Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Chordae Tendineae”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2004

Characterization of statically loaded tissue-engineered mitral valve chordae tendineae.

Chordae tendineae are essential to the proper function of the mitral valve. Native chordae contain a dense collagenous core and an outer elastin sheath. We have been using the principle of directed collagen gel shrinkage to fabricate tissue-engineered mitral valve chordae. Because the microstructure of biologic tissues determines their mechanical behavior, the morphology of collagen and elastin in tissue-engineered chordae should mimic that of native chordae. The objective of this study, therefore, was to examine the morphology of our tissue-engineered constructs in comparison to native chordae. A collagen-cell suspension was cast into silicon rubber wells with microporous anchors at the ends and cultured in an incubator. The anchors allowed shrinkage to occur only transverse to the long axis of the wells, thus creating highly aligned collagen fibril constructs. The collagen constructs were cultured for 8 weeks and characterized mechanically, histologically, and biochemically at different culture time points. Histologic sections showed that in all mature constructs collagen fibers were oriented parallel to the long axis of the constructs. At the edge of the tissue collagen fibers were in general straight, whereas in the middle of the tissue they were wavy. Transmission electron microscopy showed a progressive increase in the density and longitudinal orientation of collagen fibrils with culture time. Light and scanning electron microscopy showed the presence of an elastin sheath around the collagen core. Immunostaining demonstrated that smooth muscle cells differentiate during tissue development and TUNEL assay showed that cells in the interior of the constructs undergo apoptosis. This study has demonstrated that collagen-cell constructs, with material properties and microstructure similar to native mitral valve chordae, can be developed using static culture.

Animals↗
PubMed1997

[A case report of mitral valve repair of broad posterior leaflet prolapse due to ruptured chordae tendinea by replacement of chordae tendineae with EPTFE sutured and Carpentier-Edwards ring techniques].

A 68-year-old woman with mitral valve regurgitation due to ruptured chordae tendineae of posterior leaflet underwent mitral valve repair by replacement of chordae tendineae with EPTFE sutures and Carpentier-Edwards ring techniques. Preoperative study showed massive mitral regurgitation and moderate tricuspid regurgitation with CTR 54% of chest X-ray. The postoperative course was not eventful. Postoperative study showed trivial mitral and trivial tricuspid regurgitation. Postoperative CTR was 45%. Mitral valve repair by these techniques could be modified and applicable to mitral valve regurgitation due to ruptured chordae tendineae of posterior leaflet. There was no complication during follow-up period of 8 months.

Aged↗
PubMed1983

Scanning and transmission electron microscopic studies on isolated ruptures of chordae tendineae.

Electron microscopic studies of chordae tendineae of the mitral valve were carried out in 17 patients who underwent mitral valve replacement due to a spontaneously isolated rupture of chordae tendineae. The normal chordae, used as the control group, were obtained at autopsy from 5 patients who died from extracardiac causes and were compared with the ruptured chordae. In all patients with chordal rupture, scanning electron microscopy showed perforations of the chordae tendineae, with extensive desquamation and disruption of the endothelial cells and wide-spread destruction of the collagen fiber bundles in the central collagenous core. These pathological findings were not observed in the normal chordae from the control group. Transmission electron microscopy showed that the ruptured chordae were characterized by heterogeneous collagen fibrils with intrinsic structural alterations and disorganization in fibril arrangement. There was a wide variation in the diameters of collagen fibrils which always showed abnormal morphology, with abnormally large, peculiarly shaped fibrils. Apparent loss and/or a disordered arrangement of the typical periodicity of the fibrils were frequently observed. In addition, various degrees of degenerative changes of collagen tissue were often present. These abnormalities were never seen in the fibrils of the normal chordae, and were observed consistently in both the fibrils of the ruptured chordae and in the macroscopically intact chordae in the group with spontaneous rupture of chordae tendineae. These results suggest that a defective organization of collagen into fibrils and fibers, associated with secondary degeneration of collagen within the central collagenous core of the chordae tendineae, are important pathogenetic mechanisms for spontaneously isolated ruptures of chordae tendineae.

Adolescent↗
PubMedDate not supplied

Ultrastructure abnormalities in proteoglycans, collagen fibrils, and elastic fibers in normal and myxomatous mitral valve chordae tendineae.

