Long-term poor control of hypertension can cause structural and functional changes in the heart called hypertensive heart disease, including: early left ventricular diastolic hypoplasia, left ventricular hypertrophy, progressive development of myocardial systolic hypoplasia better eventually heart failure, some studies show that 70% of heart failure caused by hypertension; at the same time may appear associated with coronary heart disease, atrial fibrillation and other cardiac comorbidities. Pathophysiological changes 1, left ventricular hypertrophy (LVH) LVH is a compensatory change of myocardium in response to elevated blood pressure, myocardial contraction is increased to maintain adequate cardiac output, but over time can cause changes such as cardiomyocyte hypertrophy, thickening of myofibers, degenerative changes, and decrease in relative capillary density. In the early stage, myocardial remodeling occurs, i.e., centripetal remodeling, in which cardiomyocytes become hypertrophied but their number does not increase, the arrangement changes, the collagen fibers increase, and gradually the collagen accumulation exceeds 20% and fibrosis occurs to replace the cells that have lost their function, resulting in centripetal hypertrophy, and better later in which increased volume load causes centrifugal hypertrophy. Hypertensive LVH is first reflected in septal thickening, which is a common part of the cardiac circulation, and has a very important role in the systolic function of both the left and right ventricles. 2, diastolic hypoplasia Diastolic heart failure is characterized by reduced left ventricular volume and elevated end-diastolic pressure, with normal or mildly reduced LVEF. This is mainly due to the normal systolic function of the ventricle, while the reduced relaxation and compliance of the ventricular muscle reduces ventricular filling; in order to increase ventricular filling, the left ventricle must increase the filling pressure to obtain normal ventricular filling and heartbeat volume. In addition, LVH causes cardiomyocyte hypertrophy, especially myocardial fibrosis, which changes the diastolic pressure-volume relationship and increases diastolic pressure in the heart chambers. In early hypertensive disease, diastolic hypofunction accounts for about 11% of the structural and functional changes in the heart. 3, hyposystolic function is known to have LVH than those without LVH heart failure 10 times higher, this is because long-term pressure elevation caused by excessive increase in afterload, causing vascular wall thickness and cardiac centripetal hypertrophy and impaired diastolic relaxation, better eventually appear myocardial contractility decreased, the heart chamber enlarged, ventricular end-diastolic volume increased, ventricular filling pressure and atrial pressure are increased, pulmonary venous return obstruction, the occurrence of hypertension Acute or chronic left heart failure in heart disease. Clinical manifestations 1, early clinical manifestations Early manifestations are generally atypical, patients may have no obvious conscious symptoms or only mild discomfort such as headache, chest tightness, etc. These symptoms are mainly the general symptoms of hypertension, no specificity. 2, the progressive clinical manifestations of hypertension due to high arterial blood pressure, preventing the heart from pumping blood, the heart long-term high workload will appear myocardial hypertrophy and increased stiffness, better eventually lead to the pulmonary venous blood into the heart is blocked, the formation of pulmonary stasis. The increase in oxygen demand and the relative lack of blood supply during hypertrophy often lead to heart failure episodes. Diastolic heart failure and systolic heart failure have similar clinical manifestations and are not easily distinguished clinically. The clinical features of heart failure caused by hypertension are as follows: (1) Abnormal diastolic/contractile function of the left ventricle can lead to pulmonary stasis, which mainly manifests as follows: (1) exertional dyspnea; (2) shortness of breath when lying down, which improves when sitting up; (3) dyspnea with little activity, and in severe cases, patients may wake up in their sleep; (4) in severe cases, seated breathing, coughing, and coughing up pink frothy sputum. (2) Left heart failure can often involve the right ventricle function decline, forming total heart failure, the main manifestations are: ① obvious filling of the jugular vein; ② right upper abdominal pain, and hepatomegaly; ③ edema of both lower limbs, and in severe cases, general edema; ④ oliguria. The disease is a cardiac damage induced by cardiac afterload due to long-term elevation of blood pressure. It is emphasized that early blood pressure lowering up to the standard can prevent the occurrence and development of this disease. Long-term, regular anti-hypertensive treatment can improve the degree of damage to the hypertrophied heart and even completely restore the normal form. A treatment plan that solely emphasizes blood pressure lowering and neglects cardiac protection is incomplete and unscientific.