Left Ventricular False Tendons: A Morphological Study by Echocardiography

ABSTRACT

Purpose

This is a prospective study aimed to investigate the morphology of left ventricular false tendons (LVFTs) using echocardiography and explore its associations with age, sex, body mass index (BMI), congenital heart structural abnormalities, and premature ventricular contractions (PVCs).

Methods and Results

We analyzed data from 889 individuals who underwent consecutive echocardiograms at our ultrasound department between December 2023 and February 2024. Routine echocardiograms were performed to detect congenital structural abnormalities, with a focus on identifying LVFT. We examined the prevalence, number, and distribution of LVFTs, as well as their correlation with age, sex, BMI, and congenital heart structural abnormalities. LVFTs were detected in 460 of 889 cases (51.74%), totaling 672 LVFTs. LVFT prevalence significantly differed not only between sexes but also between ages. LVFT prevalence was higher in individuals with lower BMI. There was no significant difference in congenital heart structural abnormalities between the groups, but the composition of distinct types of structural abnormalities differed between the groups. The incidence of PVCs in the LVFT‐positive group was significantly higher than in the LVFT‐negative group.

Conclusions

The prevalence of LVFTs is notably higher in males than females and tends to decrease with advancing age and increasing BMI. LVFTs display diverse morphological features and may interact synergistically with certain congenital heart structural abnormalities. LVFTs can easily lead to PVCs in healthy people, but the risk of leading to malignant PVCs does not seem to be high. Correctly recognizing the morphological characteristics of LVFTs helps to distinguish similar ultrasonic images of different diseases, thus avoiding missed diagnoses and misdiagnoses in ultrasound work and clinical practice.

This study explores the prevalence and characteristics of left ventricular false tendons (LVFTs) using echocardiography in 889 individuals, revealing a 51.74% prevalence with a higher incidence in males and lower body mass index (BMI) individuals. The prevalence of LVFTs is higher in males than females and tends to decrease with advancing age and increasing BMI. In addition, LVFT is more likely to co‐occur with certain congenital heart structural abnormalities but not others, suggesting that LVFTs cannot be categorized as normal anatomical variants.

1. Introduction

Left ventricular false tendons (LVFTs) are considered “false” tendons because they differ from normal mitral valve tendons [1]. They are typically positioned between the left ventricular free wall, papillary muscle, and interventricular septum, without any connection to the mitral valves. LVFTs vary in number and may calcify with age. LVFTs are believed to originate from the internal trabecular muscle layer of the original heart [2] and contain different amounts of fibrous tissues, myocardial tissues, tiny branches of coronary vessels, and Purkinje fibers continuous with the left bundle branch conduction system. Histologically, the fiber components are smaller and looser than working myocardial fibers [2].

LVFTs can be detected in the fetal heart at 20 weeks of pregnancy by echocardiography Loukas et al. [3] further divided LVFTs into five types based on the insertion positions of the starting point and the stopping point: Type 1 (37.1%) between the ventricular septum and posteromedial papillary muscle, Type 2 (22.1%) between the two groups of papillary muscles, Type 3 (16.5%) between the ventricular septum and the anterolateral papillary muscle, Type 4 (12.5%) between the interventricular septum and free wall, and Type 5 (11.6%) in a reticular pattern (≥ 3 insertion points).

Because different diseases may have similar ultrasonic images, LVFTs are occasionally mistaken for other important pathological structures. For example, spontaneous rupture (or rupture in myocardial infarction) of LVFTs is easily confused with vegetation, thrombus, broken chordae tendineae and papillary muscles, and other structures.

LVFTs have various clinical manifestations, including arrhythmias, ventricular remodeling, and potential hemodynamic impacts [4, 5]. LVFTs may be related to functional heart murmurs. Because of the presence of conductive tissues, LVFTs can cause abnormal ventricular repolarization, such as ST‐segment elevation, T‐wave inversion, or bidirectional changes in ECG, and are closely associated with ventricular arrhythmia [6]. LVFTs may increase the incidence of left heart dysfunction and make the LV expansion more noticeable [7]. Thick LVFT can divert and accelerate the blood flow, resulting in hemodynamic disorder [8] and even thrombus and vegetation adhesion [9]. Therefore, LVFTs have varying roles in different individuals, from being completely negligible to being associated with the occurrence of adverse clinical events such as atypical chest pain and ventricular arrhythmia.