Normal and myxomatous chordae tendineae were studied using light and electron microscopy, to assess the alterations in the appearance and mutual arrangement of proteoglycans, collagen fibrils, and elastic fibers. Specific staining with ruthenium red and cuprolinic blue in a critical electrolyte concentration mode were used to localize proteoglycans. Fresh tissues were fixed in glutaraldehyde containing the cationic dyes and embedded into Spurr resin. Semithin sections of LR White (London Resin Co., Basingstoke, U.K.)-embedded tissue were used for histochemistry. In normal chordae tendineae, the fibrosa comprised close-packed collagen fibrils intermixed with elastic fibers. These were surrounded by a thin layer of elastic fibers and collagen fibrils, both of which were closely associated with proteoglycans. In myxomatous chordae tendineae, alterations were observed in the connective tissue. Proteoglycans were more abundant and were distributed throughout the tissue. The outermost layer was transformed into an undifferentiated electron-dense mass surrounding the central fibrosa, which contained degraded elastic fibers and collagen fibrils. Collagen fibrils had faint banding or lacked a banding pattern altogether. Spaces between collagen fibrils were occupied by abnormal proteoglycans or proteoglycan aggregates. Elastic fibers showed varying degrees of degeneration and were occasionally replaced by electron-lucent spaces containing microfibrils. Accumulation of abnormal proteoglycan was also observed around degenerated elastic fibres and collagen fibrils.

Aged↗
PubMed2006

Study of the traction resistance of mitral valve chordae tendineae.

OBJECTIVE: To determinate the extension and the resistance of the primary mitral valve chordae tendineae when submitted to traction. The importance of keeping the integrity of papillary muscle, chordae tendineae, and mitral valve cuspid when the replacement of this valve occurs is clear, but the knowledge of the maximum resistance that a primary tendinea chorda can withstand is not known. METHODS: Eight hearts were dissected, and one hundred and thirty two primary human chordae tendineae were measured (length and thickness) and submitted to traction under controlled conditions so that the absolute resistance, resistance relative to thickness (relative resistance), and elongation could be measured. RESULTS: The correlation between the elongation at the moment of rupture and the thickness was equal to 1.54 + 17.02 x thickness (P = 0.026); and to absolute resistance was equal to 0.95 + 1.42 x resistance (P < 0.001); and to the resistance relative to thickness (relative resistance) was equal to 1.95 + 0.08 x relative resistance (P = 0.009). The correlation between the absolute resistance and the thickness was equal to 0.26 + 14.53 x thickness (P < 0.001). CONCLUSION: The resistance of primary mitral valve chordae tendineae is associated with its thickness and elongation at the moment of rupture, but is not associated with the length. The elongation at the moment of rupture shows a relationship with the resistance relative to thickness (relative resistance) and with the thickness of the primary chordae tendineae, but not with the length of the chordae tendineae.

Adult↗
PubMed1996

[Clinicopathologic study of mitral regurgitation due to abnormal chordae tendineae].

Severe mitral regurgitation (MR) due to abnormal chordae tendineae as a primary cause is rare. This clinicopathologic study included four such cases which occurred among 6,500 consecutive autopsies on persons older than 60 years. This paper describes three of these cases. Case 1 was a 76-year-old woman with congestive heart failure, MR and atrial fibrillation. She died of acute myocardial infarction. The heart weighed 360 g. Mitral regurgitation was caused by a thick and long abnormal chorda originating from the posteromedial papillary muscle and protruding into the atrial surface of the middle scallop of the posterior mitral leaflet associated with prolapsed anterior mitral leaflet. Case 2 was an 81-year-old woman with MR and congestive heart failure. She died of acute myocardial infarction. The heart weighed 480 g. There were abnormal chordae tendineae with very few branches at the posterior commissure. Parts of both mitral leaflets on the sides of posterior commissure were also prolapsed. Case 3 was a 91-year-old man with MR and atrial fibrillation. He died of congestive heart failure. The heart weighed 530 g. Abnormal chordae tendineae with reticular structures originated from the anterolateral papillary muscle and protruded into the anterior mitral leaflet, which induced severe MR. These cases had abnormally protruding chordae tendineae, abnormal branching, and abnormal structures of the chordae tendineae, respectively. These abnormal chordae tendineae were considered to be congenital anomalies. Clinically all patients had a holosystolic murmur (Levine III-IV degrees), refractory congestive heart failure and atrial fibrillation. The etiology of the MR in these three patients was suspected to be ruptured chordae tendineae demonstrated on echocardiograms. These patients had heavy hearts (mean 457 g) with enlarged left atria and thickened mitral valves, which corresponded to the appearance of severe MR.

Aged↗
PubMed2002

Coil-like structure of the inner core of chordae tendineae.

Scanning electron microscopy was used to examine the chordae tendineae in young (approximately 20 years old) and old (approximately 85 years old) cadavers. A network of collagen fibrils was observed in both the outer and intersurface layers of the chordae tendineae. In young subjects, a regularly arranged series of disconnected collagenous ring-like structures surrounded the longitudinal collagen bundles forming the inner core of the chordae tendineae. In old subjects, the ring-like structures of the chordae tendineae were few or absent. The ring-like structures may be related to reducing mechanical stress during the tightening, twisting, and slackening of the chordae tendineae.

