False chordae tendineae]

False tendons (FT) are fibrous or fibromuscular structures which cross the ventricular cavity with no connections with valvular leaflets. They were considered for a long time as normal structures but now cardiologists are interested because of the possible association with the so-called innocent murmur, and even more so for the role they can have in eliciting ventricular arrhythmias. Some Authors believe that arrhythmias can arise from the false tendons because they contain not only fibrous tissue but also muscular and conduction tissue. Arrhythmias can be triggered either by stretching of the Purkinje fibers or by distortion of the ventricular wall, where false tendons arise. At the same time they can act as reentry circuits due to their non-homogeneous structure. Due to the fact that false tendons may arise anywhere from the ventricular cavity, they have been classified according either to anatomic or echocardiographic criteria: the latter being more complex and difficult than the former for the difficulty in locating the attachment areas. In our echocardiographic laboratory we simply distinguish two types of false tendons: type I which parallel the interventricular septum or bridges from the postero-basal portion of the septum to the posterior left ventricular wall; type II which crosses the ventricular cavity more distally, towards the apex. In the anatomic studies the prevalence of the FT is rather homogeneous, ranging from 46 to 54.9%, while it is extremely variable in the echocardiographic studies, ranging from 0.2 to 71%. This is possibly due not only to the examiner's skills, or the equipment's quality but also to the population studied. Among the patients referred to our cardiac paediatric unit we have found false tendons in 80 (29.3%) out of 273 children without cardiac disease, age ranging from i day to 13 yrs. Males were affected twice more than females, 63.7% vs 36.3%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Morphologic characterization and quantitative assessment of mitral regurgitation with ruptured chordae tendineae by transesophageal echocardiography.

To compare the accuracy of transesophageal echocardiography (TEE) with that of transthoracic echocardiography (TTE) in the detection of morphologic characteristics and in the quantitative assessment of the severity of mitral regurgitation with ruptured chordae tendineae, 40 patients with ruptured chordae tendineae (group 1) and 20 patients with moderate or severe mitral regurgitation due to other causes (group 2) were studied. All echocardiograms were recorded before cardiac surgery. Cardiac catheterization was performed in 55 patients (92%). TEE showed greater sensitivity and negative predictive value than TTE (100 vs 65%, and 100 vs 56%, respectively; p < 0.005) in the diagnosis of ruptured chordae tendineae. Visualization of the ruptured chordae (termed snake-tongue sign) was highly sensitive and specific (93 and 95%, respectively) for establishing the diagnosis of ruptured chordae tendineae. The severity of mitral regurgitation in group 1 patients evaluated by TTE color flow mapping was underestimated by 2 grades in 1 patient and by 1 grade in 6 patients, and overestimated by 1 grade in 1 patient, compared with left ventriculography. In contrast, by TEE color flow mapping it was underestimated by 1 grade in 1 and overestimated by 1 grade in 1 patient. TEE color flow mapping showed better correlation with angiography than did TTE color flow mapping (r = 0.82 vs r = 0.49).     

Mitral regurgitation due to ruptured chordae tendineae in patients with hypertrophic obstructive cardiomyopathy.

Mitral valve regurgitation in association with hypertrophic obstructive cardiomyopathy is usually caused by the systolic anterior motion of the anterior mitral leaflet. Recently, five patients were encountered with hypertrophic obstructive cardiomyopathy who had mitral regurgitation due to ruptured chordae tendineae. The diagnosis was confirmed in all patients during operation for left ventricular septal myectomy-myotomy (Morrow procedure). Preoperative identification of ruptured chordae tendineae as the cause of mitral regurgitation was established by transesophageal echocardiography in the three most recent cases. All patients had successful septal myectomy-myotomy for relief of left ventricular outflow obstruction, and mitral valve competence was restored by valve repair rather than by prosthetic valve replacement. The clinical course of these patients illustrates important management considerations as well as the utility of transesophageal echocardiography for diagnosis. Chordal rupture should be considered in the differential diagnosis of mitral regurgitation in patients with hypertrophic obstructive cardiomyopathy, especially in those with acute hemodynamic deterioration.     

Mitral regurgitation due to ruptured chordae tendineae in the aged: a clinicopathologic study

We observed 13 cases of mitral regurgitation (MR) due to ruptured chordae tendineae (RCT) among 4,000 consecutive autopsies of patients over 60 years of age (0.33%). There were four men and nine women whose average age was 79.8 yrs. Five cases had a single RCT (Group I) and eight had multiple RCT (from two to eight chordae) (Group II). The sites of RCT were in the posterior mitral leaflet (PML) in nine, the anterior leaflet in one, and both in three. All in Group I showed RCT in the PML; the posterior scallop in two and the middle scallop in three. The average heart weight was 340 g in Group I and 431 g in Group II. Sclerosis of the coronary arteries, the circumference of the mitral valve ring, and thickness of the leaflets did not differ significantly. Estimated volume of the left atrium was significantly greater in Group II than in Group I (185 ml vs 57 ml, p less than 0.05). Jet lesions were observed in 10 of the 13 cases. The etiologies of RCT were previous endocarditis in two, mitral valve prolapse in three, and spontaneous rupture in eight. Congestive heart failure was observed in three (60%) in Group I and eight (100%) in Group II (p less than 0.01). Cardiothoracic ratio more than 60% was observed in three (60%) of Group I and six (75%) of Group II. Atrial fibrillation was demonstrated in one in Group I (20%) and six (75%) in Group II (p less than 0.05), and cardiac death in one (20%) in Group I and six (75%) in Group II (p less than 0.05). Phonocardiograms showed pansystolic murmur in all cases, third heart sound in nine (69%), and fourth heart sound in four (57%). Echocardiographically, RCT was diagnosed in six of nine cases (67%). In conclusion, patients with RCT involving more than two chordae tendineae can show more severe clinical course than cases with a single RCT.