Heart valve disease is a common and frequent clinical condition. In recent years, with the improvement of medical conditions, the incidence of rheumatic heart valve disease has decreased significantly; however, with the aging of the population, valve degeneration, myocardial disease, ischemic heart disease, and metabolic disease caused by valve lesions have increased significantly, and heart valve disease has become a serious threat to people’s physical and mental health. Related data show that in people over 65 years of age, the incidence of aortic valve calcification and thickening is 29% and stenosis rate is 2%, of which 75% combined with aortic valve insufficiency; mitral valve, tricuspid valve and pulmonary valve degeneration, calcified stenosis or insufficiency also increased. Therefore, valvular degenerative disease and heart failure caused by it have become an important threat to the life and health of the aging population. Geriatric heart valve disease, also known as senile degenerative heart valve disease, is a clinical condition in which degenerative changes and fibrosis occur in the connective tissue of the valve with age, resulting in valve thickening, stiffening, deformation, and calcium deposits, leading to valve stenosis and/or closure insufficiency. The disease is a serious cardiovascular disease threatening the health of the elderly and is easily missed and misdiagnosed due to the lack of specific clinical manifestations. Geriatric heart valve disease is prone to cardiovascular complications such as arrhythmias, heart failure, infective endocarditis, and cerebrovascular accidents. Fulkerson and Nair et al. concluded that senile calcific valve disease is not associated with systemic metabolic disorders, especially calcium and phosphorus metabolism, nor with coronary artery disease, rheumatoid or other inflammatory cardiac lesions. The etiology is mainly due to the following factors: (1) bone decalcification deposited in the valve or annulus: Sugihara et al. used a human simulation of computerized systematic measurement combined with ultrasound studies and found that the calcium salts deposited on the mitral annulus were mainly from decalcification of vertebral bone. (2) Metabolic abnormalities: The Bloor study found a high incidence of calcific valve disease in patients with diabetes mellitus and deformational osteitis, and altered carbohydrate metabolism significantly reversed the degree of valve calcification. (3) Valvular degeneration: The Thompson study found that more than 90% of calcific aortic stenosis (CAS) in people over 65 years of age was due to normal valvular degeneration, and the degree of valvular calcification increased with age, and the degree of multivalvular involvement also increased significantly with age. Therefore, calcific valve disease is actually an “aging” change, a degenerative lesion that is closely related to age. (4) Gender differences: 50% to 60% of calcific valve disease is in older women, especially mitral valve lesions. One possible explanation is that the incidence of osteoporosis is higher in older women than in men of the same age, and that the tissue surrounding the mitral annulus is more sensitive to injury in older women, as in rheumatic mitral valve lesions, which occur more frequently in women than in men. (5) Increased pressure on the valve: The increased pressure on the valve and the high velocity of blood flow shear forces tend to cause annular injury, causing tissue degeneration, fibrous tissue proliferation, neutral fat infiltration, or collagen fracture, which facilitates calcium salt deposition and accelerates the calcification process. Clinically, right heart valve calcification is extremely rare, further suggesting that valve calcification is closely related to the pressure to which the valve is subjected. Thus, calcific valvular disease in the elderly mainly involves the aortic and mitral valves, probably for this reason as well. Clinical manifestations Calcific valve disease in the elderly progresses slowly, causing valve stenosis and/or closure insufficiency that is mostly not severe and has less impact on hemodynamics, and is generally less likely to attract the attention of patients and physicians. Once the clinical stage is reached, angina pectoris, syncope, and congestive heart failure are often indicative of more severe lesions. Patients in this stage have an average survival of only 3 years and a sudden death rate of about 15%. Geriatric calcific valve disease differs significantly from heart valve disease in middle-aged adults under the age of 65 in a number of ways. CAS: The most common symptoms of severe calcific aortic stenosis in the elderly are palpitations, weakness, and shortness of breath. Angina pectoris, on the other hand, is a common symptom of aortic stenosis in young and middle-aged adults. Syncope is not uncommon and may be associated with ventricular arrhythmias and conduction block; it occurs more frequently if coexisting with mitral annular calcification. In some patients, prolonged atrial fibrillation or slow arrhythmias make it easy to form thrombi, emboli, or calcified plaque dislodged in the atria, which can produce symptoms of embolism in the body circulation. When there is extensive calcification in the septal