Flail Posterior Mitral Leaflet Research Articles

Idiopathic posterior papillary muscle rupture; a case report

BackgroundPapillary muscle rupture is a rare condition. Its clinical presentation, diagnosis and management can be very challenging for the clinician.Case presentationA 73-year-old woman with hypertension presented with chest pain, ST-segment changes, and elevated serum troponin levels. Coronary angiography was normal. Echocardiography revealed normal ventricular function, flail posterior mitral leaflet, and severe mitral regurgitation. She underwent emergent mitral valve replacement.ConclusionThe diagnostic and management strategies of this uncommon presentation are discussed.

Anatomic characteristics of bileaflet mitral valve prolapse--Barlow disease--in patients undergoing mitral valve repair.

Barlow disease is a still challenging pathology for the surgeon. Aim of the present study is to report anatomic abnormalities of mitral valve in patients undergoing mitral valve repair. Between January 1st, 2007, and December 31st, 2010, 85 consecutive patients (54 men and 31 women, mean age 59 +/- 14 years--range: 28-85 years) with the features of a Barlow mitral valve disease underwent mitral repair Forty seven percent of patients were in New York Heart Association functional class III or IV. Preoperative transesophageal echocardiography was compared with anatomical findings at the moment of surgery. Transthoracic echocardiography diagnosis of Barlow disease according to the criteria described by Carpentier was confirmed at anatomical inspection. Annular calcifications were found in 28 patients while 7 patients presented single or multiple clefts. A flail posterior mitral leaflet was detected in 32 subjects, while a flail anterior leaflet in 8. Elongation of chordae tendineae was demonstrated in 45 patients and chordal rupture in 31. All patients showed at trans esophageal echocardiography the typical features of Barlow disease. Seventy-seven (90.6%) patients had severe mitral valve regurgitation, in the remaining 9.4% it was moderate to severe. Transesophageal echocardiography failed to identify clefts in 2/7 and chordal rupture in 4/31. bileaflet prolapse > 2 mm, billowing valve with excess tissue and thickened leaflets > or = 3 mm, and severe annular dilatation, are characteristics of Barlow disease, however the identification of the associated and complex abnormalities of mitral valve is necessary to obtain optimal valve repair.

Comparison of Artificial Neochordae and Native Chordal Transfer in the Repair of a Flail Posterior Mitral Leaflet: An Experimental Study

Surgical reconstruction of a flail posterior leaflet is a routine mitral valve repair, the techniques for which have evolved from leaflet resection to leaflet preservation. Artificial expanded polytetrafluoroethylene neochordae are frequently used to stabilize the flail leaflet and seldom, translocation of the native secondary chordae of the valve to the leaflet free edge is used. In this study, we sought to investigate the efficacy of the 2 techniques to correct posterior leaflet prolapse and reduce mitral regurgitation, and quantify the acute post repair leaflet kinematics. Adult porcine mitral valves (n =7) were studied in a pulsatile left heart experimental model in which isolated P2 flail was mimicked by marginal chordal transection. Baseline conditions were established in each valve under normal conditions (control) and were followed by induction of isolated P2 flail by transecting the 2 marginal chordae on the posterior leaflet free edge (disease). The flail posterior leaflet was reconstructed using artificial neochordae (repair 1) and then native chordal translocation (repair 2). Reduction in leaflet flail, changes in mitral regurgitation fraction, leaflet coaptation length, and posterior leaflet mobility were measured using B-mode echocardiography or color Doppler. At baseline, all the valves were competent with no mitral regurgitation. After transection of the marginal chordae on the posterior leaflet, isolated P2 flail was evident with 13.7% ± 13% regurgitation. Reconstruction with artificial neochordae eliminated leaflet flail and reduced mitral regurgitation to 3.2% ± 2.8%, and with chordal translocation leaflet flail was corrected and mitral regurgitation was measured at 2.3% ± 2.6%. Using either repair techniques, leaflet coaptation and mobility of the repaired leaflets were adequate and comparable with the baseline measurements. Comparable reduction leaflet flail and regurgitation, and restoration of physiologic leaflet coaptation with the 2 techniques indicate that under acute conditions, use of artificial neochordae or native chordal translocations have similar benefits.