Adult↗
PubMed1976

Morphology and relationship to extensibility curves of human mitral valve chordae tendineae.

Human mitral valve chordae tendineae in which elastic response curves are nonlinear have also been found to exhibit extensibility that increases with chordal size and decreases with chordal age. We used selective enzymatic digestion and scanning transmission electron microscopy to explain these observations. Removal of the outer elastin sheath by enzymatic digestion did not significantly affect the elastic response of this tissue. Scanning electron microscopy revealed that the collagen fibers in the central core of young chordae exhibited a very wavy pattern but the pattern in adult specimens was relatively straight. The increased waviness accounted for the greater extensibility of the young specimens. The collagen fibers from young and old chordae consisted of a network of collagen fibrils that became more collapsed when the tissue was fixed under tension. This network arrangement of the fibrils explains the nonlinearity in the elastic response of the tissue. Transmission electron micrographs showed that the density of collagen fibrils decreased as chordal size increased. The number of fibrils per 10(-8) cm2 of the central core decreased from 182.4 (SE = 1.3) to 131.3 (SE = 1.6) as average chordal cross-sectional area increased from 0.0016 cm2 to 0.0268 cm2. This difference in fibril density provides an explanation for the greater extensibility shown by the thicker chordae. The collagen fibril diameters ranged from 516 A to 552 A.

Adolescent↗
PubMed1987

Mitral valvular insufficiency associated with ruptured chordae tendineae in three foals.

Mitral valvular insufficiency associated with ruptured chordae tendineae was diagnosed in 3 foals with signs of congestive heart failure, which were believed to be secondary to the development of pulmonary hypertension associated with the valvular insufficiency. The septal leaflet of the mitral valve was affected in all 3 foals, and foal 2 also had ruptured chordae tendineae associated with the caudal mitral valve leaflet. Bacterial endocarditis and myocardial necrosis were associated with the ruptured chordae tendineae in foals 3 and 2, respectively. Idiopathic rupture was considered in foal 1. Two-dimensional echocardiography demonstrated a flail mitral valve leaflet in foals 2 and 3 and a ruptured chorda tendineae in foal 3. The ruptured chorda tendineae in foal 1 was not visualized with M-mode echocardiography.

Animals↗
PubMed1995

Labor and delivery complicated by acute mitral regurgitation due to ruptured chordae tendineae.

Acute mitral regurgitation due to ruptured chordae tendineae is a dramatic and life-threatening clinical situation. Rarely does this complication occur during pregnancy. We present a case of a 30-year-old woman in week 31 of her pregnancy who developed acute mitral regurgitation, secondary to bacterial endocarditis and ruptured chordae tendineae. This acute event resulted in preterm labor a few hours later. Delivery was uneventful and successful and was followed by open heart surgery 5 days later. A review of the literature on chordae tendineae rupture and resulting mitral regurgitation during pregnancy is presented.

Acute Disease↗
PubMed1978

Replacement of ruptured chordae tendineae of the mitral valve with autologous pericardial chordae.

Severe mitral regurgitation owing to rupture of chordae tendineae has been repaired in 10 patients by construction of new chordae from autologous pericardium. The site of rupture was the posterior leaflet in eight patients, the anterior leaflet in one patient, and both leaflets in one patient. Cardiac catheterization demonstrated severe mitral regurgitation (average 49%) and a left atrial V wave of 45 mm. Hg. The reconstruction was carried out with pericardium rolled into a chorda with one end attached to the appropriate papillary muscle and the other attached to the flail edge of the mitral valve leaflet being repaired. One patient died on the seventh postoperative day from pneumonia. The remaining nine patients are alive and well (Functional Class I) from 6 months to 9 1/2 years (average 3 years) following the operation. None requires anticoagulants.

Aged↗
PubMed1994

Ultrastructure of the rat papillary muscle-chorda tendineae junction.

The papillary muscle and chordae tendineae of the rat tricuspid valve were treated with tannic acid-glutaraldehyde fixative and examined with an electron microscope. In the junctional region, the papillary muscle cell tapered abruptly and separated into many processes. One end of bundles of elastic fibers approached these processes or lateral sides of the muscle cell and the other end extended in a longitudinal direction toward the chordae tendineae. Fine networks of elastic fibers were observed in the subendothelial layer of the junctional region.

Animals↗
PubMed1990

Direct visualization of ruptured chordae tendineae by transesophageal two-dimensional echocardiography.

