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S2B6: Biochem > Myocardial Infarction > Flashcards

Myocardial Infarction Flashcards

1
Q

What is an infarction?

What is a myocardial infarction?

What is the metabolic reason this ocurs?

A
  • Infarction
    • the process by which necrosis (cell or tissue death) results from ischemia (loss of blood supply)
  • Myocardial Infarction
    • infarction of cardiac muscle
    • etiology: lack of oxygen and various metabolits due to blockage of blood flow
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2
Q

What is the major causes of myocardial infarction?

A
  • Atherosclerosis is major cause for MI
  • Others
    • coronary embolism
    • congenital coronary anomaly
    • coronary trauma
    • coronary spasm
    • drug use (cocaine)
    • other factors (increase oxygen requirement)
      • heavy exertion, fever, hyperthyroidism, or strong emotions
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3
Q

The heart utilizes what types of molecules as fuel?

It is is most likely to use what type of molecule in the experience of ischemia?

A

carbohydrates, amino acids, and fatty acids

During ischemia: high glucose utilization

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4
Q

Myocardial utilization of what types of fuels is concentration dependent?

A

lactate and fatty acids

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5
Q

Decrease in coronary blood flow increases what process?

What is the purpose of this?

A

glycolysis

  • Purpose: return the normal contractile function of the heart
    • via glucose oxidation & glycogen resynthesis
    • translocation of GLUT4 to the plasma membrane in situations of acute ischemia
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6
Q

Why do we see an elevation of free fatty acids in the plasma ater a MI?

A
  • surge of catecholamin activity
  • inhibition fo beta oxidation of lipids in mitochondria
  • accumulation of intracellular acyl carnitine and acylcoenzyme A
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7
Q

In what situations do we see reduced myocardial uptake of free fatty acids during ischemia?

A

high glucose concentration

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8
Q

What is the reasoning behing the Glucose, insulin & potassium (GIK) treatment for a MI?

How effective is it?

A
  • If the injury zone of infarction has a low membrane resting polarization, the intracellular potassium is proportionately decreased, if [K] outside the fiber remains constant
  • the treatment with GIK forces potassium into the cell, thus restoring the normal resting potential
  • Effectiveness
    • A reduction of 28% in mortality
    • even in patients who had received thrombolytic agents, the in-hospital death rate was reduced by over 60%
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9
Q

What is the concern with administering GIK treatment?

A

fear of myocardial acidosis as a result of increased lactate production

also, the research wasn’t supported b/c not profitable

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10
Q

What is the effect of increased NO in the infarcted myocardium?

How is the majority of NO produced?

What end-products increase in the blood following MI/coronary artery occlusion?

A
  • Released primarily through inducible form of NO synthase (iNOS)
    • ​NO + Guanylate cyclase-heme-Fe –> cGMP
      • NO binds to the heme group of Guanylate cycyase
    • increase in cGMP produces the physiological & pharmacological effects
  • Helps contratcile and metabolic functions of the infarcted heart
    • necessary for the growth-promoting effect of vascular endothelial growth factor (VEGF) – important for develping collaterl arteries
  • End products
    • NO2 (nitrite)
    • NO3 (nitrate)
    • peroxynitrite & hydroxy-like intermediates
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11
Q

There is an increase in what 3 biological substances within the infarcted myocardium?

A

NO, prostacyclin, and thromboxane

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12
Q

What is the function of prostacyclin & thromboxane in

A
  • Prostacyclin
    • inhibit platelet aggregation
    • coronary vasodilation
    • prevents ventricular arrhythmias
    • decreases infarct size
  • Thromboxane
    • promotes platelet aggregation
    • causes vasoconstriction
    • initiates ventricular arrhythmias
    • increases infarct size
    • increases production of NO and prostacyclin counteracts these effects
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13
Q

What is the relationship between NO and the COX systems?

A

NO synthase & cyclooxygenase (COX) form prostanoids from arachidonic acid

cross-talk between the systems – production of NO increases production of prostacyclin & thromboxane

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14
Q

How do the NSAIDs, Aspirin & celecoxib, influence NO, prostacyclin & thromboxane?

A
  • acetylsalicylic acid (Aspirin), a COX1 and -2 (75mg/kg/day) inhibitor, reduces both prostaglandin & thromboxane formation
    • does not influencemyocardial activity of iNOS
  • celecoxib, a COX2 selective inhibitor lowers myocardial prostacyclin production
    • does not alter myocardial production of nitrit & nitrate
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15
Q

What cardiac biomarker levels are assessed for diagnosis of MI?

