When the heart contracts, the anterior wall of the left ventricle strikes the chest wall in the precordial region early in systole, causing the corresponding part of the rib question tissue to pulsate outward, called apical pulsation. After myocardial infarction of the left ventricle, the entire myocardium of the ventricular wall is necrotic. In about 10-38% of cases, the necrotic myocardium is gradually replaced by fibrous scar tissue, forming a ventricular wall tumor. The thin layer of the ventricular wall in the lesioned area bulges outward, and the heart loses mobility or shows paradoxical motion during contraction. The evolution of coronary artery obstruction, myocardial infarction, myocardial fibrosis, and left ventricular wall tumors was well understood as early as 1881. Ventricular wall tumors in the left ventricle cause loss of myocardial contractility in the lesioned area and can produce reverse beats. The ventricular wall tumor expands outward during ventricular systole and retracts during diastole, resulting in a decrease in left ventricular ejection volume. Normal myocardial contractility is enhanced, tension is increased, and myocardial oxygen demand is increased. When the volume of the ventricular wall tumor exceeds the end-diastolic volume of the left ventricle by 15% or more, the end-diastolic pressure of the left ventricle increases. Left ventricular failure is progressively worsened due to the impairment of left ventricular blood displacement. Once the thrombus is dislodged from the ventricular wall tumor, embolism of the body circulation can occur. The following diseases are also causes of reverse pulsation: 1. Myocardial infarction complicated by left ventricular wall tumor After myocardial infarction in the left ventricle, the entire myocardium of the ventricular wall is necrotic. In about 10-38% of cases, the necrotic myocardium is gradually replaced by fibrous scar tissue, forming a ventricular wall tumor. The thin layer of the ventricular wall in the lesioned area bulges outward, and the heart loses mobility or shows paradoxical motion during contraction. The evolution of coronary artery obstruction, myocardial infarction, myocardial fibrosis and left ventricular wall tumor was well understood as early as 1881. the clinical diagnosis of left ventricular wall tumor has progressed rapidly since the 1960s. closed ventricular wall tumor resection was performed by Likoff and Bailey in 1955. the first ventricular wall tumor resection was successfully performed by Cooley in 1958 under extracorporeal circulation. 2. Double outlet of the left ventricle Double outlet of the left ventricle means that both large arteries originate in the left ventricle, the opening of both arteries is in the same plane, the conus and conus muscles are bilaterally underdeveloped, and the aortic and pulmonary valves, the semilunar valve and the mitral valve are continuous with each other. It is a very rare congenital cardiovascular malformation. It is often associated with ventricular septal defect, pulmonary stenosis, tricuspid valve subluxation, right ventricular hypoplasia, atrioventricular inconsistency, and orthotropic or retrograde atria and viscera. Altered left ventricular double outlet hemodynamics resembling severe tetralogy of Fallot or complete aortic malposition with ventricular septal defect. 3. thoracoabdominal aortic aneurysm (TAA) is an aortic aneurysm that involves both the thoracic and abdominal segments, as well as an abdominal aortic aneurysm that invades above the renal artery, are referred to as thoracoabdominal aortic aneurysms. Despite a variety of surgical procedures and adjuvant modalities to reduce surgical complications, there is still a 5% to 10% perioperative mortality and ischemic complications of the kidney, lung and spinal cord.