LVFTs are considered a “normal” anatomical variation [10] with a prevalence of approximately 50% [11]; however, the effects of sex and age on the prevalence of LVFTs among adults remain unclear [3, 12, 13]. A study found that LVFTs were not associated with congenital cardiac abnormalities [13], but the researchers did not conduct a detailed analysis of specific abnormalities. At present, the clinical identification of LVFTs is mostly limited to echocardiography, which is the simplest and most effective method for detecting LVFTs. With rapid technological advancements, echocardiography offers greater potential for understanding the structure of LVFTs. To better analyze the role of LVFTs in clinical settings, it is essential to comprehensively analyze their morphology and minimize false positive and false negative diagnoses by accurately identifying and distinguishing LVFT structures.

In this prospective study, we investigated the morphological characteristics of LVFTs using echocardiography. We selected consecutive individuals who visited our ultrasound department and underwent echocardiography to observe the morphology of LVFTs. Furthermore, we analyzed the correlations between the LVFT morphology and age, sex, and body mass index (BMI).

2. Patients and Methods

2.1. Study Participants

In total, 889 individuals (including outpatients, emergency patients, inpatients, and healthy individuals) who consecutively visited our ultrasound department from December 2023 to February 2024 were selected for this study. We recorded the sex, age, height, weight, and BMI for each participant. Among the 889 patients, there were 459 males and 430 females, with ages ranging from 18 to 95 years. The cohort included 534 individuals aged > 60 years (elderly group) and 355 individuals aged ≤ 60 years (non‐elderly group). According to the World Health Organization classification of BMI, there were 65 cases of underweight (BMI < 18.5 kg/m²), 548 of normal weight (18.5 ≤ BMI ≤ 24.9 kg/m²), 244 of overweight (25 ≤ BMI ≤ 29.9 kg/m²), and 32 of obesity (BMI ≥ 30 kg/m²).

All participants underwent transthoracic echocardiography (TTE), conventional electrocardiography (ECG), and/or continuous ambulatory electrocardiography(Holter). The study protocol was approved by the Ethics Committee of Putian College Affiliated Hospital (approval no.: PUYI FU LUN 202410). Informed consent was obtained from all participants or their guardians.

2.2. TTE

TTE was performed using the PHILIPS EPIQ 7C color Doppler imaging system with the S5‐1 transducer. Patients were positioned in the left lateral decubitus and supine positions. According to the updated recommendation of ASE and EACVI on cardiac chamber quantification of adult echocardiography [14], comprehensive echocardiographic assessments were conducted with the transducer placed beside the sternum, at the cardiac apex, below the xiphoid process, and above the sternal notch at various angles. This approach enabled a comprehensive evaluation of cardiac structure and function while also screening for congenital cardiac anomalies. Special emphasis was placed on identifying the presence of LVFT at specific cardiac locations, including the apex, papillary muscles, free wall, and interventricular septum, using the parasternal long‐axis, short‐axis, apical four‐chamber, two‐chamber, and three‐chamber views.

The characteristics of the tendons, such as number, distribution, thickness, motion, and echogenic properties (e.g., presence of vegetations and calcifications), were examined. All TTE examinations were performed by a single echocardiographer. Additionally, Doppler studies were conducted to ascertain the presence of any pressure gradients produced by the tendons in relevant areas and to evaluate their hemodynamic significance.

The echocardiographic diagnosis of LVFT was based on the identification of an echogenic cord‐like fibrous and/or muscular tendon crossing the left ventricular cavity, observed in at least two echocardiographic planes, not connected to the mitral valve apparatus, being flaccid in systole, and not being trabeculae.

