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PubMed1995

Repair of complex left ventricular outflow tract obstruction with a pulmonary autograft.

The surgical relief of complex multilevel left ventricular outflow tract (LVOT) obstruction remains a challenging surgical problem. We present a new operation which combines the concepts of aortoventriculoplasty, extended aortic root replacement and the use of a pulmonary autograft. Sixteen patients underwent this operation: 11 patients after previous attempts to relieve diffuse subvalvular stenosis and five patients who presented excessive gradients over an outgrown aortic valve prosthesis. All patients, except one survived the operation. One patient developed massive right ventricular infarction and was transplanted after five days. Another patient developed complete heart block and transient tricuspid regurgitation after a septal infarction. One patient remained in congestive heart failure and died suddenly after 17 months. All other patients are in NYHA class I after a mean follow up of 21 +/- 12 months. One patient developed progressive dilatation of the neo-aortic root and was reoperated four years after initial surgery. All other patients showed laminar flow in the LVOT and excellent function of the autograft and homograft valve at follow up. This operation might present a durable or even a definitive solution in the management of these complex left ventricular outflow tract obstructions.

Adolescent↗

PubMed2003

Left ventricular outflow tract obstruction: the role of the modified Konno procedure.

The progressive nature of obstruction in the left ventricular outflow tract (LVOT) is hypothesized to be related to the complex relationship between anatomic substrate, genetic predisposition, local shear stress, and the response to injury. Consequently, recurrent obstruction after resection of subaortic membranes as well as more complex forms of LVOT obstruction (eg, tunnel-like stenosis) require aggressive resection to provide unobstructed egress of blood from the left ventricle. The modified Konno procedure is well suited to provide maximal enlargement of the entire LVOT with preservation of aortic valve function. Extension of the procedure to patients with simple forms of LVOT obstruction is, at present, not warranted because of the inability to identify patients destined to develop recurrent obstruction. As predictive models improve, however, the modified Konno procedure should be evaluated in the setting of simple LVOT obstruction at high risk for recurrent obstruction.

Anastomosis, Surgical↗

PubMed1997

Recurrent syncope induced by left ventricular outflow tract obstruction: demonstration in a patient with hypertrophic obstructive cardiomyopathy.

A 70-year-old man presented with repeated syncope induced by left ventricular outflow tract obstruction. He was referred to us because of repeated syncope with convulsion at rest. During syncope, electrocardiography showed marked ST segment depression with negative T waves in leads I, II, aVL, aVF and V2-V5 but no arrhythmias. Echocardiography revealed asymmetric septal hypertrophy and complete obstruction of the left ventricular outflow tract due to systolic anterior movement of anterior mitral leaflet and concomitant severe mitral regurgitation. During the catheterization study, syncope with convulsion developed repeatedly without antecedent cause, and was associated with a decrease in systemic blood pressure. Simultaneous pressure monitoring of the left ventricle and femoral artery showed a significant pressure gradient (maximum 110 mmHg). During each episode, systemic blood pressure rose spontaneously with the recovery of consciousness over several minutes. He received temporary atrioventricular sequential pacing and underwent successful mitral valve replacement. Four years later, he was doing well.

Aged↗

PubMed1985

Left ventricular outflow tract obstruction related to a valve prosthesis: case caused by a low-profile mitral prosthesis.

Mechanical and bioprosthetic mitral prostheses may have many potential complications. In patients with isolated mitral stenosis and a small left ventricular cavity, low-profile prostheses are recommended to avoid myocardial impingement that can result from a high-profile valve and lead to possible left ventricular inflow or outflow obstruction or ventricular arrhythmias. This case report illustrates that left ventricular outflow obstruction may also result from a low-profile mitral valve prosthesis. This obstruction was not diagnosed before cardiac catheterization. Assessment of patients with suspected prosthetic valve dysfunction is difficult and may necessitate cardiac catheterization or even direct surgical inspection for conclusive information.

