14) Cardiac function Flashcards

1
Q

Biochemical feature or facet that can be used to measure the progress of disease or the effects of treatment.

A

biomarker

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2
Q

Greek for gruel and refers to the massive accumulation of lipids in these vascular lesions.

A

athero

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3
Q

Was considered to be a bland lipid storage disease
Now thought to evolve from the inflammatory process

A

Atherosclerotic vascular disease (ASVD)

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4
Q

Acute coronary syndrome (ACS)

A

Described as a continuum of clinical signs and symptoms ranging from…

unstable angina (chest pain) to…

non-Q-wave (ECG pattern) acute myocardial infarction (AMI) and Q-wave AMI.

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5
Q

most common cause of ASC

A

atherosclerosis in coronary arteries

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6
Q

Locally acting autacoid polypeptides that mediate vasoconstriction by interacting with phospholipase C-linked receptors.

Released early in the inflammatory response preceding an ACS.

A

cytokines

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7
Q

Double-walled sac that encloses the heart

A

pericardium

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8
Q

Made up of cardiac muscle
Anchored to the heart’s fibrous skeleton

A

myocardium

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9
Q

Connective tissue and squamous cells make up the internal lining of the myocardium

A

endocardium

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10
Q

Deposition of tough, rigid collagen inside the vessel wall and around the atheroma

A

arteriosclerosis

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11
Q

Most common form of arteriosclerosis

Caused by the formation of multiple plaques within the coronary arteries

A

atherosclerosis

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12
Q

Results from the accumulation of atheromatous plaques within the walls of the arteries that supply the myocardium

A

CAD

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13
Q

cardiac biomarker release affected by…

A
  • Cytosolic enzymes
  • Subcellular location
  • Molecular mass
  • Plasma clearance
  • Concentration gradients
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14
Q

Layering or gradation of risk factors, which are described as elements or constituents that may put someone’s health in peril

A

risk stratification

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15
Q

Many cardiac biomarkers are used for evaluating….

A

risk stratification

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16
Q

characteristics of ideal cardiac biomarkers

A
  • Smaller markers are released faster from injured tissues.
  • Soluble cytoplasmic marker is preferred to structural markers.
  • Have absolute cardiac tissue specificity and should not exist in other tissues.
  • Useful to differentiate between reversible (ischemic) and irreversible (necrotic) damage.
  • Release from the myocardium should be complete following injury.
  • Amount of marker released should be in direct proportion to the size of the injury (infarct sizing).
  • Remain elevated long enough (12 to 24h) to be detected in the serum of the “late presenter.”
  • For risk stratification, there should be a correlation between outcome and the presence or absence of a marker in serum or the degree of elevation of the marker above “normal.”
  • Should be cleared rapidly to allow diagnosis of recurrent injury.
  • Should be useful for monitoring of reperfusion and re-occlusion.
  • Assays should be relatively easy and quick to perform.
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17
Q

Regulatory protein of the myofibril

A

troponin

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18
Q

3 troponins and their functions

A
  • Troponin I—Binds to actin and inhibits contraction
  • Troponin T—Binds tropomyosin
  • Troponin C—Contains 4 Ca-binding sites & regulates contraction
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19
Q

Two isoforms of TnI
Several isoforms of TnT

A

skeletal muscle

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20
Q

One isoform of TnI
Several isoforms of TnT

A

cardiac muscle

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21
Q

Binds to actin and inhibits muscle contraction

A

cTnI

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22
Q

Binds tropomyosin

A

cTnT

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23
Q

Has 3 isoforms, one of which has unique cardiac specificity

A

cTnI

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24
Q

Isoform can be demonstrated in patients with muscular dystrophy, polymyositis, and end-stage renal disease.

A

cTnT

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25
Q

(cTnI/cTnT) is NOT expressed in skeletal muscle.

A

cTnI

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26
Q

what makes troponins good cardiac biomarkers?

