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Page created on October 22, 2018. Last updated on December 13, 2018 at 14:48
Cardiac hypertrophy is an adaptive mechanism, so the heart can compensate for the increased afterload. However, after a certain limit the heart cannot compensate any longer, and regressive changes will happen instead, like lysis and loss of myocardial fibers. In extreme cases apoptosis or necrosis of myocytes will happen. All of this leads to a cardiac failure.
The left ventricle can undergo both concentric and dilative hypertrophy. The way to measure the extent of the hypertrophy is to weight the heart or measure the thickness of the wall.
- A normal heart´s weight is 250-300 g.
- In hypertrophy, it can weigh 500 g. In extreme cases it can be 650-1000 g, and we call it the bull´s heart (cor bovinum).
- Normal thickness of the left ventricle wall without papillary muscles is less than 15 mm.
- The right ventricle should not exceed 2-3 mm below pulmonary conus.
What happens inside the cardiac muscle?
The increased demand will make the cell increase its protein synthesis and assemble more sarcomeres. This also means an increased number of mitochondria to have enough “fuel”. The nuclei will also get enlarged as there will be polyploidy (more than two sets of each chromosome!)
Let’s see how the cardiac myocytes will react to pressure overload. This increased pressure will make the cells put their new sarcomeres parallel to the long axis of the cells, making the cross section of the myocytes thicker. Therefore, pressure overload leads to a concentric hypertrophy (the left ventricle gets thickened).
What about volume overload then? The new sarcomeres will be positioned in series with already existing sarcomeres, making the myocytes longer. This is the mechanism of ventricular dilation, which can happen in both right and left ventricles.
Why is this increase in muscle mass so dangerous?
As we know, hypertrophy of the heart muscles can cause heart failure. The muscles may increase in size and they will demand more blood, but the capillaries stay the same, so there will not be enough supply. This poor oxygenation will lead to compensation by increasing the wall tension, heart rate and contractility. The heart can’t continue with this tactic for long and will be vulnerable for decompensation. The cells will begin to induce foetal gene programs, causing a metabolic switch to carbohydrate metabolism, and abnormal proteins and fibrosis will appear.
More about this can be read about in the prep theory here and here.
Concentric left ventricular hypertrophy
As discussed earlier, the cause is increased afterload, which can happen because of
- Systemic hypertension
- Aortic valve stenosis
- Aortic coarctation (rare congenital disorder where the aorta gets narrowed at one point)
The morphology of this type of hypertrophy can be seen in autopsy as a thickened wall, as written earlier, with no dilation. However, if the increased afterload isn’t fixed there will be a secondary ventricular dilation.
The weight will be around 500-600 g.
Dilative left ventricular hypertrophy
Volume overload can be caused by:
- Aortic regurgitation (insufficiency)
- Chronic ischemic heart disease
- Dilative cardiomyopathy (spontaneous or induced by alcohol and drugs)
And will result in a ventricular dilation.
The wall can vary in thickness, but the weight will be extremely high (cor bovinum)! So, it’s always a good idea to measure the weight of the heart in autopsy!
Fibrosis and thrombus formation can be seen as secondary changes following dilatation.
Congestive heart failure
Hypertrophy of the heart muscles will lead to congestive heart failure as the pumping power of the heart will become impaired.
We have two types of failure: forward and backward.
The forward type is when the decreased pump function leads to insufficient supply of the organs. The backward is the congestion in the venous side.
Left sided heart failure often ends up with lung congestion, making the lungs fill up with the blood that the heart can´t pump out.
You can read more about the details of forward and backward failure in the pathophysiology topics.
It should be “fetal” I think. Fetal gene program in failing heart is a complex biological process that involves transcriptional and epigenetic regulation of cardiac genome.
It is also written “fetal” in lecture slide
You’re right, I just checked. It’s in the lecture, and, according to google, the fetal gene program of the heart is a condition where the heart goes back to metabolizing primarily carbohydrates instead of free fatty acids, like it did before birth.
My fault for not checking this the first time. Correcting again now.
søt
in “why is increase in muscle mass so dangerous”, is it supposed to say fetal or may it be fatal gene programs?
It should have been fatal obviously. Fixed now. Nice catch, and thanks!