Cardiovascular diseases are consistently linked and gradually exacerbate each other's severity. So, atherosclerosis gives rise to coronary disease, and hypertension - an increase in the left ventricle of the heart. These conditions simultaneously accelerate the development of heart failure, increase the likelihood of developing a myocardial infarction or angina pectoris.
Some of the adverse events that lead to cardiovascular disease can be recognized at an age when they can be properly corrected. Therefore, special attention should be paid to such concepts as left ventricular hypertrophy (LVH) and dilatation, as well as to study the diseases in which they appear, to try to form a prognosis and tactics for their correction.
The concept of hypertrophy and dilation
Hypertrophy and dilatation are those morphological phenomena that lead to an increase in the size of the heart, mainly due to the left ventricle andatrium, less often due to the right ventricle of the heart. Hypertrophy is an increase in the left ventricle of the heart, thickening of the myocardium, primarily the interventricular septum and posterior wall, caused by physical training or diseases that disrupt intracardiac hemodynamics (malformations and hypertrophic cardiomyopathy) and afterload (hypertension). LVH is accompanied by an increase in stroke volume and an acceleration of contraction, allowing more blood to be pushed into the receiving vessels at higher pressure.
Dilatation - stretching and thinning of the walls of the myocardium, caused by a deterioration in the nutrition of the heart muscle and their inability to withstand the actual blood pressure inside the cavities, which is accompanied by an increase in LV filling and a significant decrease in its ejection fraction. This process inevitably follows severe hypertrophy due to its decompensation or appears primarily as a result of the development of dilated cardiomyopathy.
Detection of LV enlargement
Enlargement of the left ventricle of the heart, the causes of which will be indicated below, can be determined by a simple examination of the patient, during echocardiography, ECG or x-ray diagnostics. Often this becomes an asymptomatic diagnostic finding when the patient is examined for other reasons.
Signs of hypertrophy will be an increase in the percussion borders of the heart, a shift of the apex beat to the left and an expansion of its area, which can be determined during a medical examination. With dilatation, percussion borders alsodilated, but the apex beat is diffuse and weak, may not be detected at all in overweight patients. So you can suspect an increase in the left ventricle of the heart (what is it from the point of view of medicine - read below).
Electro- and echocardiography
When an ECG is performed by a functional diagnostic physician, a conclusion is often made about hypertrophy based on the calculation of standard indices based on measuring the voltage of the R and S waves in the chest leads. Dilatation of the cavities using ECG is determined indirectly on the basis of systolic overload, which cannot reliably indicate an increase in the left ventricle of the heart. Treatment only on the basis of the ECG in this case cannot be prescribed if it is not about concomitant arrhythmias.
ECG when detecting structural pathologies of the heart is just one of the reasons to prescribe an ultrasound of the heart, which will make it possible to measure the size of the organ cavities and determine the thickness of the myocardium. In dilatation, the heart is dilated along with a decrease in wall thickness, and in hypertrophy, the myocardium thickens, often leading even to a reduction in the ventricular cavity.
X-ray diagnostics
Hypertrophy or dilatation, especially severe, can be determined by X-ray. Fluorography or radiography allows you to see the configuration of the heart. In hypertrophy due to aortic valve disease, there is a corresponding configuration with the expansion of the left ventricle and the usual size of the atrium.
When mitral valve disease is affected, the configuration is very different: it shows expansionatria with normal or only slightly enlarged LV. Hypertrophic cardiomyopathy can even be marked by a specific configuration, which, due to its large size, is called a “bull's heart”. In dilated cardiomyopathy, x-rays show signs of aortic and mitral configuration, often associated with expansion of the right borders of the heart.
The role of LVH and dilatation in the development of CHF
The relationship between hypertrophy, dilatation, acute coronary syndrome and congestive heart failure is direct and fairly easy to follow. As a result of long-term hypertension or the presence of an uncorrected defect, the normal myocardium hypertrophies and compensates for the influence of these diseases for a long time. With further increase in the left ventricle of the heart and atria, first transient and then permanent ischemia develops, which gradually leads to the death of myocardial cells. The result is a weakening of the walls of the heart, which is most pronounced in the left ventricle, causing pulmonary hypertension and first left ventricular and then total heart failure with congestion in the circulation.
Causes of LVH and dilatation
All known causes of an increase in the left ventricle of the heart must be clearly differentiated as factors in the development of either hypertrophy or dilatation. These morphological changes in the structure of the heart muscle have a different origin, but the same outcome, which depends on the degreemyocardial transformation. Among the causes of left ventricular hypertrophy should be highlighted:
- physical strength and dynamic exercises, fitness;
- arterial hypertension;
- hypertrophic cardiomyopathy;
- compensated aortic stenosis or aortic insufficiency;
- compensated heart defects.