A

cardiac troponin

sensitive & accurate

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16
Q

What charcteristics make something a good biomarker?

What do you have to know about biomarkers for them to provide good information?

A
  • indicators of normal & pthological processes
  • Provide quantitative measurements
  • used alone or in combination
  • Information
    1. plasma concentration
    2. when it is release with relation to the injury
    3. How quickly they degrade/decline in cocentration
17
Q

In addition to enzyme levels, what factors help identify a diagnosis?

A
  • patient age
  • sex
  • prior history
  • possivle drug use
18
Q

What were the first 3 enzymes used to diagnose MI?

What were the benefits & challenges of using these enzymes?

A
  • Aspartate aminotransferase (AST) & Alanine aminotransferase (ALT)
    • appear slowly in plasma
    • not specific to heart muscle
  • LDH
    • released slowly into plasma
    • tetrameric enzyme with two monomer types
      • H(heart) and M(muscle) that combine to yield
        • 5 LDH isozymes HHHH (I1), HHHM (I2), HHMM (I3), HMMM (I4), MMMM (I5)
      • tissue-specific patterns in the expression of H and M genes
      • LHD1 high in heart tissue & LDH5 high in liver
      • it is possible to separate & detect isozymes by electrophoresis
19
Q

What are the 3 isozymes of cratinine kinase?

A

CK-MM (skeletal muscle)

CK-BB (brain)

CK-MB (heart and skeletal muscle)

20
Q

Describe how the levels of CK change with relation to a MI

How are the different isozyme detected?

A

appear within 4-6 hours of an MI

peaks at 24 hours

returns to baseline by 38-72 hours

detected by eletrophoresis

21
Q

What is troponin?

At what timepoints following an MI do you see troponin?

Can elevated troponin be caused by anything other than a MI?

A
  • Troponin
    • complex of 3 proteins involved in muscle contraction in skeletal and cardiac muscle but not in smooth muscle
  • Plasma levels of cardiac troponins I and T are sensitive and specific indicators of damage to heart muscle
    • troponin levels rise within 2-6 hours after MI and remain elevated for 4-10 days
  • In addition to MI, other heart muscle damage also elevates serum troponin level
22
Q

What is an inherited cardiomyopathy?

What are the two classes?

A
  • Inhetited cardiomyopathy
    • any structural or functional abnormality of the ventricular myocardium due ot an inherited cause
  • Classes
    • Cardiac energy metabolism – mutation in genes encoding enzymes/proteins involved in fatty acid oxidation & oxidative phosphorylation
    • Mutations in genes encoding proteins involved in or affecting myocardial contraction, such as myosin, tropomyosin, the troponins, & cardiac myosin-binding protein C
      • Familial Hypertrophic Cardiomyopathy
23
Q

Fill out the provided chart

A
24
Q

What is Familial Hypertrophic Cardiomyopathy?

What is the mutation?

Clinical presentation?

A
  • FHC
    • thickening (hypertrophy) of the heart muscle
  • Mutation
    • cardiac beta myosin heavy chain gene
      • may be a missense mutation or a formation of a hybrid heavy chain
  • Clinical presentation
    • large variation
    • genetic heterogeneity (may have additional mutations in other genes)
      • cardiac actin, cardiac troponins I & T, essential and regulatory myosin light chains, cardiac myosin-binding protein C, titin
      • if additional mutation is also in betal chain, this may more severly affect the protein
25
Q

Describe the biochemical basis for the 2 most common mutations associated with Familial Hypertrophic Cardiomyopathy.

A
  • Missense mutation
    • head & head-rod regions of myosin heavy chain
    • mutatnt polypeptides caue formation of abnormal myofibrils, eventually resulting in compensatory hypertrophy
  • Alter the charge of AA side chain
    • Arginine is replace with glutamine, which presumably affects the conformation of the proetin more markedly than other substitutions
    • significantly shorter life expectancy
26
Q

Descibe dilated cariomyopathy

What mutations are associated with it?

A
  • Dilated cardiomyopathy
    • heart’s ability to pump blood is decreased b/c the LV is enlarged & weakened
    • prevents the heart from relaxing & filling with blood as it should
    • often starts in the LV and then spreads to the RV adn atria
  • Mutations
    • dystrophin
    • muscle LIM protein (w/ cystein-rich domain detected in Lin-II, Isl-1, Mec-3)
    • cyclinc response-element binding protein (CREB)
    • desmin
    • lamin have been implicated in the causation of this condition

S2B6: Biochem (1 decks)

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