Currently, there is no standardized system for classifying LVFTs. We examined their points of attachment, such as the posteromedial papillary muscle and anterolateral papillary muscle to the interventricular septum, anterolateral papillary muscle to posteromedial papillary muscle, interventricular septum to the left ventricular free wall, left ventricular free wall to the free wall, and between points on the interventricular septum. In our study, we utilized the “Written Zoom” feature on the ultrasound scanner to measure the LVFT diameter at end‐diastole. LVFT was categorized into fibrous (< 1.4 mm), fibromuscular (1.5–2.4 mm), and muscular (≥ 2.5 mm) types based on tendon diameter [6].

2.3. ECG

The total number of premature ventricular contractions (PVCs) less than 100 times in a 24‐h period is within the normal range. Additionally, all types of organic heart disease, including rheumatic heart disease, hypertensive heart disease, cardiomyopathy, coronary heart disease, valvular disease, congenital heart disease, hyperthyroid heart disease, and electrolyte imbalances, were excluded from the statistical analysis. The analyses of the correlation between PVCs and LVFTs were performed.

2.4. Statistical Analysis

Statistical analyses were performed using the Statistical Package for the Social Sciences (SPSS) version 20.0 for Windows. Categorical variables are presented as percentages (%), and intergroup comparisons were conducted using the Chi‐square test. Numerical variables are expressed as means ± standard deviation (x̄ ± s), and intergroup comparisons were performed using paired t‐tests. Binary logistic regression was adopted to analyze the influencing factors of LVFTs occurrence. p values < 0.05 were considered statistically significant.

3. Results

3.1. Prevalence of LVFT

In this study, 460 of 889 participants (51.74%), comprising 190 females and 270 males, showed false tendons in the left ventricle. The LVFT detection rates in females and males were 44.19% (190/430) and 58.82% (270/459), respectively. All participants were between 18 and 95 years old. LVFT was detected in 204 of 355 participants (57.46%) aged 60 years or younger and in 256 of 534 participants (47.94%) aged older than 60 years.

LVFT detection rates varied across BMI groups. The underweight group exhibited the highest LVFT detection rate (72.58%, 45/62), followed by the normal weight group (55.22%, 296/536). The overweight and obese groups showed lower rates at 42.40% (106/250) and 31.70% (13/41), respectively.

3.2. Analysis of Factors Affecting the Occurrence of LVFTs

Taking the examinee's age, gender, and BMI as independent variables, and whether LVFT is detected as the dependent variable (yes = 1, no = 0).

Results of univariate binary Logistic regression analysis: the detection risk of LVFT in males was 42% higher than in females (OR = 1.42, p < 0.05). The group aged 60 years or younger had a greater risk of detecting LVFT, which is statistically significant (OR = 1.80, p < 0.001); the risk of detecting LVFT in the underweight group and the normal weight group is 5.29 times (OR = 5.29, p < 0.001) and 2.44 times (OR = 2.44, p = 0.008) that of the obese group, respectively, while the risk of detecting LVFT in the overweight group compared to the obese group was not statistically significant (OR = 1.54, p > 0.05) (Table 1).

TABLE 1.

Binary logistic regression analysis of factors influencing the occurrence of LVFTs.

Variables	Univariate analysis					Multivariate analysis
	β	SE	Z	p	OR(95% CI)	β	SE	Z	p	OR(95% CI)
BMI (kg/m2)
Obese					1.00 (Reference)					1.00 (Reference)
Overweight	0.41	0.35	1.15	0.248	1.50 (0.75–2.99)	0.43	0.36	1.2	0.23	1.54 (0.76–3.11)
Normal weight	0.89	0.34	2.64	0.008	2.44 (1.26–4.74)	0.95	0.35	2.74	0.006	2.59 (1.31–5.11)
Underweight	1.67	0.43	3.84	< 0.001	5.29 (2.26–12.39)	1.75	0.44	3.94	< 0.001	5.74 (2.41–13.70)
Sex
Female					1.00 (Reference)					1.00 (Reference)
Male	0.59	0.14	4.35	< 0.001	1.80 (1.38–2.35)	0.59	0.14	4.26	< 0.001	1.81 (1.38–2.37)
Age (years)
> 60					1.00 (Reference)					1.00 (Reference)
≤ 60	0.35	0.14	2.49	0.013	1.42 (1.08–1.87)	0.47	0.15	3.24	0.001	1.60 (1.21–2.13)

Abbreviations: BMI, body mass index; CI, confidence interval; OR, odds ratio.