Adult↗

PubMed1998

Spectrum of congenital heart disease in Malta. An excess of lesions causing right ventricular outflow tract obstruction in a population-base study.

AIMS: To quantify birth prevalence and spectrum of congenital heart disease in the Island population of Malta, and compare these rates with previous studies. METHODS: All patients diagnosed as having congenital heart disease by echocardiography, cardiac catheterization, surgery or post-mortem by 1 year of age between 1990-1994 were included. There were 231 cases of live born congenital heart disease with a birth prevalence of 8.8/1000 live births. The commonest lesions were ventricular septal defect, pulmonary stenosis and tetralogy of Fallot. The rates of individual lesions were compared with two recent epidemiological studies with similar methodologies. RESULTS: Although the overall birth prevalence of congenital heart disease was similar in three studies, significantly higher rates of pulmonary stenosis, tetralogy of Fallot and double outlet right ventricle were found in Malta, all of which predispose to right ventricular outflow tract obstruction. In contrast, there were lower rates of lesions causing left ventricular outflow tract obstruction. A higher rate of ventricular septal defect was also found. The Maltese gene pool may contain an inherent predisposition towards lesions causing right ventricular outflow tract obstruction.

Double Outlet Right Ventricle↗

PubMed1984

The late prognosis after localized resection for fixed (discrete and tunnel) left ventricular outflow tract obstruction.

We studied the follow-up status of 56 patients after operation for fixed left ventricular outflow tract obstruction (LVOTO), 42 with discrete LVOTO consisting of an obstructing membranous ring in the left ventricular outflow tract (LVOT) and 14 with tunnel (diffuse) LVOTO. Forty-one of the 56 patients were available for long-term follow-up. Patients with discrete LVOTO fared better than patients with tunnel LVOTO postoperatively in their functional class status (discrete: 21 in Class I, five in Class II; tunnel: one in Class I, four in Class II; p less than 0.05), their LVOT peak systolic gradients (discrete: 22 +/- 4 mm Hg; tunnel: 98 +/- 23 mm Hg; p less than 0.02), their actuarially determined survival probabilities (discrete: 82% +/- 9% at 20 years; tunnel: 40% +/- 19% at 20 years; p less than 0.1), and their survival probabilities without an adverse event, i.e., (1) death, (2) reoperation, (3) residual gradient greater than 50 mm Hg, (4) significant aortic regurgitation, (5) bacterial endocarditis, or (6) complete heart block (discrete: 43% +/- 9% at 4 years, 36% +/- 9% at 10 years, and 15% +/- 9% at 20 years; tunnel: 0% at 4 years; p less than 0.02). Thus most patients who undergo operation for fixed LVOTO will survive late postoperatively; resection of the membrane is adequate for relief of LVOTO and for relief of symptoms in most patients with discrete LVOTO; the majority of patients with tunnel LVOTO who undergo only local resection will have an unsatisfactory operative result; most patients with discrete as well as tunnel LVOTO surviving operation will have clinically significant adverse events early or late postoperatively. This last observation dictates continuing long-term follow-up evaluations of patients operated upon for fixed LVOTO.

Adolescent↗

PubMed1994

Early changes in ventricular geometry and ventricular septal defect size following Rastelli operation or intraventricular baffle repair for conotruncal anomaly. A cause for development of subaortic stenosis.

