Ventricular hypertrophy

Ventricular hypertrophy . It is an adaptive response to pressure overload. In principle, its purpose is to maintain the wall tension, which, by virtue of Laplace’s Law , is equal to the product of the intracavitary pressure times the radius of the cavity divided by twice the thickness. Maintaining wall tension is necessary to avoid progressive dilation of the chamber, and is one of the main mechanisms by which the heart faces an increased load; this mechanism is particularly evident in pressure overload, such as that following high blood pressure or aortic stenosis.. But also in cases of volume overload, a certain degree of ventricular hypertrophy occurs, although in these cases it is “eccentric”, that is, accompanied by dilation of the cavity. In contrast, hypertrophy is “concentric” in pressure overload.


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  • 1 Types
  • 2 Causes
  • 3 Consequences
  • 4 Pathophysiology
  • 5 Diagnosis
  • 6 Sources


Hypertrophy can occur in both cardiac ventricles, but the most common is left ventricular hypertrophy. The left ventricular hypertrophy occurs caused by hypertension, stenosis or insufficiency (valve, supravalvular osubvalvular) aortic, hypertrophic cardiomyopathy, dilated cardiomyopathy, aortic coarctation, congenital heart disease and persistent ductus arteriosus and septal.

Hypertrophy of the right ventricle is part of diseases such as chronic cor pulmonale, right ventricular overload due to pulmonary arterial hypertension secondary to heart disease affecting the left side of the heart (especially stenosis and insufficiency), pulmonary thromboembolism , congenital heart disease such as isolated pulmonary valve stenosis, Fallot’s tetralogy and interatrial communication.


Cardiac hypertrophy occurs in response to stimuli that trigger signaling pathways that activate cellular responses with increased cell size, increased expression of embryonic genes , accumulation and assembly of contractile proteins , or apoptosis. It can be due to multiple causes, so varied that more than cardiomegaly , it is the disease that causes it that implicitly gives the prognosis; for example if you have rheumatic fever or high blood pressure .


Ventricular hypertrophy generates potential negative consequences for the heart: an increase in the fibrous component of the myocardium and an insufficient increase in the coronary vasculature, which leads to a reduction in the coronary reserve. Ventricular hypertrophy is not a mechanism that can be started without potential negative consequences for the heart. The two most important are:

  • An increase in the fibrous collagen component of the myocardium.
  • An insufficient increase in the coronary vasculature, which leads to a reduction in the coronary reserve. Since there is no parallel increase between the number of capillaries and the size of the myocytes , the density of the capillaries decreases; Furthermore, the coronary reserve does, that is, the ability to increase the basal coronary flow.


Cardiac hypertrophy is characterized by an increase in the individual size of myocytes ( muscle cells ) and an expansion of the extracellular matrix in response to mechanical, hemodynamic, neurohumoral, hormonal, or pathological stimuli . Myocytes and fibroblasts act as biomechanical sensors that express genesembryonic leading to physiological hypertrophy, concentric hypertrophy, eccentric hypertrophy, or apoptosis. Ventricular hypertrophy is frequently accompanied by ventricular arrhythmias, the genesis of which is especially related to the greater degree of interstitial fibrosis and relative myocardial ischemia. Increasing the fibrous component of the ventricle can alter its diastolic properties. The increased end-diastolic pressure favors the development of so-called heart failurediastolic; Furthermore, it hinders coronary perfusion, since it should not be forgotten that coronary perfusion pressure – essentially a diastolic phenomenon – is the difference between aortic diastolic pressure and ventricular diastolic pressure. When coronary heart disease is associated with ventricular hypertrophy, which often results from high blood pressure, the problem increases. Ventricular hypertrophy is frequently accompanied by ventricular arrhythmias, the genesis of which may be related to all the mechanisms discussed above, especially with the higher degree of interstitial fibrosis and relative myocardial ischemia . Perhaps this fact is to blame for ventricular hypertrophy and, according to data from the Framingham heart study, is an independent risk factor for sudden death . Therefore, it is not surprising that ventricular hypertrophy constitutes, also according to Framingham, one of the most powerful risk factors for the development of heart failure.


It is performed based on the signs and symptoms (clinical diagnosis) and is confirmed by diagnostic images, radiology , echocardiography, and the electrocardiogram indicating left ventricular hypertrophy if the sum of the S wave in V1 and the R wave in V5-V6 is greater. 3.5mV. Otherwise it will be a right ventricular hypertrophy.

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