L3. Cardiac hypertrophy in health and disease

Question 1

What are the two main types of cardiac hypertrophy?

Answer 1

Physiological and pathological hypertrophy

Question 2

What is the primary cause of physiological cardiac hypertrophy?

Answer 2

Exercise training and pregnancy

Question 3

What triggers pathological cardiac hypertrophy?

Answer 3

Pressure or volume overload, such as hypertension or valve regurgitation

Question 4

What is ‘athlete’s heart’?

Answer 4

A physiological enlargement of the heart due to consistent exercise training

Question 5

How does Laplace’s Law relate to cardiac hypertrophy?

Answer 5

It explains how the heart remodels to normalize wall stress based on chamber radius and wall thickness

Question 6

What type of hypertrophy occurs with volume overload?

Answer 6

Eccentric hypertrophy

Question 7

What type of hypertrophy is caused by pressure overload?

Answer 7

Concentric hypertrophy

Question 8

What molecular pathway mediates physiological hypertrophy?

Answer 8

Insulin and IGF-1 pathway

Question 9

Which signalling molecules are key in pathological hypertrophy?

Answer 9

Angiotensin II and Endothelin I

Question 10

What is the difference between concentric and eccentric hypertrophy?

Answer 10

Concentric hypertrophy involves thickened walls with reduced chamber size, while eccentric involves dilation with wall thickening

Question 11

What happens to cardiac output during exercise?

Answer 11

Cardiac output increases to meet the demands of working muscles

Question 12

What is the effect of detraining on an athlete’s heart?

Answer 12

Physiological remodelling reverses with detraining

Question 13

What is the significance of the resting bradycardia in athletes?

Answer 13

It is associated with sinus node remodelling due to training

Question 14

What percentage of myocardial cell volume is made up by cardiomyocytes?

Answer 14

0.9

Question 15

What distinguishes physiological from pathological hypertrophy?

Answer 15

Physiological hypertrophy is reversible and improves function, while pathological is irreversible and leads to heart failure

Question 16

What role does the IGF-1 receptor play in cardiac hypertrophy?

Answer 16

Overexpression induces physiological hypertrophy and protects against pathological remodelling

Question 17

What are the characteristics of pathological hypertrophy?

Answer 17

Fibrosis, reduced capillary networks, and activation of foetal gene expression

Question 18

What is the main difference in the capillary network between physiological and pathological hypertrophy?

Answer 18

Physiological hypertrophy maintains capillary density, while pathological does not

Question 19

What does foetal gene expression indicate in hypertrophy?

Answer 19

It signifies maladaptive remodelling in pathological hypertrophy

Question 20

How does pregnancy affect cardiac hypertrophy?

Answer 20

It induces reversible physiological hypertrophy with increased left ventricular mass

Question 21

What role do microRNAs play in hypertrophy?

Answer 21

They regulate gene expression post-transcriptionally, influencing pathological hypertrophy

Question 22

What did the TAC model reveal about miR-29 in hypertrophy?

Answer 22

Inhibiting miR-29 alleviates pathological hypertrophy and fibrosis

Question 23

How is pathological hypertrophy initially compensatory?

Answer 23

It preserves cardiac function before transitioning to decompensated failure

Question 24

What is a hallmark of heart failure with reduced ejection fraction?

Answer 24

Dilation and decreased systolic function

Question 25

How do trabeculae change during cardiac maturation?

Answer 25

They compact and contribute to coronary vessel formation

Question 26

What is the prevalence of LV trabeculation in athletes?

Answer 26

18% compared to 7% in controls

Question 27

How does eccentric hypertrophy reduce wall stress?

Answer 27

By increasing chamber radius and wall thickness

Question 28

What happens to the heart in long-term detraining?

Answer 28

Reductions in ventricular dimensions and wall thickness

Question 29

How do endothelial cells contribute to cardiac remodelling?

Answer 29

By maintaining capillary networks to match muscle growth

Question 30

What did McMullen's study on IGF-1 receptor overexpression show?

Answer 30

Improved cardiac performance and protection against fibrosis

Question 31

What is the role of CaMKII in pathological hypertrophy?

Answer 31

It promotes maladaptive cell growth by exporting histone deacetylases

Question 32

How does the sarcoplasmic reticulum contribute to hypertrophy signalling?

Answer 32

Releases calcium, which activates calcineurin and other pathways

Question 33

What is the effect of pregnancy on LV wall stress?

Answer 33

Normalised by increased wall thickness during pregnancy

Question 34

What does angiogenesis ensure in physiological hypertrophy?

Answer 34

Adequate oxygen and nutrient supply to the growing heart muscle

Question 35

What did experiments with transgenic mice show about Akt1?

Answer 35

Akt1 activation is essential for IGF-1 mediated hypertrophy

Question 36

What defines maladaptive remodelling in pathological hypertrophy?

Answer 36

Increased fibrosis and inadequate capillary formation

Question 37

What is fractional shortening a measure of?

Answer 37

The experimental equivalent of ejection fraction in cardiac studies

Question 38

How does exercise intensity affect hypertrophy type?

Answer 38

Endurance training leads to eccentric, while strength training leads to concentric hypertrophy

Question 39

What is the relationship between wall stress and oxygen consumption?

Answer 39

Higher wall stress increases myocardial oxygen demand

Question 40

How does Laplace’s Law predict heart failure progression?

Answer 40

Increased radius and reduced pressure generation exacerbate wall stress