To determine the value of transesophageal echocardiography in the detection of ruptured chordae tendineae, 28 patients who had surgical therapy for pure mitral regurgitation were evaluated prospectively by conventional transthoracic and transesophageal two-dimensional echocardiography. Seventeen patients (Group I) had ruptured chordae tendineae and 11 (Group II) had intact chordae tendineae. Transthoracic echocardiography detected ruptured chordae tendineae in 6 patients from Group I (sensitivity 35%) and flail leaflets in 11 patients from Group I (sensitivity 65%). Transesophageal echocardiography disclosed ruptured chordae tendineae in all 17 Group I patients (sensitivity 100%); the sensitivity was significantly higher than that of transthoracic echocardiography. No abnormal chordal echoes were visualized in any patient from Group II by either transthoracic or transesophageal echocardiography (specificity 100%). Transesophageal echocardiography is a highly sensitive method for detecting ruptured chordae tendineae and is superior to transthoracic echocardiography in establishing its diagnosis.

Chordae Tendineae↗
PubMed2005

Structural characterization of the chordae tendineae in native porcine mitral valves.

BACKGROUND: This study was aimed to characterize the different mitral valve chordae tendineae to provide additional understanding of their function. METHODS: Mitral valve chordae tendineae from fresh porcine hearts were stained for collagen and elastin using either a Verhoeff and van Gieson stain or Verhoeff light green stain. Cellular distribution was determined using a hematoxylin and eosin stain. Immunohistochemistry was used to verify the findings of vasculature. Biochemical assays were performed to quantify DNA, collagen, and elastin content of each of the six different types of chordae tendineae. RESULTS: Blood vessels were observed in the longitudinal and circumferential directions of the chordae. The strut chordae on the anterior leaflet of the mitral valve showed an increased degree of vascularization compared with the other chordae. All chordae had an inner layer characterized by a high concentration of collagen and an outer layer that was mostly elastin with interwoven collagen fibers. The collagen microstructure was characterized by directional crimping. Hematoxylin and eosin staining showed fibroblasts evenly distributed throughout the inner and outer layer of the chordae tendineae. Quantitative analysis showed significantly higher levels of DNA and collagen content in the anterior and posterior marginal chordae compared with the other chordae. CONCLUSIONS: The chordae tendineae were seen to have different microstructures according to chordal type. The presence of vessels characterized the chordae tendineae as complex living components that work in coordination with the papillary muscles and mitral valve leaflets to prevent mitral valve prolapse and regurgitation. They may also function to supply nutrients to the valve leaflets.

Animals↗
PubMed1988

Floppy mitral valve chordae tendineae: histopathologic alterations.

Pathologic studies of floppy or myxomatous mitral valves have focused primarily on changes in the valve cusps, with little attention given to the chordae tendineae. In a systematic study of the histopathology of floppy mitral valve chordae tendineae, 128 nonruptured chordae from 8 severely regurgitant floppy mitral valves were compared to 152 chordae from 10 normal control mitral valves and to 152 chordae from 8 control mitral valves with severe regurgitation due to ischemic heart disease. Collagen alterations were observed in 2% of normal mitral valve chordae and 3% of control regurgitant mitral valve chordae compared to 38% of floppy mitral valve chordae. Moderate or severe acid mucopolysaccharide accumulation was observed in 2% of normal mitral valve chordae and 3% of control regurgitant mitral valve chordae compared to 39% of floppy mitral valve chordae. Nonuniform histopathologic alterations, rare in normal and control regurgitant mitral valve chordae tendineae, were frequent in floppy mitral valve chordae tendineae (p less than 0.001). Histopathologic alterations provide the basis for abnormal physical properties previously demonstrated in floppy mitral valve chordae tendineae and may predispose to chordal elongation and rupture.

Aged↗
PubMed1984

Morphogenesis of chordae tendineae. I: Scanning electron microscopy.

The formation of the chordae tendineae of the left atrioventricular valve in the chick embryo is described using scanning electron microscopy. These supportive structures for the valve cusps develop between days 6 and 13 of incubation. Elevations which represent the primitive papillary muscles form on the ventricular wall. These elevations bifurcate into thin, web-like folds which are attached to the primitive valve cusps. The folds are the primordia of the chordae tendineae. Linear ridges develop on the web between the cusp and papillary muscle. These ridges alternate with depressions. The depressions become perforate to create the individual chorda from the linear ridges. Multiple perforations form initially but they typically consolidate to create one large aperture between two chordae. Some interchordal connections of tissue do persist throughout the period studied. During the period of perforation, prominent rounded cells are typical of the endocardium between the chordae. These cells are similar at the scanning electron microscope level to those present in the formation of the foramina secunda of the atrial septum. Primary, secondary, and tertiary chordae tendineae appear to develop in the same manner. First order chordae (those attached at the free margin of a cusp) are not found in the chick embryo. The majority of the chordae are second order, which insert into the ventricular surface of the cusp a short distance from the free edge. These chordae typically have a horizontal banding or grooving along their length. Third order chordae which extend from the papillary muscle to the ventricular wall are also present. It is suggested that chordal development is a programmed cellular and hemodynamic event.

Animals↗