Causes
The term left ventricular hypertrophy (IVS) describes the increase in muscle mass in the left ventricle.
In many cases, the IVS arises as a long-term compensatory mechanism in response to an overload :
- of pressure (as happens in hypertensives and in those who practice power sports, such as weight lifting)
- or volume (as happens with endurance athletes, such as cyclists, marathon runners, swimmers and cross-country skiers).
The heart, in fact, is a muscle and as such can undergo structural modifications (hypertrophy, hypotrophy, shortening and lengthening of its own fibers) in relation to work and biochemical stimuli (hormones, such as GH, catecholamines, insulin, and enzymes, such as angiotensin II) to which it is subjected.
In other cases, left ventricular hypertrophy is caused by intrinsic factors, such as hypertrophic obstructive myocardiopathy.
The most common cause of left ventricular hypertrophy is prolonged arterial hypertension . If the peripheral resistances increase the left ventricle must contract with greater intensity to overcome them, completely empty themselves and push the blood into the periphery. This phenomenon, in the long run, causes cardiac changes which, added to the coronary ones induced by hypertension, strongly increase the cardiovascular risk (up to triple it compared to hypertensive subjects but without IVS).
Further haemodynamic causes of left ventricular hypertrophy are represented by stenosis of the aortic valve (a flap that separates the left ventricle from the aorta, the large blood vessel that carries oxygen-rich blood to the various parts of the body) and its regurgitation. The partial obstruction (stenosis) of the aortic or semilunar valve requires a more vigorous contraction of the left ventricle, necessary to overcome the resistance offered to its emptying. When regurgitation is present, however, the aortic valve does not close properly and the left ventricle fills more than necessary, requiring more effort to pump blood to the periphery.
In patients with a previous cardiac infarct, left ventricular hypertrophy is the result of an adaptive heart response, implemented to compensate for the function of those muscle areas lacking contractile capacity.
From the morphological point of view, it is usual to distinguish left ventricular hypertrophy in concentric, eccentric and asymmetric.
- Concentric hypertrophy is the consequence of a prolonged pressure overload, which leads to an increase in wall thickness, a reduction in the capacity for ventricular distension and a reduction in the intraventricular diameter. It can be physiological, in response to predominantly isometric or pathological power training, due, for example, to high blood pressure.
- Eccentric hypertrophy is the consequence of a prolonged volume overload that leads to an increase in wall thickness and intraventricular diameter (the thickness / radius ratio does not increase as in the previous case but remains within the normal range). Eccentric hypertrophy recognizes non-pathological causes, as occurs in predominantly isotonic or pathological resistance training, for example in valvular insufficiencies, in obesity and in the late phase of hypertensive heart disease.
- Asymmetric hypertrophy is characterized by asymmetric hypertrophy of the septum and is found, for reasons not yet clear, in a small percentage of hypertensive patients.
Symptoms
To learn more: Symptoms Left ventricular hypertrophy
Tendentially, left ventricular hypertrophy develops gradually, and is more common among elderly and hypertensive people.
Especially at an early stage, it does not cause any particular signs or symptoms; when these appear they can include chest pain, palpitations, dizziness, fainting, shortness of breath and reduced resistance to physical effort.
Care and therapy
See also: Drugs for the treatment of Ventricular Hypertrophy
Just as it happens with our muscles, the phenomenon of left ventricular hypertrophy, secondary to hypertension or long-term training is, at least partially, reversible (not always completely because the fibrotic component, typical of hypertensive IVS, regresses with difficulty).
It is therefore essential that the medical therapy of hypertension be started early; better still to intervene in the preventive field, controlling the diet, the level of stress, abolishing smoking and increasing the level of physical activity. In fact, while on the one hand the regression of left ventricular hypertrophy reduces the cardiovascular risk in hypertensive patients, on the other it keeps it at levels that are higher than those who, despite having high blood pressure, have never suffered from IVS. We must also not overlook the fact that the regression of IVS of hypertensive origin is almost never complete, precisely because of the poor reversibility of the fibrotic component.
In the presence of overt hypertension, therefore, action will be taken with adequate dietary strategies (reduction of salt in the diet) and pharmacological strategies (ACE inhibitors, Angiotensin II receptor antagonists, B-blockers, etc.).
If left ventricular hypertrophy is caused by stenosis of the aortic valve, surgery may be necessary to remove it and replace it with an artificial, animal or human origin. Even in the presence of aortic valve regurgitation, surgical repair or replacement should be considered.
Role of Sport
As regards fitness for sports in the presence of left ventricular hypertrophy, it is necessary to first of all evaluate the benign origin of the disease, distinguishing it from hypertrophic myocardiopathy (CMI), which represents one of the most common causes of sudden death in young athletes.
The distinction between the two conditions is made by the doctor on the basis of various elements collected during the anamnesis (type of sport practiced, familiarity with the pathology) and diagnostic examinations for assessment.
To cite some examples, an athlete's heart can be distinguished from a heart affected by hypertrophic myocardiopathy due to the increase in the ventricular cavity (which may be normal or diminished in the presence of CMI) and for a parietal thickness of less than 16 mm (can be superior in the presence of CMI).
To confirm his / her diagnosis, the doctor may request the suspension of the training activity for a few months, in order to assess the degree of reversibility of the left ventricular hypertrophy (if low it indicates probable CMI and vice versa).