Results of the multivariate binary logistic regression analysis indicate that age, gender, and BMI were all independent influencing factors for LVFTs, suggesting a close association between these factors and the occurrence of LVFTs. When age exceeds 60 years, the risk of LVFT detection increased by 60% (OR = 1.60, p = 0.001); males had an 81% higher risk of developing LVFT compared to females (OR = 1.81, p < 0.001); the risk of detecting LVFT in the underweight index group is 5.74 times higher than in the obese group (OR = 5.74, p < 0.001), and for the normal weight group, it is 2.59 times higher (OR = 2.59, p = 0.006) (Table 1).

3.3. Correlation Between PVCs and LVFTs

Excluding organic heart diseases, 23 PVCs were detected in 587 participants (3.92%, 23/587). The incidence of PVCs in the LVFTs positive group (5.65%, 16/283) was higher compared with the LVFTs negative group (2.30%, 7/304), which is statistically significant (Table 2). Additionally, in the LVFTs positive group, there were five cases of paired PVCs (1.76%, 5/283), whereas, in the LVFTs negative group, there was one case of paired PVCs and one case of multifocal PVCs (0.65%, 2/304). There was a statistically significant difference in the incidence of malignant PVCs between the two groups. However, the practical significance of this difference may be minimal, as the confidence interval was relatively narrow and included zero (Table 3).

TABLE 2.

Comparison of PVCs between LVFTs positive and negative groups.

PVCs	LVFTs		Total
	Present	Absent		Statistical significance
Present	16	7	23	χ 2 = 4.37, p < 0.05, 95% CI:0.19%–6.51%
Absent	267	297	564
Total	283	304	587

Abbreviations: LVFTs, left ventricular false tendons; PVCs, premature ventricular contractions.

TABLE 3.

Comparison of malignant PVCs between LVFTs positive and negative groups.

Malignant PVCs	LVFTs		Total
	Present	Absent		Statistical significance
Present	5	2	7	χ 2=9.02, p < 0.05, 95% CI:−0.65% to 2.87%
Absent	278	302	580
Total	283	304	587

Abbreviations: LVFTs, left ventricular false tendons; PVCs, premature ventricular contractions.

3.4. Echocardiographic Appearance of LVFT

Among the 460 cases where LVFT was detected, 672 tendons were identified, with a maximum of five false tendons detected in a single heart. Within a single heart, one tendon was the most common, followed by two tendons, with five tendons being the least common (Table 4). The thickness of LVFTs varied, ranging from 0.41 to 3.9 mm. Based on thickness, 658 tendons (97.9%) were categorized as fibrous type, 13 (1.93%) as fibromuscular type, and 1 (0.15%) as muscular type. One end of the LVFT was most often located in the interventricular septum, while the other end was connected to the free wall of the apex or to the anterior or posterior papillary muscles. LVFTs exhibited transverse, longitudinal, or oblique traversing of the left ventricular cavity; multiple tendons either ran parallel or formed a mesh‐like shape (Table 5).

TABLE 4.

Prevalence of LVFTs and the number of false tendons.

Number of LVFTs	Number of patients (%)
1	316 (68.70%)
2	98 (21.30%)
3	28 (6.09%)
4	14 (3.04%)
5	4 (0.87%)

Abbreviation: LVFTs, left ventricular false tendons.

TABLE 5.

Attachment sites of LVFTs.

