Over the past two decades, pharmacologic therapy has achieved significant success in reducing mortality in systolic heart failure, but the question of how to reduce mortality in patients with diastolic heart failure remains unresolved. The exact diagnosis of diastolic heart failure is a clinical challenge, and the interpretation of clinical findings is complicated by different diagnostic criteria. In this article, we will discuss the diagnosis and treatment of diastolic heart failure in the context of recent national and international heart failure guidelines and clinical research findings. I. Concept and diagnosis of diastolic heart failure In 2008, the European Society of Cardiology (ESC) defined heart failure as a clinical syndrome containing the following features: 1. Typical symptoms: dyspnea at rest or during exercise, weakness, ankle edema; 2. Typical signs: tachycardia, shortness of breath, pulmonary rales, pleural effusion, increased jugular venous pressure, peripheral edema, hepatomegaly; 3. Objective evidence of structural or functional abnormalities: enlarged heart chambers, third heart sound, heart murmur, abnormal echocardiogram, elevated brain natriuretic level. This definition focuses on the clinical manifestations and diagnosis of heart failure, emphasizes the three major symptoms of heart failure and lists the signs of heart failure in detail, and adds brain natriuretic tests to the objective tests. The 2006 Heart Failure Society of America (HFSA) definition of heart failure focuses more on the etiology and development of heart failure, stating that heart failure is a clinical syndrome caused by cardiac insufficiency, generally as a result of myocardial insufficiency or myocardial loss. It is characterized by dilatation or hypertrophy of the left ventricle, resulting in neuroendocrine malfunction, circulatory abnormalities and typical symptoms: fluid retention, dyspnea, and weakness (especially with exercise). If left untreated, the level of cardiac function and symptoms usually worsen. The severity of clinical symptoms can vary significantly during the disease progression and may not correspond to the status of cardiac function. These definitions all include diastolic heart failure (DHF). Although most heart failure has both systolic and diastolic insufficiency, when symptoms of heart failure are present, it is still classified as systolic and diastolic heart failure based on left ventricular ejection fraction (LVEF). In contrast, heart failure with not low ejection fraction (≥45-50%) is not always due to diastolic insufficiency, so in 2008 the European ESC recommended replacing diastolic heart failure with heart failure with preserved ejection fraction (HF-PEF). It was also proposed that echocardiography has an important role in the diagnosis of HF-PEF, and three conditions need to be met for the diagnosis of HFPEF: 1. signs and/or symptoms of chronic heart failure; 2. normal or mildly impaired left ventricular systolic function (LVEF ≥45-50%); and 3. evidence of diastolic insufficiency (poor left ventricular relaxation or diastolic restriction). This diagnostic criterion is the same as that of the 2005 ESC for diastolic heart failure. Therefore, HF-PEF and DHF are only conceptually different and the clinical diagnosis is not yet difficult to distinguish. The diastolic heart failure mentioned in this paper includes all heart failure with preserved LVEF. II. Etiology and pathophysiological changes of diastolic heart failure Diastolic heart failure and systolic heart failure have similar clinical symptoms, but there are major differences in etiology, epidemiology, pathophysiological changes, treatment and prognosis. About half of the patients with heart failure have diastolic heart failure, which occurs mainly in older women, most of whom have hypertension, and diabetes mellitus is also a common cause. The pathophysiology of diastolic heart failure is characterized by left ventricular centripetal remodeling and normal left ventricular end-diastolic volume. Systolic heart failure, on the other hand, is characterized by a decrease in left ventricular ejection fraction (LVEF) due to off-center left ventricular remodeling. Patients with diastolic heart failure have impaired cardiac diastolic function, including impaired left ventricular perfusion volume due to active myocardial hypoplasia and passive myocardial activity stiffness. The hemodynamic manifestations are an upward shift of the left ventricular end-diastolic pressure-volume relationship curve to the left and increased left ventricular stiffness due to impaired diastolic mechanical motion. III. How to look for evidence of diastolic insufficiency The diagnosis of diastolic insufficiency remains difficult and crucially requires confirmation of a slowing of ventricular diastolic velocity, characterized by increased left ventricular filling pressures in the presence of normal left ventricular volume and systolic function. Echocardiography is of great value in differentiating diastolic from systolic heart failure. Elevated levels of brain natriuretic peptide (BNP) are also useful in the diagnosis of heart failure, including diastolic heart failure: increased left ventricular pressure and volume increase ventricular wall tension, which prompts the release of BNP from the ventricular myocardium. several studies have demonstrated that plasma BNP levels are elevated in patients with diastolic heart failure, but to a lesser extent than in systolic heart failure. The early diagnosis of diastolic heart failure using echocardiography was standard M-mode and 2-dimensional anatomical imaging, including left atrial diameter and volume, left ventricular mass, left ventricular wall thickness, and left ventricular systolic function, with the most important changes being mitral flow velocity and pulmonary venous flow index. Measurement of mitral flow velocity using pulsed Doppler includes four parameters: peak transvalvular flow velocity in early diastole (E), peak transvalvular flow velocity in late diastole (A), early perfusion deceleration time (DT), and A-wave time frame. Normal E/A is 0.75 to 1.5 and DT