Determinants & Consequences of Ventricular Hypertrophy Flashcards Preview

Physiology > Determinants & Consequences of Ventricular Hypertrophy > Flashcards

Flashcards in Determinants & Consequences of Ventricular Hypertrophy Deck (21):

Explain the normal growth of the heart?

-Embryo - Cell proliferation - Hyperplasia: ceases after a few moths of life
- Childhood - Cell hypertrophy: increase in cell diameter
- parallel to body growth
- doubles in size in 6 months
- triples in size by 1 year
- LV thickens more than RV
- endocrine control via growth hormones/IGF & thryoxine


What does normal heart size depend on?

- body size (lean body mass) or body surface area
- family history/genetics (0.9 correlation b/t MZ twins)
- athletic conditioning
- BP
- AngII, catcholamines


What is Left Ventricular Hypertrophy?

Hypertrophy is when the LV ass increases relative to the body size.

Relative wall thickness = LV wall thickness/ LV chamber size (diameter)


What is cardiac remodeling and hypertrophy?

- Changes in size, shape & function of the heart after cardiac injury (hypertrophy when increase in LV mass)


What are some causes of remodeling?

- Causes of remodeling may be:
- myocardial infarction
- cardiac damage (ie myocarditis)
- volume overload
- pressure overload


Explain the difference between eccentric and concentric hypertrophy?

Concentric Hypertrophy:
- ↑ LV mass
- ↑ relative wall thickness without LV enlargement
- often due to pressure overload
- more sarcomeres in parallel

Eccentric Hypertrophy:
- ↑ LV mass
- normal relative wall thickness
- ↑ chamber size and normal relative wall thickness
- often due to volume overload
- myocyte stretching: more sarcomeres in series


What is remodeling compared to hypertrophy?

Hypertrophy involves increased myocardial cell size, not number - there are more mitochondria, myofibrils and sarcoplasmic reticulum. Additionally, there are increased fibroendothelial cell numbers and an increased interstitial matrix.

- normal LV mass
- ↑ relative wall thickness


The Dallas Heart study classification of 2010 saw 4 patterns of hypertrophy; What are they?

1. Thick, 2. Dilated, 3. Thick & Dilated, 4. Intermediate/neither


Explain the differences between concentric and eccentric hypertrophy including long term effects?

In concentric (thick) hypertrophy there is compensation for pressure load (high afterload). The thicker wall reduces or normalises wall stress (under Laplace's Law) so as to maintain systolic function, cardiac output and LVEDP.
There is a controversy because animals with no hypertrophy do better in response to pressure load so it can be argues that the compensatory mechanism is insufficient.

In eccentric (dilated) hypertrophy the compensation is for volume load in order to maintain stroke volume by increasing LVEDV and increasing EF, however subjects with hypertension may also have eccentric hypertrophy.

Over the long term, hypertrophy has a decompensation as the LV dilation causes increased LDEDV, LVESV and decreased EF. This leads to reduced systolic function and cardiac output which will increase LVEDP and eventually lead to heart failure.


What are some environmental and genetic causes of LVH?

- Concentric: pressure overload - high afterload (due to hypertension or aortic stenosis)
- Eccentric: volume overload - high preload (mitral and aortic regurgitation or ventricular septal defect
- following myocardial infarction
- following cardiac injury (myocarditis)
- obesity, diabetes, renal failure
- infiltration

- hypertrophic cardiomyopathy
- Fabry's disease


How do you identify LVH?

Clinically - forceful apex beat, S4, S3
ECG - tall voltages, T wave inersion
CXR - large heart in eccentric LVH but may be normal size in concentric LVH
Cardiac CT


What are the mechanisms of LVH?

- Angiotensin
- Aldosterone
- Catecholamines
- Local Factors
- Cellular & Molecular Mechanisms
- Possibly Stem cells (?)


What are some consequences of LVH?

Increased risk of:
- Ischaemic Heart Disease
- Cardiac Failure
- Atrial Fibrillation
- Stroke
- diastolic dysfunction


How does diastolic dysfunction occur with LVH?

- Thick muscle is stiff muscle
- Increased LVEDP required to achieve same LVEDV (preload) so there is and increased LA Pressure and pulmonary vein pressure
- More likely to have pulmonary congestion
- More sensitive to fluid loading (heart failure) or dehydration (low BP)
- Atrial 'kick' more important: Atrial Fibrillation.


How do you treat LVH?

Treat the underlying condition (valves etc)
Treat hypertension so that the BP is within a target range
Weight loss.


What are some specific causes and mechanisms of aetiology for LVH?

Left Ventricular Remodeling:
- Following myocardial infarction (heart attack)
- Increased LV volume and more spherical in shape
- Myocyte hypertrophy and apoptosis
- Interstitial Fibrosis

Causes of LV remodeling include associations with:
- Renin-Angiotensin-Aldosterone
- Adrenergic Nervous System
- Endothelin
- Cytokines
- Local Factors
It can be prevented or reduced by angiotensin blocking or beta adrenergic blocking.
The consequences of LV remodeling can include increased heart failure and mortality.


What are some specific causes of Right ventricular hypertrophy?

- transposition of great arteries
Pulmonary Hypertension:
- lung disease
- pulmonary embolus
- chronic L heart failure
Right Heart Valves:
- Pulmonary Stenosis/Regurgitation
- Tricuspid Regurgitation


What are the features of hypertrophic cardiomyopathy?

- Autosomally dominant with a positive family history in ~60%
- mutation in genes for sarcomere proteins
- >900 mutations in 12 genes (since 1990) the most common of which are:
- beta cardiac myosin heavy chain
- cardiac myosin binding protein
- cardiac troponin I & T

- Increased LV wall thickness especially of the septum
- cellular hypertrophy
- myocyte disarray
- LV outflow tract obstruction
- Diastolic dysfunction
- Ventricular arrhythmias - sudden death

- Clinical expression is seen in the heterogeneous phenotype and partially correlates to the mutations
- The same mutation can cause many different phenotypes, from mild asymptomatic LVH to severe LVH with:
- outflow obstruction
- ventricular arrhythmias
- shortness of breath
- heart failure
- syncope
- sudden cardiac death (most common cause of SCD in athletes)


What is the mechanism of hypertrophic cardiomyopathy?

The mechanism for hypertrophic cardiomyopathy is unclear at this point but has an association with intracellular calcium & its transport, ATP utilization and is likely to be involved in regulation of normal growth.


What is dilated cardiomyopathy?

- multiple causes
- most 'idopathic'
- Many are possible genetic
--> sarcomere proteins (different mutations to HCM)
--> Desmosomes - cytoskeleton- connections between cells


Explain correlations between exercise and the heart?

-Moderate exercise reduces the risk of heart attack, stroke and DM and with increased exercise training, bradycardia can be normal as a greater range in HR is possible.

Athletes Heart:
In competitive athletes (Esp. Endurance trainers), echo findings may overlap those seen in HCM where the thickness of the wall is