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CARDIO TEST 2 > Lecture 7: Cardiomyocyte Growth Remodelling > Flashcards

Lecture 7: Cardiomyocyte Growth Remodelling Flashcards

1
Q

What is eccentric cardiac growth?

A

The lumen/internal chamber of the heart increases - proportional to the centre of the lumen

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2
Q

What is concentric cardiac growth?

A

Growth of muscle/thickening of wall, at expense of lumen size - cannot pump as much blood

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3
Q

What is increase in heart size proportional to?

A

Body size

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4
Q

How many people experience statistically significant hypertrophy?

A

10%

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5
Q

What can hypertrophy be a response to?

A

Altered mechanical conditions, compensatory strategy to optimise thermodynamic state or to reduce wall stress

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6
Q

What is physiologic hypertrophy?

A

Adaptation to CV training

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7
Q

What kind of people does physiologic hypertrophy occur in?

A

Elite athletes

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8
Q

What does physiologic hypertrophy involve?

A

Alteration in complex central and peripheral mechanisms

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9
Q

How many athletes does cardiac remodelling occur in?

A

50%

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10
Q

How many athletes does LV enlargement occur in?

A

15%

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11
Q

What does endurance training lead to?

A

Increase LV EDV = Increase LV wall thickness

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12
Q

What does strength training lead to?

A

Increase LV EDV

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13
Q

What has the biggest influence on LV EDV?

A

Body size - 50%, followed by genetics -25%, sport - 14%

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14
Q

What is altered in elite athletes by training?

A

Amount of perfusion volume

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15
Q

What doesn’t influence LV EDV?

A

Not influenced by competitive performance achievement level

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16
Q

What is pathologic hypertrophy?

A

Heart growth due to chronic events and acute events

17
Q

What are the chronic events that lead to pathologic hypertrophy?

A

Hypertension, renal disease, hormonal disturbance

18
Q

What are the acute chronic events that lead to pathologic hypertrophy?

A

Valve disease, infarction

19
Q

What happens with LV hypertrophy?

A

Systemic load effect

20
Q

What happens with LV and RV hypertrophy?

A

Trophic/hormonal effect

21
Q

What causes the heart to have a volume load and what growth does this lead to?

A

Obesity, eccentric

22
Q

What causes the heart to have a pressure load and what growth does this lead to?

A

Hypertension, concentric

23
Q

What myocyte growth does eccentric hypertrophy lead to?

A

Longer myocyte

24
Q

What myocyte growth does concentric hypertrophy lead to?

A

Fat myocyte

25
Q

What happens in sub cellular remodelling?

A
  • Myosin heavy chain – alpha (fast) to beta (slow)
  • Major changes in calcium transport
  • Reduced maximum velocity of shortening to economize on energy
  • Reactivation of fetal and embryonic expression patterns
  • Ultimately short term adaptations and don’t work forever
  • No real change in calcium current due to channels balancing each other out
26
Q

What happens if there are fewer L-type calcium channels?

A

Calcium release is suppressed

27
Q

Does more t-type calcium channels make up for lost l-type channels?

A

Not necessarily - might not be positioned correctly

28
Q

What are the protein expression changes in hypertrophy (activation)?

A

Same calcium current, less l-type channels, more t-type channels, less SR calcium release channels

29
Q

What are the protein expression changes in hypertrophy (relaxation)?

A

Fewer SR calcium ATPase, increased Na/Ca exchanger

30
Q

What happens in relaxation in hypertrophied hearts?

A

SR calcium uptake delayed, longer calcium and myosin interaction, increased reliance of Na/Ca exchanger, prolonged relaxation

31
Q

What is the consequence of prolonged relaxation?

A

Next beat may come along before relaxation has finished, diastolic beat compromised

32
Q

What happens to SV in heart failure?

A

For same EDV, SV is reduced, sympathetic NS kicks in to compensate and curve is recovered - compensation cannot occur forever 0 decompensation phase

33
Q

What happens in the positive feedback system?

A

Ongoing exposure to growth promoting mediators, maintained growth signalling, increase heart muscle mass and wall thickness, arrhythmia vulnerability, ultimate functional decompensation, dilation and failure

34
Q

What are the three ways that myocytes can be lost?

A

Myocyte lysis through NECROSIS: cell swelling, membrane rupture, oxygen deficiency

Myocyte suicide through APOPTOSIS: programmed cell death, mitochondrially mediated – related to critical energy deficit state

Myocyte self-eating through AUTOPHAGY: metabolic stress induced internal breakdown – goes beyond recycling and breaks itself down

35
Q

What doesn’t occur as a result of physiologic hypertrophy?

A

Increased LV systolic function

CARDIO TEST 2 (10 decks)

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