To investigate the relationship between left ventricular pseudotendinous cords and their characteristics and early repolarization syndrome. Methods Thirty-one patients with early repolarization syndrome (ERS group) and 100 healthy subjects (control group) were selected by simple randomization method, and the incidence of left ventricular pseudotendinous cords, the composition ratio of the location and number of left ventricular fibromuscular tracts, the length and width of left ventricular pseudotendinous cords, and the angle between left ventricular pseudotendinous cords and ventricular septum were statistically analyzed.
The difference in the incidence of left ventricular pseudotendinous cords between the ERS group and the control group was not significant (P > 0. 05); the difference in the composition ratio of different numbers of left ventricular pseudotendinous cords, length and width between the two groups was not significant (P > 0. 05); the difference in the composition ratio of the location of left ventricular pseudotendinous cords between the two groups was significant (P < 0. 001); the left ventricular pseudotendinous cords starting from the middle of the septum and ending at the middle of the left ventricular free wall were about 47% in the ERS group and only 2% in the control group; the angle between the left ventricular pseudotendinous cords and the septum was significantly higher in the ERS group than in the control group (P < 0. 001). The angle between the left ventricular pseudotendon and the septum was significantly higher in the ERS group than in the control group (P < 0. 01).
Conclusion The position and angle of the left ventricular pseudotendinous cord are independent risk factors for early repolarization syndrome, which is presumed to be related to the inconsistent repolarization caused by the pull of the left ventricular pseudotendinous cord on the start and end points, resulting in earlier repolarization of part of the subendocardial myocardium than the normal excitation sequence.
I. Study subjects
1. Early repolarization syndrome group: 31 patients with early repolarization syndrome between December 1999 and April 2002, mean age (33.5 ± 9.7) years, 30 males and 1 female, except for acute myocardial infarction, variant angina, acute pericarditis and electrolyte disturbance, were selected.
2. Control group: 100 healthy normal subjects were randomly selected by lot, 58 males and 42 females, with an average age of (31. 6 ± 7. 2) years, without any electrocardiographic abnormalities.
II. Study methods
1. Detection of left ventricular pseudotendinous cord
Echocardiography was performed in both groups of subjects. The HP 5500 color Doppler echocardiograph with a probe frequency of 2.5 MHz was used to examine the long-axis view of the parasternal left ventricle, the short-axis view of the parasternal left ventricle, the apical four-chamber view, the two-chamber view, and the sagittal view of the long axis of the left ventricle by moving the probe up or down and adjusting the direction of the acoustic beam appropriately to perform multi-sectional and multi-angle examinations. The diagnosis of left ventricular pseudotendinous is made when a hyperechoic band in the left ventricular cavity is observed in 2 or more views.
The number, location, length, width and angle of the left ventricular pseudotendinous cords were recorded, and the length, width and angle of the left ventricular pseudotendinous cords were measured at the end of diastole. The left ventricular pseudotendinous cord attachment point to the ventricular septum was designated as the starting point according to the order of normal myocardial excitation, while the other point was the stopping point, and if both attachment points were in the ventricular septum, the point above was the starting point.
The measurement of the angle between the left ventricular pseudotendinous cord and the septum was centered on the starting point, and the endocardium of the left ventricular surface of the septum and the septal surface of the left ventricular pseudotendinous cord were selected for the angle measurement.
The anteroposterior and inferior diastolic diameters of the left ventricle at end-systole and end-diastole were measured, and the diastolic percentage was calculated (diastolic percentage = (end-diastolic diameter – end-systolic diameter)/end-diastolic diameter).
4. Barium esophageal fluoroscopy was performed in patients with early repolarization syndrome to observe the presence of esophageal hiatal hernia or diaphragmatic hernia.
Statistical analysis
The incidence, number and location of left ventricular pseudotendinous cords between the two groups were tested by chi-square test, and the length and width of left ventricular pseudotendinous cords between the two groups and their angle with the septum were tested by t-test.
