The fetal ventricular spot is an ultrasound image presentation rather than a cardiac malformation, let alone a diagnosis of cardiac anomaly. The echogenicity of fetal ventricular spots is similar to that of bone echoes, and the intracardiac spots can be classified into three levels: Level I, lower than bone echoes; Level II, the same as bone echoes; and Level III, stronger than bone echoes. It can occur in one or both ventricles; it is usually found in the left ventricle, but can also occur simultaneously (1.5%-7.6%). The strong echogenic spots are between 1-6 mm in diameter and are mostly located near the tendons and papillary muscles. Most of the strong echogenic spots shrink with increasing gestational weeks and the echogenic intensity gradually decreases. They disappear almost completely by full-term gestation, while a few may persist until delivery and can even be observed on postpartum ultrasound. In most fetuses, intraventricular hyperintensities may not be clinically significant. Simple intraventricular strong echogenic spots without the combination of other malformations have a relatively low chance of fetal anomalies. Chromosomal examination is recommended in pregnant women older than 35 years of age. During embryonic development of the ventricle the left and right ventricles undergo separation, continuous absorption and enlargement of the ventricular cavity, and progressive formation of the atrioventricular valve and subvalvular structures (papillary muscles, tendons). The atrioventricular valve is formed by the endocardial cushions, the central endocardial cushion forms the anterior mitral valve and tricuspid septal valve, and the other valve leaflets are formed by the lateral endocardial cushions. The inner wall of the ventricle is constantly absorbing and dilating, and part of the meatus forms the papillary muscle and the tendon cords between the valve and the papillary muscle. The mechanism of the occurrence of strong light spots in the fetal left ventricle, although not completely clear, may be related to intraventricular tendon cord thickening, papillary muscle mineral deposition, early ischemia of the terminal branches of the coronary arteries within the papillary muscle, and incomplete perforation of the papillary muscle tendon cords. Health care measures: 1. No special therapeutic care is needed during the fetal period; 2. Normal delivery can be awaited without special delivery measures; 3. Cardiac ultrasonography is performed after birth. Treatment: No treatment is required. Long-term prognosis: Complete normal life, study and work.