Arising from	Attaching to	Number of LVFTs (%)
Interventricular septum	Posteromedial papillary muscle	134 (19.94%)
Interventricular septum	Anterolateral papillary muscle	198 (29.46%)
Top interventricular septum	Apex free wall	143 (21.28%)
Mid‐interventricular septum	Apex free wall	135 (20.09%)
Base‐interventricular septum	Apex free wall	28 (4.17%)
Anterolateral papillary muscle	Posteromedial papillary muscle	11 (1.64%)
Anterolateral papillary muscle	Free wall	2 (0.30%)
Posteromedial papillary muscle	Free wall	12 (1.79%)
Interventricular septum	Interventricular septum	2 (0.30%)
Free wall	Free wall	5 (0.74%)
Mesh‐shaped		2 (0.30%)

Abbreviation: LVFTs, left ventricular false tendons.

The mechanical features of LVFTs were examined. Among the 460 LVFTs, two remained flaccid throughout the entire cardiac cycle, while the remaining were stretched in diastole and flaccid in systole. Doppler examination revealed no pressure gradients in the blood flow produced by the false tendons at corresponding locations of LVFT throughout the cardiac cycle in all participants, suggesting hemodynamic insignificance.

Among 460 LVFT‐positive participants, 13 (2.82%) exhibited congenital cardiac structural abnormalities, whereas among 429 LVFT‐negative individuals, 27 (6.29%) showed congenital cardiac structural abnormalities. This lower ratio in the LVFT‐positive group compared to the LVFT‐negative group suggests no clear tendency for LVFT‐positive participants to have congenital cardiac structural abnormalities such as patent foramen ovale (Table 6).

TABLE 6.

Co‐occurrence of LVFTs and congenital heart structural abnormalities.

Congenital cardiac structural abnormalities	LVFTs
	Present	Absent
Patent foramen ovale	7	9
Atrial septal defects	1	3
Ventricular septal defects	1	2
Bicuspid aortic valve	1
Simple ventricular septal membranous tumors	1
Pulmonary valve septal defects	1
Noncompaction of the left‐ventricular myocardium	1
Hypertrophic cardiomyopathy		6
Coronary artery fistulas		4
Persistent left superior vena cava		2
Pericardial cysts		1

Abbreviation: LVFTs, left ventricular false tendons.

4. Discussion

LVFTs serve as useful anatomical landmarks within the left ventricle, aiding in the differentiation of morphological left and right ventricles (RVs) during segmental analysis of congenital heart disease. Research in clinical medicine, anatomy, and electrophysiology has revealed a closer relationship between LVFTs and various clinical manifestations, highlighting the advantages of echocardiography in this field. Therefore, a thorough understanding of LVFTs and efficient detection methods are essential skills for echocardiographers.

In this study, the LVFT detection rate was 51.74% among 889 participants. LVFTs are more common in males than in females. Our results also align with previous studies [13], indicating that LVFTs are more likely to occur in younger individuals. This may be due to several reasons: firstly, LVFTs may undergo degeneration and absorption with age, leading to a lower occurrence rate in older age groups; secondly, the image quality of echocardiography in younger populations may allow for better identification of LVFTs.

Among the 43 participants with congenital heart structural abnormalities in this study, only 15 were LVFT‐positive, accounting for 34.88%. This suggests no significant co‐occurrence of LVFT and congenital heart structural abnormalities. However, Philip et al. [13] reported a much higher proportion of LVFT‐positive individuals, reaching 61.8%, in individuals with congenital heart abnormalities, likely due to their focus on infants and young children primarily affected by congenital heart abnormalities. Although the occurrence rate of congenital heart structural abnormalities in the LVFT‐positive group was lower compared to the LVFT‐negative group, the types of combined structural abnormalities differ. LVFTs were more likely to co‐occur with certain congenital heart structural abnormalities, such as bicuspid aortic valve and pulmonary valve septal defects. However, this does not exclude the possibility of coincidence, given the relatively short study period. Further studies focusing on elucidating the relationship between LVFT occurrence and congenital heart structural abnormalities are needed.