Acute mitral regurgitation due to flail mitral leaflet mimicking: a diagnosis of pneumonia

A 47-year-old man admitted to our department with the persisting complaints of shortness of breath and dry cough. He had been treated with sulbactam-ampicillin with the diagnosis of pneumonia for 3 weeks. He began to define paroxysmal nocturnal dyspnea and orthopnea despite treatment for 4 days. On physical examination, he had an apical systolic murmur and fine crackles heard over the mid-upper chest. Electrocardiography demonstrated sinus rhythm with left atrial abnormality. Chest X-ray revealed bilateral symmetric pulmonary infiltration and pleural effusion with normal cardiac contours (Fig. 1a). Transthoracic echocardiography was obtained immediately and showed probable ruptured chorda tendineae resulting in severe mitral regurgitation with normal systolic functions. Further investigation with transesophageal echocardiography disclosed flail posterior mitral leaflet with eccentric mitral insufficiency jet flow directing to opposite site of affected leaflet (Fig. 1b,c). The patient responded well to mitral valve repair after an uneventful surgery. This case is a very good example of the radiographic features of bilateral mid-upper lobe pulmonary edema caused by mitral valve regurgitation mimicking pneumonia. The pulmonary edema associated with mitral valve regurgitation is usually bilateral but can also be seen isolated or predominantly in right upper lobe [1–3]. Because our patient presented with a confusing medical history and the possibility of cardiac disease is not considered, the initial diagnosis of pneumonia was made incorrectly. We think that careful cardiac auscultation might help the exact diagnosis, in fact the centerpiece of physical examination. In conclusion, this presenting case emphasizes the mitral regurgitation as an etiologic factor in the differential diagnosis of bilateral pulmonary infiltration and the role of proper cardiac auscultation. So, familarity with the pulmonary findings in patients with acute mitral regurgitation is crucial for rapid diagnosis and optimal patient care.

Intraoperative rupture of the endoaortic clamp balloon in a patient undergoing port-access mitral valve repair

A 66-year-old man (t65 cm, 71 kg) had a 10-year history of mitral valve disease with minimal symptoms. Over the last year, he developed increased shortness of breath and fatigue with physical activity; in the last several months, he was unable to climb a flight of stairs without dyspnea. He underwent a cardiac catheterization, which showed a mildly dilated left ventricle (LV) with an estimated ejection fraction of 83%, 3 + to 4+ mitral regurgitation with a flail posterior mitral leaflet, and a mean pulmonary capillary wedge pressure of 13 mmHg, increasing to 24 mmHg with a V wave to 45 mmHg. Coronary anatomy was normal. He was referred for mitral valve repair or replacement, and a Port-Access, minimally invasive procedure using the Heartport EndoCPB system (Heartport Inc, Redwood City, CA) was planned, The patient was admitted on the same day of surgery. Bilateral radial artery catheters and a pulmonary artery catheter (Swan-Ganz; BaxterEdwards Inc, Deerfield, IL) were inserted. Midazolam, 5 rag, was administered intravenously for sedation. On arrival in the operating room, arterial blood pressure was 125165 mmHg (mean arterial pressure, 80 mmHg); mean pulmonary artery pressure, 30 mmHg; cardiac index, 2.2 L/min/m 2, and heart rate, 60 beats/rain. After preoxygenation, general anesthesia was induced with fentanyl, 500 pg; midazolam, 5 rag; and cisatracurium, 16 mg. The trachea was intubated, and the lungs were ventilated with isoflurane in oxygen. A biplane transesophagoal echocardiography (TEE) probe (Hewlett-Packard, MA) was inserted. The baseline two-dimensional and color-flow Doppler examination confirmed severe mitral regurgitation and valvular changes suggestive of myxomatous degenerative disease, with ruptured chordae and a flail posterior leaflet. The aortic valve appeared normal without regurgitant flow, and the ascending and descending parts of the thoracic aorta were without echocardio~:aphic evidence of significant atheromatous disease. Access to the heart was achieved through a 6-era submammary incision, and the chest was entered through the fourth right intercostal space. The left femoral vessels were exposed through a groin incision, and after systemic anticoagulation with heparin, the Heartport Endoarterial Return cannula was inserted into the femoral artery. A guidewire was advanced from the femoral vein to the right atrium, visualized by TEE, and the Heartport Endovenous Drainage cannula was advanced into the fight atrium with the tip at the superior caval atrial junction. The Heartport Endoaortic Clamp was advanced over a guidewire and positioned in the ascending aorta with the tip slighdy above the sinotubular ridge, as seen by TEE. The surgeon inserted a retrograde cardioplegia catheter through a right atrial purse-string cannulation site into the coronary sinus, guided by TEE and pressure waveform.