Causes of dilatation of the heart are much less, and they should be divided into primary and secondary. The primary ones include hereditary dilated cardiomyopathy, a disease associated with a defect in the structural proteins of muscle cells. For this reason, the myocardial wall cannot withstand the blood pressure inside the cavities of the heart, which is why it gradually stretches and becomes thinner. Secondary causes of dilatation include decompensation of congenital and acquired defects, acquired dilated cardiomyopathy (alcoholic, toxic or radiation).
Degrees of hypertrophy
Above is an explanation of the concept of what an increase in the left ventricle of the heart means, however, how it should be interpreted should be understood in more detail. If with dilatation the prognosis for the development of heart failure with a drop in ejection fraction is inevitable, then with LVH this can be avoided in most situations. Therefore, to form a prognosis, it is proposed to more fully assess the extent of hypertrophy according to echocardiographic criteria.
Normal LV wall thickness in women is 0.6 – 0.9 cm, andin men, 0.6 - 1.0 cm in the region of the interventricular septum (IVS) and the posterior wall of the left ventricle (PLV).
With a mild degree of hypertrophy in women, there is a thickening of the LVL and IVS up to 1.0 - 1.2 cm, with an average degree - 1.3 - 1.5 cm, and with a severe degree - more than 1.5 cm.
In men, a mild degree of LVH is observed when the thickness of the IVS and ZSLZh is within 1.1 - 1.3 cm, the average degree is 1.4 - 1.6 cm, and in severe - 1.7 or more.
Physiological hypertrophy
In the framework of sports medicine, there is such a thing as physiological functional hypertrophy caused by intensive training of the body, myocardium and skeletal muscles. This process allows the heart to contract more strongly and push more blood into the receiving arteries, which ensures that the muscles of the body are intensively nourished than in an untrained patient.
Physiological hypertrophy is the more pronounced, the harder the sport, and the more dynamic or static loads it requires. However, what distinguishes it from pathological hypertrophy is that it leads to an increase in the ejection fraction of the left ventricle of the heart. That is, a portion of blood that has entered the left ventricular cavity is pushed out more completely than in an untrained patient, faster and stronger. If a he althy person has an ejection fraction of about 65-70%, then for an athlete it can be 80-85% or higher.
This is what determines the ability of the heart to overcome intense physical activity. However, physiological LVH is rarelygoes beyond the boundaries of a mild degree according to echocardiography, and is also characterized by a rich network of collaterals in the myocardium. Because of this, the risk of developing heart failure in the absence of other more important factors, such as hypertension, is quite low. In this case, hypertrophy is needed to increase the fraction of the left ventricle of the heart, and not to overcome the total peripheral vascular resistance, as in the case of hypertensive hypertrophy.
Combined hypertrophy
If an athlete has hypertension, professional training should be stopped, as LVH will take on the character of not a compensatory mechanism, but a pathological one. The only reason inherent in the increase in the left ventricular ejection fraction of the heart will now work against the increase in exercise tolerance. There will be an increase in myocardial volume, after which the subepicardial areas will begin to experience constant ischemia. This will inevitably lead to the appearance of angina, will increase the risk of early development of myocardial infarction.
LV enlargement treatment
In the debatable question of how to treat an enlarged left ventricle of the heart, there will not soon be an adequate unambiguous answer for the reason that this condition is not considered as a disease, with the exception of heart defects and dilatation. In hypertension, the main drugs that reduce pressure can prevent the development of LVH. All ACE inhibitors (Enalapril, Lisinopril, Quinapril, Ramipril), angiotensin receptor blockers (Candesartan,"Losartan", "Valsartan"), diuretics ("Indapofon", "Hydrochlorothiazide", "Furosemide", "Torasemide").
Prevention of LVH
The doctor, prescribing a combination of drugs for the treatment of hypertension or heart failure, thereby slows down the development of hypertrophy and dilatation. This means that the prevention of hypertrophy is effectively achieved during the pharmacological treatment of hypertension, malformations, acute coronary syndromes and subsequent angina pectoris.
In situations where a certain heart defect has been identified in a patient, it is reasonable not to wait for the time of decompensation, when hypertrophy transforms into dilation, but to correct the disease surgically. In the case of decompensation of hypertrophic (especially concentric or obstructive) or dilated cardiomyopathy, young patients are available for heart transplantation or temporary implantation of left ventricular prostheses.
