Quiz 3: Cardiac Flashcards

1
Q

AMI

A

Acute Myocardial Infarction Common Symptoms: intense chest pressure, with impending sense of doom and pain to the left arm; other symptoms may include chest heaviness or burning, pain radiation to other areas, indigestion, vomiting, nausea and diaphoresis

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2
Q

Angina Pectoris

A

• Stable Angina: Myocardial ischemia, Chest discomfort upon exertion

• Unstable Angina: Can occur without exertion (more severe), Transient ischemia

  • Platelet aggregation
  • Coronary artery spasms
  • Coronary thrombosis
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3
Q

ECG AMI Diagnosis

A

• ECG changes depend on the location and severity of myocardial necrosis

• 100% specificity, 50% sensitivity (myocardial infarctions that do not produce characteristic ECG changes)

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4
Q

Biochemical Markers of AMI

A
  • AST - Aspartate aminotransferase
  • LDH - (LD) Lactic dehydrogenase
  • CK - Creatine kinase
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5
Q

Creatine kinase (CK)

A
  • Takes at least 6 hours for there to be an “enzyme leak”.
  • Enzymes should be re-assessed every 8 hours for the first 24 hours
  • Enzyme is helpful in gauging the size of the AMI CK Isoenzymes found with Agarose gel electrophoresis with fluorescent detection.

CK3 skeletal muscle

CK2 heart muscle

CK1 brain

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6
Q

Measuring CK Levels

A
  • Immunoinhibition/precipitation - Antibody to M subunit - Multiply results by 2 - Interference from CK-1 (BB)
  • Most modern methods use two-site (“sandwich”) heterogeneous immunoassay - Measures CK-MB mass, rather than activity - Gives rise to a pseudo-percentage, often called the “CK- MB index”
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7
Q

AST

A

AST: Found in liver and heart – now more commonly measured as a liver enzyme

• Increased levels in AMI, but not specific

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8
Q

LDH Ratios (Normal and Disease State)

A
  • Normal ratios: LD1 < LD2; LD5 < LD4
  • LD1 > LD2 – Myocardial infarction, hemolytic anemia, pernicious anemia
  • LD5 > LD4 –Liver disease
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9
Q

5 LDH Isoenzymes

A

LD1 – heart, rbc’s, kidney

LD2 – heart, rbc’s, kidney (Less than LD1) (LD2 makes up the largest fraction)

LD3 – lungs and other tissues

LD4 – wbc’s, lymph nodes, muscle, liver

LD5 - liver, skeletal muscle

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10
Q

Less Common Biomarkers for AMI

A
  • C-reactive Protein
  • Fibrinogen
  • Lipoprotein (a)
  • Homocysteine
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11
Q

C-Reactive Protein

A
  • Evaluation of inflammatory processes, arthritis and autoimmune disease
  • Also found in atherosclerotic plaque, may enhance expression of adhesion molecules, alter LDL cholesterol uptake by macrophages
  • High sensitivity methods with detection limits of 0.2 mg/L allow differentiation of low level inflammation implication in coronary artery disease (CAD)
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12
Q

Fibrinogen

A
  • Large glycoprotein - final step in the coagulation cascade
  • Normal levels are 200-400 mg/dL
  • Levels also correlate positively with other risk factors, increasing with LDL cholesterol and decreasing with increased HDL cholesterol levels
  • Elevated fibrinogen associated with 1.5 fold increased risk of AMI or coronary death
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13
Q

Lipoprotein (a)

A
  • LDL particle containing the apolipoprotein B-100 molecule and an apoprotein (a) molecule
  • Plasma concentration is from 1-100 mg/dL, but most values are < 20mg/dL
  • When chronically elevated, Lp (a) may be proatherogenic
  • Recent studies show that asymptomatic individuals with high levels had a risk of CAD events 1.7 times those with lower levels
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14
Q