BACKGROUND: Obstruction to left ventricular outflow can be seen after surgical repair of congenital heart disease in which a ventricular septal defect (VSD) is closed by means of a baffle to the systemic great artery arising from the right ventricle (Rastelli operation, intraventricular repair, for conotruncal anomaly). We investigated the hypothesis that obligatory volumetric changes that occur after this operation lead to acute alterations in ventricular geometry and VSD size, resulting in subsequent subaortic stenosis in patients who were thought before operation to have a large, nonrestrictive VSD orifice. METHODS AND RESULTS: Preoperative and postoperative echocardiograms and medical records of 24 patients with conotruncal anomaly who underwent conventional Rastelli operation or intraventricular repair in which the VSD was used as part of a new left ventricular outflow were reviewed. Eleven patients had transposition of the great arteries with pulmonic stenosis, 7 had double-outlet right ventricle, and 6 had subaortic atresia or stenosis with a normal-size left ventricle and underwent Norwood's palliation in infancy. All had large, nonrestrictive VSDs at preoperative cardiac catheterization. The mean age at the time of surgery was 32 +/- 24 months. The following measurements were made from two-dimensional echocardiographic images obtained before and 5 +/- 4 days after surgery from the subcostal views at end diastole: (1) VSD diameter; (2) short-axis left ventricular internal diameter (LVID); (3) left ventricular posterior wall thickness (LVPW); and (4) systemic great artery diameter (arising from the right ventricle). VSD diameter diminished significantly after surgery (11.6 +/- 3.6 versus 10.1 +/- 3.7 mm, P < .0001), as did LVID (34.9 +/- 5.0 versus 31.7 +/- 5.1 mm, P < .001). LVPW thickness increased significantly (5.7 +/- 1.0 versus 6.7 +/- 1.1 mm, P < .0001), while great artery diameter was unchanged (16.2 +/- 4.0 versus 16.7 +/- 3.8 mm, P = NS). Percent change in VSD dimension correlated with percent change in LVPW/LVIDD ratio (degree of ventricular "contraction"). Nine patients subsequently developed subaortic obstruction at the VSD orifice level and had a greater degree of early diminution in VSD size (21 +/- 8% versus 10 +/- 8%, P < .002) as well as postoperative change in LVPW/LVID ratio (0.24 +/- 0.04 versus 0.20 +/- 0.02, P < .002) than those who did not develop subsequent subaortic obstruction. CONCLUSIONS: The left ventricle undergoes geometric change after Rastelli operation or intraventricular repair, surgeries in which the VSD is used as the new left ventricular outflow. These changes are manifested as increased wall thickness, decreased cavity dimensions, and a decrease in VSD size. Patients who subsequently develop left ventricular outflow obstruction have the greatest degree of ventricular contraction and VSD diminution early after surgery.

Child, Preschool↗

PubMed1993

Left ventricular outflow tract obstruction after mitral valve repair. Results of the sliding leaflet technique.

BACKGROUND: Left ventricular outflow tract obstruction (LVOTO) occurs in 4% to 5% of patients after prosthetic ring mitral valve repair. Major anatomic factors incriminated in the genesis of LVOTO include degenerative mitral valve insufficiency with excess leaflet tissue, nondilated left ventricular cavity, and narrow mitro-aortic angle. We have previously reported a 14% incidence of LVOTO after prosthetic ring mitral valve repair in this high-risk group of patients. Serial echo Doppler studies demonstrated an overlapping and/or inversion of the left ventricular functional compartments generating systolic anterior motion of the posterior leaflet and paradoxical opening (eversion) of the anterior leaflet. In an attempt to eliminate LVOTO after mitral valve repair, a new surgical procedure was developed in 1988 by Carpentier: the sliding leaflet technique, which reduces the height of the posterior leaflet. The purpose of this study was to analyze the results of the new technique in terms of the occurrence of LVOTO: METHODS AND RESULTS: Eighty-two patients undergoing prosthetic ring mitral valve repair between 1988 and 1991 and identified as high risk for LVOTO were operated on using the sliding leaflet technique. There were 52 men and 30 women. Ages ranged from 28 to 75 years. The surgical techniques used included prosthetic ring annuloplasty (n = 82), leaflet resection (n = 82), chordal shortening or transposition (n = 36), and other (n = 19). Intraoperative and/or immediate postoperative echo Doppler studies were obtained in all cases. Two patients (2.4%) died, and 2 (2.4%) required reoperation. Nonsignificant LVOTO was identified in 2 cases (2.4%), in whom instantaneous maximal subaortic gradients were 20 and 18 mm Hg, respectively. CONCLUSIONS: This study was not done on a concomitant series of patients but on patients with the same type of pathology. It demonstrates that (1) the sliding leaflet technique eliminates significant LVOTO in the high-risk patients; (2) the sliding leaflet technique is associated with a low mortality; and (3) no reoperations for mitral insufficiency were required in this series.

