This type is characterized by hypertrophy of the ventricular myocardium, typically in the left ventricle, especially in the septum, and occasionally as concentric hypertrophy. The left ventricular chamber volume is normal or reduced. Occasionally, the lesion occurs in the right ventricle. It is usually autosomal dominant. The etiologic pathology is dominated by myocardial hypertrophy and increased heart weight. Myocardial hypertrophy is seen in both the septum and the free wall, with the former being the most common, often asymmetric (non-concentric) hypertrophy, that is, varying degrees of hypertrophy in various parts of the ventricular wall, with the left ventricle being the most common and the right ventricle being the least common. If the septum is highly hypertrophied and protrudes into the left ventricular cavity, causing obstruction of the left ventricular outflow tract during systole, it is called “hypertrophic obstructive cardiomyopathy”, formerly known as “idiopathic hypertrophic subaortic stenosis”. The septum is less thickened and does not cause significant obstruction of the left ventricular outflow tract during systole, which is called “hypertrophic nonobstructive cardiomyopathy. The anterior papillary muscle can also be hypertrophic and is often displaced to affect normal valve function. In highly hypertrophic myocardium, the left ventricular cavity is reduced. There is a variant of hypertrophic cardiomyopathy in which myocardial hypertrophy is more prominent in the apical region. In this type, the subepicardial coronary arteries are normal, but the number of coronary arteries in the ventricular wall is increased and the lumen is narrowed. Microscopically, myocardial cells are disorganized, with abnormal nuclei, many branches, increased mitochondria, extreme hypertrophy of myocardial cells, increased intracellular glycogen content, and interstitial fiber hyperplasia. In 2/3 of the patients, the mitral leaflet was enlarged and grew, and a fibrous plaque on the left intraventricular wall opposite the anterior mitral leaflet was the result of a collision between the mitral valve and the ventricular septum. The disease can occur at all ages, but myocardial hypertrophy is more severe in those under 40 years of age than in those over 40 years of age, and the cause of this hypertrophy in relation to age is not known. As the disease progresses, myocardial fibrosis increases, ventricular wall hypertrophy decreases, and the degree of narrowing of the heart chambers decreases, showing advanced manifestations. Pathophysiology: 1. Left ventricular outflow tract obstruction During systole, hypertrophic myocardium narrows the ventricular outflow tract. In the non-obstructed type, this effect is not yet obvious, but in the obstructed type it is more prominent. During ventricular systole, the hypertrophied septal muscle projects into the ventricular cavity, and in the left ventricle, the anterior leaflet of the mitral valve in the outflow tract is displaced forward in close proximity to the septum, causing narrowing of the left ventricular outflow tract and incomplete mitral valve closure, which is more pronounced in mid- and late systole. In the early stage of left ventricular ejection, the outflow tract obstruction is light and ejects about 30% of the heartbeat volume, while the remaining 70% ejects when the obstruction is obvious. Therefore, the carotid wave shows a rapidly rising ascending branch, descends and then goes up again into all traces, and then slowly descends. Outflow tract obstruction causes a pressure difference between the left ventricular cavity and the outflow tract during systole, with no pressure difference between the outflow tract and the aorta. In some patients, outflow tract obstruction is not obvious at rest, but becomes obvious after exercise.2. Abnormal diastolic function The hypertrophic myocardium has reduced compliance and poor dilatation ability, so that ventricular diastolic filling is impaired and end-diastolic pressure can be increased. Diastolic chamber stiffness increases and left ventricular dilatation decreases, resulting in reduced heart beat volume, increased filling and compression of coronary arteries within the ventricular wall. Myocardial ischemia is caused by myocardial oxygen demand exceeding the coronary blood supply, narrowing of the coronary arteries in the ventricular wall, prolonged diastole, and increased tension in the ventricular wall. Clinical manifestations are slow in onset. About 1/3 of them have family history. Most of the symptoms begin before the age of 30. Men and women are equally affected. The main symptoms are: (1) dyspnea, mostly after exertion, due to reduced left ventricular compliance, increased end-diastolic pressure, followed by increased pulmonary venous pressure and pulmonary stasis. Mitral valve insufficiency associated with septal hypertrophy may aggravate pulmonary stasis. (2) Precordial pain, which mostly occurs after exertion, resembles angina pectoris but is atypical, due to increased oxygen demand of hypertrophied myocardium and relatively insufficient blood supply of coronary arteries. (3) Weakness, dizziness and fainting, which occur mostly during activity, are caused by the accelerated heart rate, which further shortens the diastolic phase of the already poorly filled left ventricle, which further shortens the diastolic phase of the already poorly filled left ventricle, aggravating the underfilling and decreasing the cardiac blood output. The sympathetic nerve action strengthens the contraction of the hypertrophied myocardium during activity or emotional excitement, aggravating outflow tract obstruction and causing a sudden decrease in cardiac output. ④ Palpitations, due to cardiac decompensation or arrhythmia. ⑤ Heart failure, mostly seen in advanced patients, due to decreased myocardial compliance, significantly increased end-diastolic ventricular pressure, followed by increased atrial pressure, and often combined with atrial fibrillation. In advanced patients, myocardial fibrosis is extensive and ventricular systolic function is also reduced, predisposing them to heart failure and sudden death.