The heart is a muscle and as with any muscle, when it has to work against a higher pressure over a prolonged period of time, it becomes more muscular. This increased muscle mass is seen as an increased thickness in the walls of the heart and is known as hypertrophy. Doctors sometimes erroneously refer to this as an enlarged heart. This is not true – the heart is not bigger but it is heavier; the walls are just more muscular and therefore appear thicker than normal. This is why a more muscular heart does not appear abnormal on a chest x-ray. As the left ventricle is the chamber of the heart that pumps blood around the whole of the body, any sustained increase in pressure that the left ventricle works against will result in the development of left ventricular hypertrophy (LVH). Similarly the right ventricle has to pump blood to the lungs and if it has to do so against a higher pressure for a long time then this will lead to right ventricular hypertrophy (RVH).
What are the causes of hypertrophy
The commonest cause of LVH is hypertension (high blood pressure). Another important cause is a valvular abnormality called aortic stenosis – abnormal narrowing of the aortic valve which controls the outflow of blood from the heart when the heart contracts which results in increasing the work that the heart has to do to pump the blood out.
Common causes of RVH are pulmonary hypertension (increased blood pressure in the pulmonary circulation) and pulmonary stenosis – a rare abnormal narrowing of the the pulmonary valve which controls the outflow of blood from the right heart.
LVH is seen far more commonly than RVH.
Mild LVH may also be a normal finding in afrocaribbean or african-american patients.
It is also well recognised that athletes may also mild left ventricular hypertrophy. This is known as athlete’s heart.
Sometimes the heart may look more muscular, not because it has had to work harder, but because the muscle itself is genetically abnormal (hypertrophic cardiomyopathy) or because the muscle has been infiltrated by abnormal substances (cardiac amyloidosis, Fabry’s disease, haemochromatosis ect)
What are the problems associated with hypertrophy?
The reason hypertrophy of the heart is important is two fold:
Firstly, hypertrophy may be a sign that the heart is having to work harder and thereby should prompt a search for the underlying cause. Additionally the hypertrophy may prompt a search for a possible infiltrative condition which in itself may be dangerous and require treatment.
Secondly, the hypertrophy itself may cause harm. As the heart becomes more muscular, it becomes stiffer. Hence although it can contract strongly to pump blood out of the heart, it takes much longer to relax because of its stiffness. This is otherwise known as diastolic dysfunction and and this therefore means that a hypertrophied heart does not fill as well with blood as a normal heart. When the heart does not fill with as much blood as it should, it pumps out less blood then expected and this reduction in output will be sensed by the kidneys which will try and counteract this by producing hormones which in turn will put more strain on the heart. This can then be counterproductive and thereby cause even more hypertrophy and eventually an extremely muscular heart may start outstripping its own blood supply and therefore lead to the heart weakening over a period of time.
Another problem is that a hypertrophied heart is more likely to be electrically irritable and therefore there is a higher incidence of all the known heart rhythm disturbances in the hypertrophied heart.
How do we diagnose hypertrophy?
As the heart does not enlarge as such, hypertrophy can not be diagnosed on a simple chest X-ray
The definitive test is an echocardiogram (an ultrasound examination of the heart) which allows visualisation and measurement of the abnormally thick walls of the heart. The problem however is that echocardiography is a specialised investigation which is not as easily available as chest x-rays or ECGs
An ECG can however be helpful. As the cardiac electrical impulses have to travel through a larger muscle mass, the size/amplitude of the ECG complexes may be significantly increased. The presence of very large complexes on the ECG should always prompt further investigation in the form of an echocardiogram – firstly to confirm the hypertrophy and secondly to determine the underlying cause. The absence of very large ECG complexes does not however exclude hypertrophy and therefore in patients who have high blood pressure, an echo is useful regardless.
We know from many studies that the presence of LVH on ECG or Echo is associated with increased risk of adverse outcomes such as heart attacks, strokes, heart failure, dangerous heart rhythm disturbances and sudden death.
How do we treat hypertrophy?
The first thing is to work out the cause and aggressively treat the cause. As most patients will have LVH due to high blood pressure, treating any underlying causes of the blood pressure as well as controlling the blood pressure through lifestyle changes and medications can help regress the hypertrophy.
Lifestyle changes are immensely important and include attention to diet (including avoidance of smoking and alcohol), regular cardiovascular exercise and weight loss, and attention to good sleep hygiene and stress management)
Whilst most anti-hypertensive medications have similar effects on lowering of the blood pressure numbers, research indicates that they don’t all have the same effect on regression of LVH. In particular, angiotensin receptor blockers (these usually end in ’sartan’ such as losartan, valsartan, candesartan and telmisartan) are perhaps the most effective agents at regressing hypertrophy. Calcium blockers (which end in ‘ine’; such as nidefidipine, lercanidipine and amlodipine) and ACE inhibitors (which end in ‘il’ as in ramipril, perindopril, lisinopril and enalapril) are also effective although not as effective as the sartans. Diuretics (end in ‘ide’ e.g. bendrofluazide, indapamide and hydrocholorthiazide) and Beta blockers (end in ‘ol’ e.g atenolol, bisoprolol and timolol) however are perhaps the least effective agents and this is one reason why they are no longer prescribed as first line agents in hypertension treatment.
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Tags: LVH, Left ventricular hypertrophy, high blood pressure, hypertension, RVH, right ventricular hypertrophy