LVFTs exhibit diversity in both number and morphology, with thinner tendons being more common and thicker ones less prevalent. Among LVFT‐positive participants, single tendons were most common (47.32%), followed by two tendons (28.27%), while multiple tendons (up to five) were rare. Histologically, LVFTs can manifest as fibrous, fibromuscular, or muscular, with the fibrous type predominating in our study. The thinnest LVFT measured 0.41 mm, while the thickest measured 3.9 mm. Furthermore, the common attachment sites of LVFTs vary among different studies. Although most studies suggest a common connection between the interventricular septum and the posteromedial papillary muscle [11], our results showed that most LVFTs connected the interventricular septum and the apex free wall (306/672, 45.54%). LVFTs with both ends in the interventricular septum (Figure 1) and mesh‐shaped LVFTs were infrequent. Interestingly, we observed a case where one of the chordae tendineae of the mitral valve merged with an LVFT at the base of the papillary muscle (Figure 2), suggesting that LVFTs may undergo migration and/or incomplete absorption during embryonic development.

FIGURE 1.

Left ventricular false tendon with both ends in the interventricular septum (arrow). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; IVS, interventricular septum.

FIGURE 2.

Representative case with one of the chordae tendineae of the mitral valve merged with the left ventricular false tendon at the base of papillary muscles (arrow). AML, anterior mitral leaflet; IVS, interventricular septum；Ao, aorta; LA, left atrium; LV, left ventricle; PPM, posterior papillary muscle; RV, right ventricle.

According to the Framingham Study [15], 79% of LVFTs are stretched in diastole and flaccid in systole, 14% are in tension for the entire cardiac cycle, 1% remain flaccid for the entire cycle, and some LVFTs cannot be assessed through echocardiography. In our study, only one LVFT remained flaccid throughout the cardiac cycle. The remaining exhibited alternating laxity and tension during systole and diastole, respectively. Moderate stretching of LVFTs can support cardiac structure and prevent adverse left ventricular remodeling. However, excessive stretching can affect papillary muscle function and potentially cause LVFT rupture or myocardial scarring at its attachment site [16]. Although our study suggests that LVFTs do not significantly affect hemodynamics, previous reports indicate that LVFTs, especially mesh‐shaped ones, may increase the risk of thrombosis and vegetation formation [9].

Despite the simplicity of diagnosing LVFT via ultrasound, misdiagnosis and missed diagnosis are common due to the diverse morphology of LVFTs. Distinguishing LVFTs from other linear echogenic structures within the left ventricular cavity, such as trabeculations, mural thrombus, subaortic membrane, vegetations, tumors, elongated aortic valve or mitral valve leaflets, chordae tendineae of the mitral valve, and right sinus of Valsalva aneurysm, is important. Accurate measurement of the relevant ventricular septal thickness is of crucial importance when LVFTs attached to the interventricular septum or connecting the interventricular septum to the left ventricular free wall or papillary muscles, particularly in the case of combined sigmoid ventricular septum. These LVFTs may obstruct the left ventricular outflow tract or impede forward blood flow, making differentiation from hypertrophic obstructive cardiomyopathy challenging. Therefore, differentiating these structures is essential to minimize false‐positive diagnoses.