IV. Results
1 The incidence of pseudotendinous cords was extremely high (117/131, 89%), and the difference in the incidence of left ventricular pseudotendinous cords between the male and female groups was not significant
The difference in the incidence of left ventricular pseudotendinous cords between the early repolarization syndrome group and the control group was not significant (P > 0. 05), and the difference in the length and width of left ventricular pseudotendinous cords was not significant (both P > 0. 05); however, the difference in the angle between the left ventricular pseudotendinous cords and the septum between the two groups was significant (P < 0. 01).
3. There were four types of left ventricular pseudotendinous cords according to their locations: from the mid ventricular septum to the mid left ventricular free wall, from the basal ventricular septum to the apical segment of the left ventricular free wall, from the basal ventricular septum to the mid left ventricular free wall, and from the mid ventricular septum to the apical segment of the left ventricular free wall, and the difference in the composition ratio of the four locations of the left ventricular pseudotendinous cords between the early repolarization syndrome group and the control group was significant ( P < 0. 001). 4. There was no significant difference between the early repolarization syndrome group and the control group in the number of cases of left ventricular pseudotendinous cords ( P > 0. 05). The difference in the percentage of anterior-posterior left ventricular diastolic and percentage of long-diastolic diastolic between the early repolarization syndrome group and the control group was not significant (P > 0. 05), while the difference in the percentage of anterior-posterior left ventricular diastolic and percentage of long-diastolic diastolic between the groups was significant (P < 0. 01). In the resting state, the heart rate of patients with early repolarization syndrome was slower than that of the control group, and the difference was significant. There was no esophageal hiatal hernia or diaphragmatic hernia in the early repolarization syndrome group. V. Discussion Early repolarization syndrome is mainly characterized by ST-segment elevation on ECG, mostly seen in young and strong men, and some of them may show symptoms such as chest tightness and chest pain, which are easily misdiagnosed as acute myocardial infarction, variant angina and acute pericarditis. According to statistics, about 64% of early repolarization syndromes are misdiagnosed as organic heart disease at the first diagnosis, and the exact etiology is not well understood. The mechanism of its occurrence may be as follows: In early repolarization syndrome, the ventricular depolarization has not yet finished, and some of the ventricular muscle has already started to repolarize, making the ventricular repolarization procedure abnormal; (2) Increased parasympathetic tone; (3) The possibility of additional collateral tracts; ④ The stimulation of the epicardium by esophageal hernia or diaphragmatic hernia causes early depolarization and repolarization of the subepicardial myocardium. The left ventricular pseudotendinous cord is a fibrous structure attached to the left ventricular cavity, except for the tendinous cord connecting the papillary muscle to the mitral leaflet. The detection rate of left ventricular pseudotendinous cords in the population reported in the domestic and international literature ranged from 0.2% to 71%. The left ventricular pseudotendinous cords are divided into milky white and dark red according to their histological characteristics, and generally contain conduction tissue, but a few thin milky white cords are composed entirely of dense connective tissue. The conduction tissue within the left ventricular pseudotendinous cords may be an extension of the bundle of Hirschsprung, which is distributed in the ventricular wall and conducts excitation from the sinoatrial node in a timely manner and effectively coordinates left ventricular systolic and diastolic motions. Salazar J reported a case of a large left ventricular pseudotendinous cord in a 2-year-old child that resulted in altered cardiac repolarization, depression of the ST segment in the inferior wall and V 4 to V 6, and inversion of the T wave. Mobilia G et al. reported two young male patients with left ventricular pseudotendinous cords presenting with large T waves in the anterior chest leads. Although the exact relationship with cardioplegia is not certain, it is also suggested that left ventricular pseudotendinous may be associated with cardioplegia. The results of this study showed that the incidence of left ventricular pseudotendinous in the early repolarization syndrome group was not statistically different from that of normal controls, suggesting that left ventricular pseudotendinous is not a characteristic anatomical structure for early repolarization syndrome, similar to that reported by Lin FC et al. The left ventricular pseudotendinous location composition ratio in the early repolarization syndrome group was not statistically different from that of normal controls. There was a statistical difference between the early repolarization syndrome group and the control group. In the control group, 75% of the left ventricular pseudotendinous cords started at the base of the septum and ended at the apex; however, in the early repolarization syndrome group, 