Homocysteine

A
  • Amino acid byproduct of the metabolism of the essential amino acid methionine
  • Assoc. with Vit. B6/12 and Folic Acid
  • A link was established between moderate levels and atherosclerosis, and studies show homocysteine is associated with cardiovascular events
  • Homocysteine lowering therapy has had conflicting results with respect to outcomes
  • Measurement remains controversial
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15
Q

Myoglobin

A
  • Intracellular heme protein that aids in the transport of oxygen
  • Abundant in both cardiac/skeletal muscle
  • Elevations detected within 1-4 hours (peak) after AMI symptoms; returns to normal after 12 hours
  • Nonspecific (increases in MI and Renal damage) but sensitive marker–primarily used for negative predictive value.
  • Usually measured by sandwich, nephelometric, turbidimetric, or fluorescence immunoassay
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16
Q

Troponin Complex

A
  • A contraction-regulating protein found on the thin filaments of striated muscle, made of three non-identical subunits (T,I, and C)
  • Troponin has become the most sensitive and specific test for myocardial damage
  • Troponin C is the calcium-sensitive subunit and contains four Ca++ binding sites
  • Troponin I is the inhibitory subunit, binds actin in the relaxed state
  • Troponin T binds to tropomyosin and actin
17
Q

Troponin T and I

A
  • Proteins found in thin filament of muscle
  • Early release due to cytosolic pool
  • Sustained release due to myofibrils
  • Cardiac troponin not released from skeletal muscles
18
Q

Troponin I

A
  • Specific for cardiac muscle
  • It rises 3-6 hours post AMI, peaks at 14-20 hours and remains elevated 5-10 days
  • Studies also show its utility in risk stratification
  • TnI is useful in clinical conditions where other markers are ambiguous such as in chronic renal patients.
  • Most commercial assays measure TnI
19
Q

Troponin T

A
  • Troponin T is also specific for cardiac muscle, rises 3-4 hrs post MI and peaks in 10- 24 hours. Remains elevated for 10-14 days.
  • Troponin T has been shown to be useful in risk stratification; and in detecting peri-operative MI during procedures
  • May also be elevated in renal disease
20
Q

cTnT vs cTnI

A
  • cTnT remains positive after AMI longer than cTnI.
  • Abnormal cTnT found more frequently in patients with chronic renal failure than cTnI due to non-ischemic myocardial damage.
21
Q

Congestive Heart Failure

A
  • A condition where the heart can’t pump enough blood to the body’s other organs
  • Can result from: - Coronary artery disease - Past MI with scar tissue that interferes with function - High blood pressure - Heart valve disease - Cardiomyopathy - Infection of the valves and/or heart muscle As a result of decreased cardiac function, body fluids may build up in the lungs and limbs.
22
Q

BNP

A

1 of 4 natriuretic hormones

Antagnonists to renin-angiotensin- aldosterone system Decrease blood pressure by vasodilation and renal excretion of Na and water Helps diagnose presence and severity of congestive heart failure, increased in CHF due to enhanced atrial & ventricular synthesis. Brain natriuretic peptide (BNP) are naturally occurring peptide hormones synthesized in the brain, increased in patients with kidney disease

23
Q

POCT for Cardiac Markers

A
  • Whole blood platforms.
  • Quantitative and qualitative assays available
  • Can significantly reduce assay TAT.
  • Precision and sensitivity less than central laboratory platforms
24
Q

POCT for AMI

A
  • STEMI: ECG, no cardiac markers needed
  • NSTEMI: troponin increased dramatically, POCT adequate
  • UA/NSTEMI: variability in performance of POCT devices.
25
Q

Relative Appearances of Markers

A
26
Q

ECG Markers

A
27
Q

Negative Risk Factors

A

HDLc > 60mg/dL

LDLc < 100mg/dL

28
Q

Congestive Heart Failure

A
  • B-Natriuretic Peptide (BNP) is active, increases Na and water excretion, causing vasodilation and drop in BP; antagonist to renin-angiotensin-aldosterone which increases BP
  • N-terminal pro-BNP is inactive

Released by ventricular walls due to hypertension and volume overload