LVFTs are increasingly associated with various clinical conditions. For instance, when persistent T‐wave inversion is observed on an electrocardiogram without evidence of coronary artery atherosclerosis, hypertrophic cardiomyopathy, pericardial diseases, or other related conditions, LVFT should be considered as a potential cause. During cardiac surgery, surgeons should avoid suturing LVFTs, as they may contain branches of the conduction system and branches of coronary arteries. LVFTs have been considered one of the causes of functional (so‐called harmless) murmurs. Functional murmurs may be associated with multiple factors, including a dilated ascending aorta, hypertension, left ventricular systolic hyperfunction, reduced blood viscosity, and thick LVFT located in the left ventricular outflow tract. However, in this study, no pressure gradient was detected in the LV cavity including the outflow tract, middle segment, and apex, regardless of the distribution, number, and thickness of LVFT. Similar to endocardial Purkinje fibers, Purkinje fibers in LVFT are also autonomous and therefore serve as potential ectopic agitation [17]. The attachment point of LVFT with mechanical traction may induce premature ventricular beats [18, 19] or more serious arrhythmia by reentrant mechanisms such as ventricular tachycardia and fibrillation [19, 20]. In this study, the analysis of the correlation between PVCs and LVFTs suggested that LVFTs could easily lead to PVCs in healthy individuals, but the risk of leading to malignant PVCs did not seem to be high. LVFT may be a contributing factor to arrhythmia during left ventricular catheterization. A cat‐based study found that long‐term LVFT traction can cause myocardial thickening of [21] and even scarring at the insertion site. The moderator band (MB) of the RV has the function of regulating RV tension, thus preventing RV overexpansion [22]. Because LVFTs are similar in structure to MB, especially between papillary muscles, they likely delay the remodeling of the heart and the occurrence of mitral regurgitation to stabilize the left ventricular cavity. Another rat‐based immunohistochemistry experiment [23] showed that LVFTs are also the source of natriuretic peptide, which can delay the remodeling of the left ventricle, stabilize the papillary muscle position, and reduce mitral valve regurgitation through the inhibition of endothelin‐1, angiotensin II, and aldosterone. However, Lo Presti et al. [5] found that the presence or absence of LVFTs did not affect the incidence of moderate or heavy mitral regurgitation after acute myocardial infarction. Understanding these anatomical variations is crucial for assessing cardiac structure and function in patients. Although research has found associations between LVFT and electrophysiological, mechanical, and hemodynamic effects, the exact relationship remains unclear. Current research suggests that LVFTs may have both beneficial and detrimental effects on cardiac structure and function, necessitating a comprehensive assessment of their characteristics.

The results of this study found that more than one‐half of the tested population had LVFTs and that LVFTs were related to gender, age, and BMI. The detection rate of LVFT was significantly higher in men than in women and tended to decrease with increasing age and BMI. Although no clear tendency for LVFT‐positive participants to have congenital cardiac structural abnormalities compared to the LVFT‐negative group, LVFT may play a synergistic role in certain specific congenital heart structural abnormalities such as congenital heart valve malformation and diaphragmatic structural abnormalities. The case with one of the chordae tendineae of the mitral valve merging with the LVFT at the base of papillary muscles reflected the variation of LV chordae tendineae and also suggested that LVFT may require dynamic observation.

This study had several limitations. First, as a prospective study, the inclusion of consecutive patients introduces unavoidable random variability, resulting in a higher ratio of older participants. Second, the diagnosis of LVFTs primarily relied on imaging rather than histological confirmation. Third, the short timeline of the study limits the accumulation of a large number of cases, necessitating further studies with a higher sample size. Fourth, no follow‐up was conducted. Fifth, considering that different researchers may use different techniques or equipment, which could affect the consistency and generalizability of the research findings, the key steps in this study, such as operation and data collection analysis, were carried out solely by one researcher. Although this may increase the subjectivity of the results and limit the applicability of the findings to other clinical settings or centers, this echocardiography expert, who is highly experienced and follows strict quality control measures, implemented standardized operating procedures to ensure the reliability and consistency of the data. In addition, where possible, validate results through replication. As echocardiography technology continues to advance, the role of LVFTs in cardiac structure and function will be better elucidated.

In summary, the detection rate of LVFT is significantly higher in males than in females and tends to decrease with increasing age and BMI. Due to the diverse morphology of LVFTs and their co‐occurrence with certain congenital heart structural abnormalities, LVFTs cannot be simply classified as benign anatomical variations.

5. Conclusions

Understanding the morphological diversity of LVFTs contributes to the ultrasound diagnosis and differential diagnosis of LVFTs in echocardiography, providing LVFT‐related evidence for some non‐specific clinical manifestations and expanding the ideas for further exploring the new clinical significance of LVFTs.

Ethics Statement

The study protocol was approved by the Ethics Committee of Putian University Affiliated Hospital (approval no.: PUYI FU LUN 202410).

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

All data analyzed during this study are included in this article. All data are available on request at the archive of the Information Management Database of the Affiliated Hospital of Putian University, Putian, China.