Hypertrophic Cardiomyopathy with Obstruction: Important Diagnostic Clue Provided by the Direction of the Mitral Regurgitation Jet

We present an unusual case of hypertrophic cardiomyopathy complicated by mitral regurgitation resulting from chordal rupture with flail posterior mitral leaflet. The diagnosis was suggested by the presence of an anteriorly directed mitral regurgitation jet on transthoracic color flow imaging, in addition to the typical posterolateral-lateral jet caused by systolic anterior mitral motion. The flail posterior leaflet was confirmed by transesophageal echocardiography, and the patient underwent mitral valve repair in addition to myectomy. This combination of hypertrophic cardiomyopathy and flail mitral leaflet usually requires surgical intervention, and prompt diagnosis is important. The presence of an anteriorly directed mitral regurgitant jet should always raise suspicion of posterior mitral leaflet abnormality. (J Am Soc Echocardiogr 1998;11:61-5.)

Cardiac disease in patients with reversible cerebral ischemic events.

The establishment of a possible association between ischemic cerebral attacks and prolapsing mitral valve has been studied in 45 consecutive patients aged 60 years or less with transient cerebral ischemic attacks and reversible ischemic neurological deficits. The study comprised cardiac history, auscultation, electrocardiography and echocardiography. We found only one patient (2%) with mitral valve prolapse but 19 patients (42%) with cardiac abnormalities. Two of the patients with cardiac abnormalities had a flail posterior mitral leaflet, one had ventricular septal defect and one had sclerotic aortic valves. We conclude that all patients with transient cerebral ischemic attacks should be subjected to heart examination, if possible including echocardiography.

Quantitation and significance of horizontal cardiac motion in M mode and two dimensional echocardiography

Cardiac structures are continuously moving during the cardiac cycle so that constantly changing acoustical interfaces are being recorded by the theoretically static echographic beam. The characteristic movement of the base of the heart toward the apex in systole appears as horizontal motion when imaged in two dimensional echocardiographic parasternal long axis views. The quantitative characteristics of horizontal motion were studied in 50 control patients, 25 patients with decreased cardiac output, 20 with volume overload and 10 with pericardial effusion. The angle of cardiac shift at the aorto-interventricular septal junction was 8 ± 2 ° (mean ± standard deviation) in control patients, and this change constituted 21 ± 6 percent of the area within the arc containing the standard M mode information. Horizontal shifts were decreased in patients with decreased cardiac output (4 ± 2 °; p < 0.001) and increased in patients with volume overload (11 ± 4 °; p < 0.001) or pericardial effusion (10 ± 3 °; p < 0.025). With use of the concept of horizontal motion, the interventricular septal hinge point was noted to be in the area of the membranous interventricular septum, rather than at the junction of the upper and middle thirds of the interventricular septum in 80 percent of normal subjects, 72 percent of patients with decreased cardiac output, 60 percent of those with pericardial effusion, 52 percent of those with left-sided volume overload and 40 percent of those with right-sided volume overload. The concept of horizontal cardiac motion was also pertinent to the interpretation of aortic valve opening, the transposition of aortic root information to apparent left ventricular outflow tract level, one form of pseudosystolic anterior mitral motion, abnormal left atrial echoes, echoes mimicking flail posterior mitral leaflet and interpretation of left atrial wall motion at the left atrial-left ventricular junction. In conclusion, horizontal cardiac motion is a significant physiologic phenomenon of potential clinical importance. It causes important changes in the echographic recording of acoustical information.

Abnormal mitral valve motion associated with ventricular septal defect following acute myocardial infarction

It is often difficult to make the clinical distinction between acute mitral regurgitation caused by papillary muscle dysfunction or rupture and ventricular septal defect complicating an acute myocardial infarction. A case of a patient with rapidly progressive congestive heart failure and a loud murmur is presented. Echocardiography strongly suggested the presence of a flail posterior mitral leaflet. However, the patient was subsequently found to have rupture of the interventricular septum. This diagnosis was made with bedside right heart catheterization and was later confirmed by left ventriculography and direct inspection at the time of surgery. The mitral valve apparatus was completely normal. Thus this case demonstrates the apparent lack of specificity of the accepted echocardiographic criteria for flail mitral leaflet and acutely ruptured interventricular septum, and the potential necessity of cardiac catheterization to distinguish between these entities.

The role of cross‐sectional echocardiography in the diagnosis of flail mitral leaflet

Cross-sectional echocardiography was performed on two patients with mitral regurgitation in whom M-mode echocardiographic findings were not specific for the etiology of mitral regurgitation. In one patient, flail motion of the free edge of the anterior mitral leaflet into the left atrium was demonstrated only by cross-sectional echocardiograms. In the second patient, the flail posterior mitral leaflet was suggested to be a result of bacterial endocarditis. Cross-sectional echocardiograms clearly identified a flail motion of a mass of vegetation attached to the posterior mitral leaflet. Thus, cross-sectional echocardiography can provide critical information in recognizing patients with a flail mitral leaflet.