Lecture 8: Cardiac Hypertropy Flashcards
What is cardiac hypertrophy?
Enlargement of the heart Can ebe: - global - left ventricular - right ventricular
What does normal cardiac growth depend on?
Timing: - Parallels body growth - Doubles in size after 6mo - Triples in size after 1yr Characteristics: - Macroscopic - Micropscopic Controls: - Number of cells - Hypothalamic-pituitary axis (Growth hormone/IGF, thyroxine Correlates: - Body size - BP - Ang2 - Catecholiamines - Family history
What are the macroscopic & microscopic normal growth characteristics?
Macroscopic:
- From ovoid to spheroid in shape
- Greater change in left than right ventricle (greater wall thickening & greater increase in ventricular capacity)
RV: 2 - 20ml
LV: 2 - 40ml
Microscopic:
- Myocardial cell division (hyperplasia) ceases after first few months
- Further growth through hypertrophy (increased fibre diameter)
RV: 10 - 16 um
LV: 10 - 20 um
- Increased proportion of fibroendothelial cells (from 1:1 to 2.5:1)
What are the extrinsic and intrinsic growth determinants?
~Extrinsic~ Hemodynamic - SV - systolic wave form Non-hemodynamic - hormones - neural ~Intrinsic~ Genetic Autocrine, paracrine
What are the causes of cardiac hypertrophy?
Myocardial infarction Hypertension Valve disease Obesity Unknown
What are the phases of cardiac hypertrophy?
A spectrum:
Development
Compensated
Decompensated (failure)
What are the patterns of hypertrophy?
Concentric - cavity size is the same but pressure overload causes thicker walls
Eccentric - cavity size is larger & thicker walls occur as a result of volume overload
What are the two most important risk factors for CV death?
- Age
2. LV hypertrophy
What are the consequences of cardiac hypertrophy?
Greater risk of CV death
- Underlying disease
- Electrical instability
What is the development phase of hypertrophy?
Increased work: - preload (volume) - afterload (pressure) Increased strain on: - ventricular wall - individual muscle cells Cellular response: - increased myocardial cell size - increased number of fibroendothelial cells (especially around epicardial vessels - can't dilate) - increased interstitial matrix Subcellular response: - regression to fetal patterns of gene expressions - more mitochondria - extra myofibrils more SR - switch from low to high ATPase myosin
What is the compensated phase of hypertrophy?
Normalisation of strain on individual sarcomeres and cells
Normalisation of workrate:mass ratio
Normal CO but myocardial cells:
- develop less tension at a given length (less interactions between actin & myosin)
- develop tension more slowly (reduced ability of actin to activate myosin ATPase activity)
What is the decompensated phase of hypertrophy?
Falling workrate:mass ratio
Symptomatic deterioration
Heart failure
Death