membrane, conduction dysfunction may occur by involving the AV node, the bundle of Hirschsprung and the conduction tissue in its vicinity. Systolic murmurs are often present in the aortic valve region, and the best area of auscultation is often at the apex of the heart rather than at the base (Callavardin effect). It is more likely to be heard in the axilla than in the neck, and its loudness is mild to moderate and may be musical. Due to valve calcification, loss of elasticity and fixation, there is often no early systolic jet (karate) sound. The aortic regurgitant murmur is less frequent (only 4%), but once a diastolic murmur is present, it indicates a more severe degree of aortic valve calcification. MAC: Most mitral valve calcifications in the elderly have no obvious clinical symptoms. When the mitral annulus is involved, mitral valve activity can be limited. When severe annular calcification involves the posterior valve and affects its activity, atresia of the mitral valve can occur. The Aronow study found that the presence of a diastolic murmur in the apical region of the elderly was associated with a 90% probability of MAC and was significantly more severe than that of a systolic murmur only. The signs of mitral valve insufficiency due to calcific valve disease are similar to those of chronic mitral stenosis in general, and the presence of mitral regurgitation can lead to atrial arrhythmias with left atrial enlargement. In China, it was reported that 68.2% of MAC patients with atrial fibrillation had left atrial enlargement. Those with mitral regurgitation are prone to complications of bacterial endocarditis. Nair reported that the incidence of cerebral embolism due to MAC is about 11%. Complications: Arrhythmias, heart failure, infective endocarditis, cerebrovascular accidents and other complications can occur. (1) Arrhythmias: About 80% of patients with degenerative heart valve disease have arrhythmias, such as atrial arrhythmias, atrioventricular block, and sick sinus node syndrome, etc. Severe arrhythmias can lead to heart failure or even sudden death. (2) Heart failure: Some reports show that 35% to 50% of patients have congestive heart failure, with cardiac function mostly between class II and III. The annual morbidity and mortality rate of patients with combined heart failure is 15%. (3) Sudden cardiac death: This is the most serious complication of degenerative heart valve disease. The disease can cause fatal arrhythmias, heart failure, and severe valve stenosis and insufficiency leading to sudden death. Sudden death is reported to occur in about 20% to 25% of patients. (4) Infective endocarditis Due to the development of detection methods, the incidence of infective endocarditis caused by this disease has increased compared to the past, and is about 15%. (5) Embolic stroke: Data show that once the mitral annulus is calcified, the risk of cardiogenic embolic stroke increases two to four times. A domestic study confirmed that mitral valve calcification complicated by cerebral infarction accounted for 26.8% of cases, indicating that mitral valve calcification is the basis for thrombosis. Diagnosis The diagnosis is often delayed because there are no clinical symptoms in the early stage of the disease, and late symptoms such as angina pectoris, heart failure and syncope lack specificity. However, with the development of ultrasound technology, the diagnosis rate of this disease has been significantly improved, and calcification caused by other cardiovascular diseases can be excluded by combining with ECG and X-ray. Treatment Currently, it is not possible to effectively halt the progression of this disease. Treatment mainly includes: ① For patients with compensated cardiac function and no clinical symptoms, dynamic observation of changes in the disease is possible, and treatment is generally not necessary. (2) Active treatment of various predisposing factors such as hypertension, coronary artery disease and diabetes mellitus, and active prevention and treatment of various comorbidities such as heart failure, arrhythmia, infective endocarditis, embolism, etc. (3) Pacemakers should be installed in a timely manner for patients with complications such as atrioventricular block and sinus syndrome, and patients in the symptomatic stage should be followed up regularly to avoid accidents. ④Symptomatic patients with severe valve calcification and significant hemodynamic disorders should be advised to undergo surgery or other interventional treatments. (1) Internal drug therapy: mainly symptomatic treatment. When heart failure occurs, digitalis or other positive inotropic drugs, vasodilators and diuretics can be applied. In case of angina attack, calcium antagonists of nitroglycerin and beta-blockers can be given. For slow arrhythmias and atrioventricular block, especially for syncope, an artificial pacemaker should be installed promptly. Drugs that improve calcium and phosphorus metabolism and/or calcium antagonists have not been shown to have a preventive or therapeutic effect on calcification. (2) Valve replacement: It is now recognized as an effective treatment. With improvements in surgery, the morbidity and mortality rate has been greatly reduced (approximately 3% to 18%). Currently, more than 730,000 elderly