not CURE CAD, its good for those with unstable angina. Requires a longer assessment- not good for early phases of acute MI. Q

87
Q

What are some risk factors to CAD that are unique to females?

A

hormone use, and menopausal satus.

MI risk increased in post-menopausal women and those with hysterectomies with removal of ovaries.

88
Q

Is there an increased atherogenic risk in females taking oral contreceptoves?

A

yes, slightly but is only clinically significant in those who smoke or have known thrombotic disesae

89
Q

Is the stress testing for CAD associated with a lower sensitivity and specificity in males or females?

A

females, but when age, sxs and EKG status of individuals have been properly classified, the predictive value stress testing compares favourable with both sexes.

90
Q

After a succesfull angioplasty, do F have similar symptomatic improvement, decreased requirement for additional revascularization/restenosis and similar survival rates as males?

How about for coronary artery bypass surgery?

A

yes

No- its less sucessfull when related to operative mortality and graft closure and angina sxs post-operatively.

91
Q

How does aging affect cardiac structure and function

A

there is an increase aterial amd myocardial stiffness,
increased fibrosis and cell loss with cardiac condution system
there is thickening and calcification of cardiac valves and a reduction in the maximal HR.

92
Q

T or False, the elderly with non-coronary atherosclesis (cerebrovascular diease, peripheral vascular disease, and abdominal aneurysms) are more likely to have CAD

A

Yes,

whether or not its clinically apparent.

93
Q

How can review of BP help dx CAD in elderly?

A

both systolic and diastolic HTN are formidable risk factors for stroke and CAD, and tx can be effective in reducing risk. Pulse pressure also increases risk. (related to arterial shear stress)

94
Q

Does PTCA have a higher or lower primary success rate in elderly vs younger people?

A

increased.

however angina is more likley to recur in elderly, and recur sooner than it would after CABG.

95
Q

how is the long-term results after CABG in the elderly compared to the youth

A

they mirror. those who undergo this surgery and who experience an uneventful recovery period have been sown to have an equivalent survival to those with similar age with no CAD.