A
  • High level of diagnostic specificity and sensitivity.
  • Possess early release kinetics after an AMI
  • Remain elevated for a long interval of time
  • Very low to undetectable concentrations in serum from healthy patients
  • Relatively few interfering substances
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27
Q

Drawing blood samples periodically, usually at prescribed time intervals over the course of the patient’s admission

A

serial sampling

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28
Q

Total CK
rise
peak
return to normal

A

4-6 hours
24 hours
3-4 days

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29
Q

CK-MB
rise
peak
return to normal

A

4 hours
18 hours
2 days

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30
Q

Myoglobin
rise
peak
return to normal

A

1-3 hours ★ (earliest)
8-12 hours
1 day

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31
Q

TnT
rise
peak
return to normal

A

4-6 hours
10-24 hours
10 days ★ (longest)

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32
Q

TnI
rise
peak
return to normal

A

4-6 hours
10-24 hours
4 days

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33
Q

sources of error for cTnI

A

False positive
Heterophile antibodies
Rheumatoid factor

False negative
Bilirubin
Hemoglobin
Circulating cTnI autoantibodies
Interfering factor (IF)

do not affect TnT

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34
Q

causes of elevated troponins besides ACS

A
  • Trauma
  • HTN
  • Hypotension, often with arrhythmias
  • CVA
  • Rhabdomyolysis (cardiac)
  • Cocaine-induced rhabdomyolysis
  • Post-op noncardiac surgery
  • Renal failure
  • DM
  • Burns
  • Severe asthma
  • Sepsis
35
Q

WHO criteria for making AMI dx and European revisions

A
  1. History of characteristic chest pain
  2. Diagnostic changes in the EKG
  3. Changes in serum enzyme levels

Revisions
1. Promote troponin to a pivotal role
2. Relegate CKMB to a secondary role
3. Eliminate the need for CK

36
Q

non-cardiac CKMB elevations

A
  • Severe skeletal muscle injury following trauma or surgery (ie crushing injury)
  • Chronic muscle disease in patient with muscular dystrophy, end-stage renal disease, or polymyositis
  • Healthy people who exercise and participate in physical activity such as long-distance running
  • Extensive rhabdomyolysis
  • Early dermatomyositis
37
Q

CK index

A

CKMB(100)/total CK

do not use if total CK is normal

38
Q

CK index >5%, <5%, and RR

A

> 5% —MI
<5% —crushing injury
RR —<3%

39
Q

First cardiac biomarker to appear in circulation that may be used for assessment of ACS.

A

myoglobin

40
Q

myoglobin may be pos for…

A

MI or crushing injury

41
Q

myoglobin advantages

A
  • High sensitivity and negative predictive value
  • Useful for early detection of MI and reperfusion
42
Q

myoglobin disadvantages

A
  • Low specificity in presence of skeletal muscle injury and renal insufficiency
  • Rapid clearance after necrosis
  • Labor-intensive process on urine; doesn’t make very much sense to run as an early detection marker
43
Q

mainly expressed in the heart ventricles, discovered in porcine brain

A

BNP

44
Q

pathway of BNP synthesis

A
  • Initially synthesized as preproBNP (134 amino acids)
  • Cleaved into proBNP (108 aa)
  • Cleaved again into NT-proBNP (76 aa) and BNP (32 aa)
45
Q

part of the body’s defense against volume overload and hypertension

A

BNP

46
Q

BNP functions

A

Dilate blood vessels

Increase the excretion of sodium and fluids

Reduce concentrations of neurohormones (ie. ADH) that lead to:
* Vessel constriction
* Fluid retention
* Elevated blood pressure

47
Q

Elevated plasma —– indicates the presence of heart failure and provides information about its severity.

A

NT-proBNP

48
Q

Heart is unable to pump sufficient blood to meet body’s metabolic needs and normal filling pressure.

A

CHF

49
Q

2 types of CHF

A

Diastolic — heart cannot fill properly
Systolic — heart cannot contract/pump properly

50
Q

s/s of CHF

A

Dyspnea
Increased fatigue
Edema

51
Q

best biomarkers for CHF

A

BNP/NT-proBNP

52
Q

essentially obsolete cardiac biomarker due to lack of tissue specificity

A

LD

53
Q

found in high concentrations in the heart, kidney, and erythrocytes

A

LD-1

54
Q

Nonspecific, acute-phase reactant. Shows up during inflammatory processes.

A

CRP

55
Q

Measuring blood levels of hs-CRP provides better ….. than measuring any other biomarker.

A

risk assessment of cardiovascular disease

56
Q

Produced when circulating albumin comes in contact with ischemic tissue in the heart or other organ.

