The term “megalocardia” is not a medical term, but rather our description of the manifestation of a giant heart. Giant hearts can occur as a result of a variety of pathologies in the heart and lungs, and heart valve disease is more likely to lead to “giant heart” because of its greater circulatory impact and longer duration, when most patients experience heart failure. So how does heart enlargement occur? First, we need to understand how the heart compensates. Myocardial hypertrophy. Myocardial hypertrophy is primarily the result of an increase in the size of cardiomyocytes. Cardiomyocytes do not normally proliferate. The contraction of hypertrophied myocardium per unit weight heart valve disease increases the load on the heart, and a series of compensatory activities occur in the body, through which the function of the cardiovascular system can be maintained in a relatively normal state, and the patient does not experience significant discomfort, this is the compensatory state, mainly the compensation of cardiac function and metabolism (such as enhanced myocardial contractility and accelerated heart rate) and morphological and structural compensation (myocardial hypertrophy). In normal subjects, compensatory activity of the cardiovascular system is mobilized only during exercise or labor. Patients with heart valve disease, on the other hand, require mobilization of this compensatory activity in the base case. In the early stages of cardiac overload or myocardial damage, the first thing that occurs is mainly functional and metabolic compensation, but at the same time another form of compensation begins to appear, namely myocardial morphological-structural compensation, which is manifested as a decrease in sex but an increase in total cardiac contractility due to the increased weight of the whole heart, so that the hypertrophied heart can remain in a functionally stable state for a considerable period of time, keeping the output per beat and per minute Therefore, the hypertrophied heart can remain in a functionally stable state for a considerable period of time, so that the output per beat and per minute are maintained at a level that is adapted to the needs of the body and the patient does not experience heart failure for a considerable period of time. Therefore, cardiac hypertrophy is a form of compensation that plays an important role in cardiovascular system diseases. Pathologists have long observed two forms of myocardial hypertrophy: centripetal hypertrophy and distal hypertrophy (enlargement of the heart). The mechanism is as follows: when the ventricles are subjected to excessive pressure loads, the increase in systolic ventricular wall pressure can cause a juxtaposition of myocardial fibers in the myocardial fibers, which can thicken (the number of myocardial fibers can also increase when the total weight of the heart exceeds a certain supervening value) and increase the thickness of the ventricular wall, resulting in centripetal hypertrophy. In this way, the thickened ventricular wall keeps the wall tension normal during systole, so that cardiac output does not decrease. When the ventricle is subjected to excessive volume load, the increase in diastolic wall tension can cause crosstalk hyperplasia in the myocardial fibers, increasing the length of the myocardial fibers and thus enlarging the ventricular cavity, i.e., distal hypertrophy, which results in “giant heart disease”. When heart valve disease is chronic, myocardial hypertrophy appears before heart failure. For a considerable period of time, such as years or even decades, myocardial hypertrophy can compensate for cardiac overload or myocardial damage, leaving cardiac function in a compensatory phase. If the cause of the valve lesion continues to act, the above-mentioned compensation is still not enough to overcome the heart dysfunction, the cardiac output will be significantly reduced and the clinical symptoms of heart failure will appear, at this time the heart has developed from the compensated state to the decompensated state, the heart will continue to expand, such “giant heart disease” needs to be removed from the valve lesion as soon as possible surgery.