Echocardiography, Transesophageal↗

PubMed2002

An intraoperative diagnosis of dynamic left ventricular outflow tract obstruction using transesophageal echocardiography leads to the treatment with intravenous disopyramide.

UNLABELLED: Hypertrophic obstructive cardiomyopathy (HOCM) is an uncommon familial disorder, traditionally characterized by asymmetric septal hypertrophy and left ventricular outflow tract (LVOT) obstruction (1). It is now recognized that HOCM may also include those patients with secondary left ventricular hypertrophy (LVH) and dynamic LVOT obstruction. In particular, a syndrome with similar clinical and echocardiographic findings has been identified in elderly patients exhibiting concentric LVH with chronic hypertension, aortic stenosis, or sigmoid-shaped septum (2). IMPLICATIONS: During surgery, dynamic left ventricular outflow obstruction (LVOT) can potentially occur frequently, but diagnosis may be less frequent. When circulatory disturbance occurs with suspicion of LVOT obstruction, transesophageal echocardiography can provide exact proof of diagnosis and basis for immediate treatment.

Anti-Arrhythmia Agents↗

PubMed1999

Does left ventricular outflow tract obstruction influence outcome of interrupted aortic arch repair?

BACKGROUND: In previous studies left ventricular outflow tract obstruction (LVOTO) has been recognized as an important factor affecting survival and reoperation probability in patients having repair of an interrupted aortic arch (IAA). METHODS: All 72 patients who underwent operation for IAA from January 1, 1985 to June 30, 1997 were reviewed. The presence or absence of LVOTO was noted and the immediate and long-term results were analyzed. RESULTS: Type A IAA was found in 23 patients and type B IAA in 49 patients. Anomalous right subclavian artery was noted in 15 patients, all of whom had type B IAA. LVOTO was identified in 36 patients before arch repair and was associated with the presence of type B IAA and anomalous right subclavian artery (p = 0.02 and 0.007, respectively). There were 2 hospital deaths (within 30 days) for a mortality of 2.8% (confidence limit [CL] = 0% to 6.6%). There were 7 late deaths over 3,737 patient-months of follow-up (9.7%, CL = 2.9% to 16.6%). Actuarial survival for the whole cohort was 84.8% (CL = 73.2% to 94.4%) at 12 years. There was 87% 10-year survival (CL = 60% to 93%) for patients with LVOTO at presentation compared with 83% (CL = 62% to 92%) for patients without LVOTO (p = 0.85, hazard function 0.87). Twenty-eight patients have required at least one reoperation. The use of conduits to restore right ventricular to pulmonary artery continuity predicted the need for reoperation (p = 0.0001). Patients with presence of a nonseptatable heart were also more likely to need reoperation (p = 0.027) when compared to the rest of the cohort. Freedom from reoperation was 47.3% (CL = 30% to 62%) at 12 years. In patients with LVOTO, freedom from reoperation (55% at 10 years, CL = 33% to 72%) was not significantly different from those patients without LVOTO at presentation (29% at 10 years, CL = 7% to 56%; p = 0.97, hazard function 0.7). Actuarial freedom from recurrent arch obstruction requiring reintervention was 82.7% (CL = 66.7% to 98.7%) at 12 years. CONCLUSIONS: Neonatal complete repair of patients with IAA is possible with low mortality. LVOTO was not a significant risk factor for hospital or late death in patients having complete repair of IAA during this period. The use of conduits for right ventricular to pulmonary artery continuity and the presence of a nonseptatable heart are important risk factors for further operation and will continue to provide added morbidity to these patients.