A

Ischemia-Modified Albumin (IMA)

57
Q

Albumin cobalt binding test

A

used to measure IMA

Cobalt is added to serum and does not bind to ischemia-modified albumin, thus leaving more free cobalt to react with the reagent dithiothreitol

58
Q

Secreted by activated leukocytes

Enriched in unstable atherosclerotic lesions.

A

myeloperoxidase

59
Q

Elevated results are seen in patients with AMI (>50 ng/mL).

A

myeloperoxidase

60
Q

Myeloperoxidase is useful for both short- and long-term …… and may help identify …… at risk for major adverse cardiac events.

A

risk stratification for CVD

troponin-negative patients

61
Q

This has shown to be a good indicator of cytokine storm syndrome (CSS) severity and mortality risk in COVID-19 positive patients.

A

IL-6

62
Q

Typically measured during pregnancy to detect Down syndrome.

A

Pregnancy-Associated Plasma Protein-A (PAPP-A)

63
Q

A zinc-binding metalloproteinase and insulin like growth factor (IGF).

A

Pregnancy-Associated Plasma Protein-A (PAPP-A)

64
Q

Increased circulating PAPP-A is associated with ——

A

ACS

65
Q

Found primarily in the fatty plaques that may line the walls of coronary arteries in patients with atherosclerosis

A

oxidized LDL

66
Q

Circulating levels of —— are strongly associated with angiographically documented CAD in patients 60 years of age or younger.

A

Ox-LDL

67
Q

Includes the recruitment of circulating macrophages into atherosclerotic lesions and stimulation of smooth muscle cell growth

Appears to function in the early stages of the inflammatory process

A

Placental Growth Factor (PlGF)

68
Q

May serve as a strong candidate biomarker for plaque instability, myocardial ischemia, and patient prognosis in ACS

A

Placental Growth Factor (PlGF)

69
Q

In the heart, participates in vascular remodeling, plaque instability, and ventricular remodeling after cardiac injury.

A

Matrix Metalloproteinase-9

70
Q

Is released into the circulation when the myocardium is injured

low specificity in the presence of skeletal muscle injury and renal insufficiency

A

Heart-Type Fatty Acid-Binding Protein (H-FABP)

71
Q

may provide a sensitive guide to the underlying pathophysiology of coronary heart disease.

A

FFAU

72
Q

FFAU

A

fatty acids unbound to albumin

73
Q

How do omega-3 FAs reduce risk of CVD?

A
  • Decrease risk for arrhythmias
  • Decrease risk for thrombosis
  • Decrease triglycerides and remnant lipoprotein levels
  • Decrease rate of growth of the atherosclerotic plaque
  • Improve endothelial function
  • Slightly lower blood pressure
74
Q

Produced by macrophages and expressed in atherosclerotic lesions

enzyme that co-traffics with LDL in circulation

A

Lipoprotein-Associated Phospholipase A2 (Lp-PLA2)

75
Q

Biological function is unclear.
Roles may be to:
* Respond to tissue injury and vascular lesions
* Prevent infectious pathogens from invading cells
* Promote wound healing

A

Lipoprotein (a)

76
Q

Most important role in atherothrombosis is to inhibit clot formation at site of injury.

A

Lp (a)

77
Q

Competes with plasminogen for binding sites thus interferes with clot lysis and increases the risk of AMI

A

Lp (a)

78
Q

Screen for ——- if there is a(n):
* Family history of premature CVD
* Family history of hyperlipidemia
* Established CVD with normal routine lipid profile
* History of recurrent arterial stenosis

A

Lp (a)

79
Q

Plasma ——– levels may predict cardiovascular events years in advance in a population without diagnosed CVD.

A

adiponectin

80
Q

High blood levels are associated with reduced risk of heart attacks.

Low blood levels are found in individuals who are obese, and who are at increased risk.

A

adiponectin

81
Q

Causes vasodilatation

Plays a role in fat metabolism and obesity

A

leptin

82
Q

The higher the blood leptin level, the ——– the risk of developing CVD.

A

greater

83
Q

found to have an independent protective association with unstable CAD

A

leptin

84
Q

advantages of cardiac POC

A
  • Rapid identification of AMI
  • Decreased turn-around time for analysis
  • Rapid exclusion of ACS
  • Rapid stratification of cardiac patients
  • Rapid identification and exclusion of CHF