Determinants and Consequences of Ventricular Hypertrophy Flashcards

1
Q

What is involved in normal heart growth?

A

Cell proliferation as an embryo and cell hypertrophy during childhood

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2
Q

What does normal heart size depend on?

A

Body size, genetics, athletic conditioning, blood pressure, angiotensin II and catecholamines

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3
Q

When does remodelling and hypertrophy occur?

A

In response to myocardial infarction, myocarditis, volume overload, pressure overload

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4
Q

What is hypertrophy?

A

Increase in LV mass relative to body size

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5
Q

What is relative wall thickness?

A

Wall thickness over chamber size

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6
Q

What is remodelling?

A

Increased relative wall thickness without an increase in mass

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7
Q

What is concentric hypertrophy?

A

Increase in mass and increase in relative wall thickness - chamber size stays the same. Due to more sarcomeres in parallel.

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8
Q

What is eccentric hypertrophy?

A

Increase in mass but normal relative wall thickness - chamber size increases. Due to more sarcomeres in series.

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9
Q

When does concentric hypertrophy occur?

A

Usually due to pressure overload

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10
Q

When does eccentric hypertrophy occur?

A

Usually due to volume overload

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11
Q

What happens in hypertrophy?

A

Increased myocardial cell size, increased fibroendothelial cell number, increased interstitial matrix

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12
Q

Why does concentric hypertrophy occur?

A

To compensate for pressure load- thicker wall reduces stress - able to maintain CO and and EDV

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13
Q

Why does eccentric hypertrophy occur?

A

To maintain SV by having a larger EDV

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14
Q

What happens in decompensation?

A

Reduced systolic function and cardiac output - leads to cardiac failure

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15
Q

What are the causes of LVH?

A

pressure overload (aortic stenosis, hypertension), volume overload (valve regurgitation, septal defect), myocardial infarction, myocarditis, obesity, diabetes, renal failure, infiltration, hypertrophic cardiomyopathy (genetic), fabry’s disease (genetic)

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16
Q

What are the features of LVH on examination?

A

forceful apex beat, 3rd and 4th heart sound, tall voltages on ECG, inversion of T wave, large heart size on X-ray (if eccentric) - more accurate diagnosis using echo, MRI and CT

17
Q

What are the mechanisms of LVH?

A

Not very well understood- involves angiotensin, aldosterone, catecholamines, local factors, cellular and molecular mechanisms

18
Q

What are the consequences of LVH?

A

Increased risk of ischaemic heart disease, cardiac failure, atrial fibrillation, stroke - also causes diastolic dysfunction

19
Q

What happens in diastolic dysfunction?

A

The thickened muscle is stiffer, so a higher LVEDP is required to achieve the same LVEDV - the pressure backs up in to the LA and the pulmonary veins and causes pulmonary congestion

20
Q

What is the treatment for LVH?

A

Have to target underlying conniption - repair or replace valve, treat hypertension, weight loss

21
Q

When does left ventricular remodelling occur?

A

Following a myocardial infarction - the damage to the heart muscle and the following scar leads to dilation of the heart - can prevent this occurring with ACE inhibitors

22
Q

When does right ventricular hypertrophy occur?

A

Congenitally (transposition of great arteries), pulmonary hypertension (lung disease, pulmonary embolism, left heart failure), right heart valve problems (pulmonary stenosis/regurgitation or tricuspid regurgitation)

23
Q

What is hypertrophic cardiomyopathy?

A

An autosomal dominant genetic condition that causes left ventricular hypertrophy due to myocyte disarray - may be mild or severe, can cause ventricular arrhythmias

24
Q

What is athlete’s heart?

A

eccentric hypertrophy - may cause ventricular arrhythmia and sudden death