Left ventricular false tendons (LVFTs) are linear fibrous or fibromuscular bands stretching across left ventricular cavity. Although LVFTs have been associated with various heart pathologies and investigated embryologically and histologically, there is only one report in the literature connoting possible hereditary transmission of this entity. We reported a father and his daughter having similar types of LVFTs with regard to location and thickness. With this report, we will contribute in the literature in respect to potential genetic inherence of LVFTs.
Left ventricular false tendons (LVFTs) are linear fibrous or fibromuscular bands that extend between ventricular septum and papillary muscle, left ventricular free wall, or apex [
Although there is no consensus on the implication of LVFTs in heart diseases, they have been associated with various clinical manifestations in otherwise structurally normal hearts such as functional murmur, preexcitation, idiopathic ventricular tachycardia, infective endocarditis, cavitary thrombi, regional myocardial hypertrophy, repolarization abnormalities, and genesis of J-waves [
Our knowledge about LVFT continuously grows. In order to understand clinical implication of LVFT, we need to evaluate this entity in all its aspects. The questions rose regarding its clinical implication let researches to extend histologic characteristic and embryologic development of LVFT. The lacking information regarding genetic transition of LVFT is the missing link of this chain. We offered an insight into genetic aspect of this entity by reporting these cases.
An 18-year-old previously healthy girl presented with complaint of palpitation. She has experienced palpitation 2 or 3 times a month for 3 years. She did not declare other triggering factors for palpitation with the exception of caffeine. She stated that her palpitation episode sometime lasts one hour, and it is rarely accompanied by dizziness. On physical examination, the followings were noted: normal S1 and S2 without added sounds (S3 or S4) and murmur on cardiac auscultation, blood pressure 118/76 mmHg, heart rate 78/min, and normal breathing sounds. A 12-lead electrocardiogram showed sinus rhythm with normal QRS morphology. Transthoracic echocardiography revealed a structurally normal heart with the exception of a broad false tendon within the left ventricle extending between apical lateral wall and basal septum (Figures
B-mode echocardiographic image from the father (a) and his daughter (b). (a) and (b) Modified parasternal long axis view by B-mode recording. The arrow indicates the false tendon stretching from the left ventricular apical free wall to the ventricular septum. The star indicates the papillary muscles. LA: left atrium; RV: right ventricle.
M-mode echocardiographic image from the father (a) and his daughter (b). (a) and (b) M-mode recording from the midsegment of the left ventricle. The arrow indicates the false tendon; The star indicates the papillary muscles.
B-mode echocardiographic image from the father (a) and his daughter (b). (a) and (b) Modified apical four chamber view by B-mode recording. The arrow indicates the false tendon stretching from the left ventricular apical free wall to the ventricular septum. LA: left atrium; RV: right ventricle.
B-mode echocardiographic image from the father (a) and his daughter (b). (a) and (b) B-mode image from the short axis. The arrow indicates the false tendon stretching from the left ventricular free wall to the ventricular septum.
The father of the girl in case 1, 52 years old, was admitted in our outpatient clinic due to a periodic examination of coronary artery disease. He had coronary bypass surgery history. At the time of admission, he was asymptomatic with regard to coronary artery disease. On physical examination, the followings were noted: normal S1 and S2 without added sounds (S3 or S4) and murmur on cardiac auscultation, blood pressure 132/82 mmHg, heart rate 72/min, normal breathing sounds, and no peripheral edema.
A 12-lead electrocardiogram revealed nonspecific ST changes in precordial leads. Transthoracic echocardiography showed normal systolic contraction in all left ventricular wall segments. There was no evidence of left ventricular cavity enlargement or hypertrophy according to the measurements suggested by chamber quantification guideline [
Although there are several reports in the literature regarding embryologic development, histologic evaluation, and its clinical association of LVFT, to date, genetic aspect of LVFT has not been scrutinized thoroughly. Many years ago, genetic transmission of LVFT became the main topic of conversation upon a presentation of resembling LVFTs in a mother and her son in Russian literature [
Clinical implication of LVFTs is still not well understood although several reports have showed their association with some heart diseases [
Maximum thickness of the left ventricular false tendon in both cases.
Subjects | PSLAX (mm) | SAX (mm) | A4C (mm) | Average (mm) |
---|---|---|---|---|
Father | 8 | 3 | 9 | 6.6 |
Daughter | 6 | 2 | 7 | 5 |
PSLAX: parasternal long axis; SAX: short axis; A4C: apical four chambers.
LVFTs are classified into 5 types with varying percentages based on the points of attachment. Type 1 (66%) extends between posteromedial papillary muscle and ventricular septum, type 2 (12%) between anterolateral papillary muscle and posteromedial papillary muscle, type 3 (11%) between anterolateral papillary muscle and ventricular septum, type 4 (9%) between left ventricular free wall and ventricular septum, and type 5 (1%) between one left ventricular free wall and another left ventricular free wall [
Although there is no consensus on clinical importance of LVFTs [
Several heart diseases and electrocardiographic abnormalities have been associated with LVFTs [
By reporting these cases, we draw attention of clinicians on the potential genetic inheritance of LVFTs. Clinical studies are warranted to confirm the genetic inheritance and reveal the pattern of genetic transmission of LVFTs.
The authors declare that they have no conflicts of interest.