Aorta, Thoracic↗

PubMed2005

Inheritance analysis of congenital left ventricular outflow tract obstruction malformations: Segregation, multiplex relative risk, and heritability.

The left ventricular outflow tract (LVOTO) malformations, aortic valve stenosis (AVS), coarctation of the aorta (COA), and hypoplastic left heart (HLH) constitute a mechanistically defined subgroup of congenital heart defects that have substantial evidence for a genetic component. Evidence from echocardiography studies has shown that bicuspid aortic valve (BAV) is found frequently in relatives of children with LVOTO defects. However, formal inheritance analysis has not been performed. We ascertained 124 families by an index case with AVS, COA, or HLH. A total of 413 relatives were enrolled in the study, of which 351 had detailed echocardiography exams for structural heart defects and measurements of a variety of aortic arch, left ventricle, and valve structures. LVOTO malformations were noted in 30 relatives (18 BAV, 5 HLH, 3 COA, and 3 AVS), along with significant congenital heart defects (CHD) in 2 others (32/413; 7.7%). Relative risk for first-degree relatives in this group was 36.9, with a heritability of 0.71-0.90. Formal segregation analysis suggests that one or more minor loci with rare dominant alleles may be operative in a subset of families. Multiplex relative risk analysis, which estimates number of loci, had the highest maximum likelihood score in a model with 2 loci (range of 1-6 in the lod-1 support interval). Heritability of several aortic arch measurements and aortic valve was significant. These data support a complex but most likely oligogenic pattern of inheritance. A combination of linkage and association study designs is likely to enable LVOTO risk gene identification. This data can also provide families with important information for screening asymptomatic relatives for potentially harmful cardiac defects.

Analysis of Variance↗

PubMed2001

Surgical results in patients with double outlet right ventricle: a 20-year experience.

BACKGROUND: The objective of this study was to review our surgical strategy in children with double outlet right ventricle and to assess risk factors for early and late mortality and reoperation. METHODS: Patients (n = 124; June 1980 to January 2000; age range, 7 days to 16 years; mean, 2.8 years) who underwent repair of double outlet right ventricle. The patients were divided into three groups. Group 1 (n = 47) had noncomplex patients with atrioventricular concordance, a single ventricular septal defect, balanced ventricles, no straddling atrioventricular valves, and no major pulmonary artery anomalies. Group 2 (n = 39) included patients with double outlet right ventricle and a subpulmonary ventricular septal defect (Taussig-Bing). Group 3 (n = 38) had patients with complex anomalies including straddling atrioventricular valves, atrioventricular septal defects or a hypoplastic valve or ventricle, or a combination of atrioventricular septal defects and hypoplastic valve or ventricle. RESULTS: Four types of definitive repairs were performed: (1) intraventricular tunnel repair with a baffle from the left ventricle to the aorta (n = 53); (2) use of a valved or nonvalved conduit (n = 20); (3) arterial switch operation with a patch committing the left ventricle to the neo-aorta (n = 16); and (4) cavopulmonary shunt and Fontan procedures (n = 33). Two patients with late postoperative cardiomyopathy had heart transplantation. Potential risk factors included location of the largest ventricular septal defect, presence of additional ventricular septal defects, ventricular outflow obstruction or hypoplasia, or both ventricular outflow obstruction and hypoplasia, previous palliation, and type of definitive operation. There were six early deaths (4.8%) and four late deaths (3.2%), and two heart transplants (1.6%). Overall 15-year survival was 95.8%, 89.7%, and 89.5% for groups 1, 2, and 3, respectively (p = 0.08). Thirteen patients (11.4%) have required 15 reoperations. Mean follow-up for survivors was 76.6 +/- 52.8 months. Up-to-date follow-ups are available on 114 surviving patients. Ninety-five of these patients (83.3%) were in New York Heart Association class I, and the remaining 19 patients (16.7%) were in New York Heart Association class II. Freedom from reoperation was 87%, 72%, and 100% at 15 years for groups 1, 2, and 3, respectively (p = 0.11). CONCLUSIONS: Survival was high for all patients with double outlet right ventricle undergoing intraventricular tunnel repair, arterial switch operation, and repair with a conduit or a modified Fontan procedure. Careful attention to preoperative anatomy dictates the best surgical approach and will enhance outcomes.