47% of the left ventricular pseudotendinous cords started at the middle of the septum and ended at the free wall of the mid-left ventricle, whereas only 22% of the cases started at the base of the septum and ended at the apex; although the reason why the location of the left ventricular pseudotendinous cords in the early repolarization syndrome group was significantly different from that in the control group is not clear, it at least indicates that the abnormal location of the left ventricular pseudotendinous cords contributed to the development of early repolarization syndrome. In the early repolarization syndrome group, the left ventricular pseudotendinous position played a role in the development of the syndrome. In addition, the angle between the left ventricular pseudotendinous cord and the septum was significantly increased in the early repolarization syndrome group, which was statistically different from that of the control group, suggesting that the increased angle may also be related to early repolarization syndrome. The mechanism may be : The left ventricular pseudotendinous cord crosses the left ventricular cavity, and since the percentage of diastole in the anterior and posterior diameters of the left ventricle is greater than the percentage of diastole in the long diameters, and the difference is statistically significant, the diastolic amplitude in the circumferential direction of the left ventricle is greater than in the longitudinal direction, and when the left ventricle is in diastole, the ends of the left ventricular pseudotendinous cord are more easily stimulated by pulling, and the local myocardium is elongated, and the elongation of myocardial cells can be directly This results in earlier repolarization than the normal sequence of myocardial excitation at the site of stretching, especially in the middle part of the left ventricular free wall, resulting in a voltage gradient between the endocardium and the subendocardium, leading to ST-segment elevation. In the control group, because the end point of the left ventricular pseudotendinous cord was located in the free wall of the apical segment of the left ventricle, the direction of downward transmission of excitation along the ventricular septum was approximately the same; moreover, the percentage of diastole in the longitudinal direction of the left ventricle was relatively small because of the fixed apical position, and the pulling effect on the ventricular wall was weaker, so there was no early repolarization syndrome in the control group, although the incidence of left ventricular pseudotendinous cord was similar to that of the early repolarization syndrome group. The present study also showed that the incidence of early repolarization syndrome was much higher in men than in women, which is consistent with previous reports. In the present study, the incidence of early repolarization syndrome was much higher in men than in women, and the results of heart rate variability analysis in 40 male patients with early repolarization syndrome showed that vagal hyperactivity was present in patients with early repolarization syndrome. Whether there is an inherent difference in vagal function between the sexes or whether male patients are more prone to vagal hyperactivity cannot be determined. The present study showed that the heart rate of patients with early repolarization syndrome was slower than that of the control group at rest, indirectly suggesting the possibility of vagal hyperactivity in patients with early repolarization syndrome. However, the exact relationship between vagal hyperactivity and early repolarization syndrome and its specific mechanism of action have not been addressed in previous studies. We believe that vagal hyperactivity may lead to slower heart rate and more adequate LV diastole, i.e., a further increase in the percentage of transverse diastole, and when the left ventricular pseudotendinous cord is located in the mid-left ventricular free wall, it is more likely to increase its pulling force on the local myocardium and elongate the local myocardium, resulting in further early repolarization of the subendocardial myocardium in the mid-left ventricular free wall, leading to elevation of the ST segment. This is also consistent with reports that ST-segment elevation becomes more pronounced in early slowing. Although the length and width of the left ventricular pseudotendinous cords in the early repolarization syndrome group were not statistically different from those in the control group, the two widest left ventricular pseudotendinous cords were found in the early repolarization syndrome group, whether this is also related to the fact that the left ventricular pseudotendinous cords contain conduction tissue, which excites the subendocardial myocardium in the free wall of the left ventricle through the additional conduction channel formed by the left ventricular pseudotendinous cords across the left ventricular cavity, causing it to advance. It is not known whether the early repolarization syndrome is related to the inconsistent repolarization of the myocardium as a whole. Therefore, we believe that the location of the left ventricular pseudotendinous cord and its angle to the septum are the main factors in the early repolarization syndrome, and that the focus on the characteristics of the left ventricular pseudotendinous cord may have implications for the study of multiple arrhythmia mechanisms.