people worldwide undergo valve replacement each year. The 5-year survival rate after valve replacement is 70.8% for those older than 75 years old, and 99.6% for those whose heart function has improved from class IV to class II. The prognosis for those with severe coronary artery disease who undergo coronary artery bypass grafting at the same time is more obvious. ①Surgical indications: At present, it is mostly advocated that a transvalvular pressure difference of ≥50 mmHg and an orifice area of ≤0.75 cm2 are the “gold standard”. Patients with severe mitral regurgitation without symptoms of MAC should be evaluated for exercise tolerance, and patients with symptomatic mild to moderate mitral regurgitation should also be monitored hemodynamically to objectively assess whether the patient has pulmonary artery and pulmonary venous hypertension in combination with exercise. ② Factors affecting the prognosis of surgery: Age: High morbidity and mortality rate in advanced age. Age > 70 years is 2.5 times the postoperative mortality rate of the < 70 years group; cardiac function: preoperative cardiac function is significantly reduced, the mortality rate is 5-20 times that of patients with normal cardiac function; coronary artery disease: severe coronary artery disease (coronary stenosis > 70%) its postoperative mortality rate is 2.7 times higher than that of non-coronary artery disease; lung, liver, kidney disease or diabetic peripheral vascular disease has a poorer prognosis; ⑤ transvalvular pressure difference. In general, surgical survival is inversely related to transvalvular pressure difference. The major causes of death during perioperative valve replacement are, in order, reduced cardiac output, severe ventricular arrhythmias, prosthetic valve endocarditis, cerebral complications, and renal failure, while the main factors associated with death are, in order, unsatisfactory myocardial protection, cardiac block time ≥120 min or extracorporeal circulation time ≥160 min, previous history of valve surgery, cardiothoracic ratio ≥0.7, preoperative cardiac function III and IV class and aortic stenosis, etc. Balloon valvuloplasty (PBAV): Since its clinical application in 1986, PBAV has become an important non-surgical interventional treatment. It is safe and low cost. It is easy for patients to accept, especially for elderly patients who are not suitable for surgical treatment. The main complications are bleeding, hypotension, embolism and regurgitation, but they are mild. Acar has performed PBAV in 56 elderly patients >78 years old with a success rate of 93%. The complication of pericardial tamponade was 1.8%. Acute myocardial infarction was 3.6%, vascular trauma was 5.3%, and the overall morbidity and mortality rate was 7.1%. However, postoperative valve restenosis after PBAV is an important unresolved problem. waller believes that balloon dilation mainly dilates the aortic wall and ruptures calcified plaque, and postoperative restenosis may be due to elastic retraction of the overexpanded aortic wall. Some follow-up results show that valve restenosis occurs in about 80% of patients at 5 to 17 months after surgery. Because of this excessive rate of late restenosis, some scholars in recent years have suggested that PBAV is only a palliative therapy for short-term symptomatic relief. Indications: Percutaneous balloon aortic valvuloplasty is indicated for patients with aortic stenosis with or without mild regurgitation, one of the four symptoms of angina, syncope, heart failure, and cardiac enlargement, and an aortic orifice area <0.75 cm2 and a transvalvular pressure difference of 6.67 kPa (50 mmHg), or a transvalvular pressure difference <9.33 kPa (70 mmHg) despite mild symptoms and refusal or intolerance of surgical who refuse or cannot tolerate surgical valve replacement. Contraindications: ①Aortic stenosis combined with moderate or severe aortic regurgitation. (ii) Cardiac catheterization is contraindicated. ③Severe coronary artery disease or other valvular disorders requiring surgical treatment. PBAV success criteria: ① aortic transvalvular pressure difference decreased by ≥ 50%; ② orifice area increased by ≥ 25%; ③ murmur reduced or disappeared; ④ cardiac output increased. Prognosis and prevention of age-related heart valve disease (1) Prognosis: There is no reliable method to stop the occurrence and development of this disease. In most cases, the clinical symptoms of the disease are mild, and once symptoms appear, the disease deteriorates rapidly and most deaths are due to serious complications such as arrhythmias and heart failure. (2) Prevention: Because the etiology and pathogenesis are not fully understood, preventive measures have not yet made breakthroughs, mainly: Actively treat susceptibility factors, such as hypertension, hyperlipidemia, diabetes mellitus, coronary artery disease, subaortic stenosis, etc. Active prevention and treatment of its complications, such as cardiac insufficiency, arrhythmia, infective endocarditis, thrombosis, etc. It is believed that in the near future, with further research on the pathogenesis, effective measures to delay cardiac degeneration and treat valvular calcification will be found, resulting in a significant reduction in its incidence and morbidity and mortality rate.