Adolescent↗

PubMedDate not supplied

[Left ventricular outflow tract obstruction caused by accessory mitral valve tissue].

An asymptomatic 15-year-old woman was studied because of a systolic ejection murmur. The echocardiogram showed a mobile, leaflet-like structure attached to the ventricular surface of the anterior mitral leaflet, chordae tendineae and papillary muscle. This structure moved to the left ventricular outflow tract during systole occupying the subaortic area. Conventional Doppler examination revealed left ventricular outflow obstruction caused by the accessory mitral valve tissue that produced a pressure gradient of 25 mmHg between the aorta and left ventricle. The diagnosis was not obvious clinically and was based on the echocardiographic data.

Adolescent↗

PubMed1975

Ultrastructure of crista supraventricularis muscle in patients with congenital heart diseases associated with right ventricular outflow tract obstruction.

Ultrastructural studies were made of operatively resected crista supraventricularis muscle in 59 patients with congenital heart diseases, or whom 54 had obstruction to right ventricular outflow. Relationships of anatomic diagnosis, age, peripheral arterial oxygen saturation (PAO2), peak right ventricular systolic pressure gradient and right ventricular end-diastolic pressure (RVEDP) to hypertrophic changes, abnormalities of cellular and myofibrillar orientation, and degenerative alterations were determined. Changes directly related to hypertrophy were: cell diameters greater than 20 mu, irregular cell shape, lobulated nuclei, multiple intercalated discs, dilated T tubules, abnormal Z bands, and increased numbers of ribosomes. Abnormalities of cellular or myofibrillar orientation were focal in distribution and occurred in 12 patients, most of whom had elevated RVEDP, decreased PAO2, markedly enlarged cells, and interstitial fibrosis. Interstitial fibrosis was prominent in 19 patients and was associated with cellular hypertrophy, elevation of RVEDP, and increased age of the patients. Degenerative changes (myofibrillar lysis, abnormally small mitochondria, myelin figure formation, and proliferation of sarcoplasmic reticulum in cardiac muscle cells ocurred in six patients and correlated with increased age, decreased PAO2, and elevated RVEDP. Mitochondria containing glycogen deposits were present in 17 patients, most of whom had decreased PAO2. The variability of morphologic manifestations of chronic cardiac hypertrophy and the relationships of hypertrophic changes to orientation abnormalities and degenerative alterations are discussed.

Adolescent↗

PubMed1979

Left ventricular outflow tract obstruction in transposition of the great arteries: an angiographic study of 74 cases.

Recent advances in techniques of angiocardiography now allow highly accurate assessment of the anatomy of the left ventricle in patients with transposition of the great arteries. The cineangiograms of 225 children with transposition were reviewed using axial cineangiographic techniques and 33 percent were found to have significant left ventricular outflow tract obstruction with or without coexisting ventricular septal defects. The varieties of left ventricular outflow tract obstruction and the associated ventricular septal defects found in this group of patients are described, illustrated and correlated. The advantages of axial angiocardiography in the diagnosis of transposition are pointed out, and the techniques used to produce the axial angiocardiograms are reviewed.

Adolescent↗

PubMed1993

Is there an anatomic basis for subvalvular right ventricular outflow tract obstruction after an arterial switch repair for complete transposition? A morphometric study and review.

The study was initiated by reports on right ventricular outflow tract obstruction in complete transposition of the great arteries after an arterial switch repair. We investigated 39 heart specimens with native, unoperated transposition of the great arteries. Of these, 14 hearts had a ventricular septal defect; 25 had an intact ventricular septum. In each heart specimen the narrowest site of the subaortic outflow tract was measured and compared with the circumference of the aortic orifice. Obstruction was considered to be present if the outflow tract circumference was less than that of the aortic orifice. In addition, the diameter of the ascending aorta immediately above the level of the valve orifices was measured and compared with that of the pulmonary trunk. An obstruction was present in the subaortic right ventricular outflow tract of two hearts (5.1%): one of the obstructions, in a neonatal heart with intact ventricular septum, was caused by a prominent supraventricular crest and anterior trabeculations; the other obstruction was an additional extensive muscular hypertrophy, in the heart of a 13-year-old patient with a similar anatomy, and a septal defect. A mismatch between the diameters of the ascending aorta and the pulmonary trunk was present in 15 of 32 hearts measured. Our observations and a review of the literature confirm that subvalvular right ventricular outflow tract obstruction in hearts with native transposition of the great arteries is infrequent. Nevertheless, the anatomic characteristics of the right ventricular outflow tract are such that the tract is intrinsically narrow and muscular hypertrophy may easily lead to obstruction. After an arterial switch operation, subvalvular obstruction could be caused by dynamic processes analogous to those observed after relief of isolated pulmonary valve stenosis. Anatomic subvalvular obstruction could be due to either an obstruction that was not identified before operation or (a purely speculative hypothesis) subtle degrees of mismatch in size between the proximal aorta and the pulmonary trunk, which may be considered irrelevant at time of operation but may also set into pace a process of ongoing adaptive infundibular hypertrophy.

Academic Medical Centers↗

PubMed1999

Fixed left ventricular outflow tract obstruction in presumed hypertrophic obstructive cardiomyopathy: implications for therapy.

BACKGROUND: A subset of patients presenting with a presumed diagnosis of hypertrophic obstructive cardiomyopathy (HOCM) have a fixed left ventricular outflow tract (LVOT) obstruction. Recognition of this pathophysiologic abnormality is important in choosing therapy. METHODS: Of patients referred for treatment of HOCM, 4 had fixed LVOT obstruction. Clinical and echocardiographic data and surgical findings were reviewed. RESULTS: In the 4 patients with clinical features consistent with HOCM or HOCM-like conditions, echocardiography showed fixed LVOT obstruction with an early-peaking LVOT Doppler signal or absence of severe systolic anterior motion of the mitral valve. The causes of fixed obstruction included accessory mitral tissue with associated fibrous ring (1 patient), fixed subaortic tunnel stenosis (2 patients), and a discreet subaortic ridge (1 patient). After surgical relief of the fixed LVOT obstruction, all patients had relief of the ventricular outflow tract gradient. CONCLUSIONS: Not all patients with a presumed diagnosis of HOCM have isolated dynamic LVOT obstruction but may have isolated or additional fixed obstruction. Careful two-dimensional and Doppler echocardiography are needed to identify this subset of patients who are best treated surgically.

Adult↗

PubMed2006

Left ventricular outflow tract obstruction after bioprosthetic mitral valve replacement with posterior mitral leaflet preservation.

We present a case of transient left ventricular outflow tract obstruction after mitral valve replacement with a high-profile bioprosthesis; only the posterior native mitral valve leaflet was preserved. A 76-year-old woman was admitted to our institution with pulmonary edema. Two weeks earlier, she had undergone mitral valve replacement at our hospital due to severe mitral stenosis and 2+ mitral regurgitation complicated by cardiac failure and atrial fibrillation. The patient was taking digoxin, furosemide, and warfarin at the time of readmission. Echocardiography showed a narrowed left ventricular outflow tract. Doppler echocardiography revealed a peak 64-mmHg gradient between the septum and the strut of the bioprosthesis. The patient was successfully treated medically. This case indicates that the risk of left ventricular outflow tract obstruction after bioprosthetic mitral valve replacement is not always eliminated by removal of the anterior mitral valve leaflet when the posterior mitral leaflet is preserved.

Aged↗