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PubMed1981

Effect of negative intrathoracic pressure on left ventricular outflow tract obstruction in muscular subaortic stenosis.

To study the effect of respiration and negative intrathoracic pressure on the left ventricular outflow tract gradient in patients with muscular subaortic stenosis, we studied nine patients using various respiratory maneuvers at the time of cardiac catheterization. Deep inspiration decreased the left ventricular outflow tract gradient from 60 +/- 11 to 34 +/- 6 mm Hg (p less than 0.01) and decreased the left ventricular ejection time (corrected for heart rate) from 0.42 +/- 0.01 to 0.38 +/- 0.01 second (p less than 0.001). The Müller maneuver decreased the left ventricular outflow tract gradient from 69 +/- 13 to 7 +/- 3 mm Hg (p less than 0.001) and decreased the corrected left ventricular ejection time from 0.42 +/- 0.02 to 0.24 +/- 0.01 second (p less than 0.01). In keeping with this amelioration of left ventricular outflow tract obstruction, echocardiography showed a reduction or abolition of the systolic anterior motion of the anterior mitral leaflet, and auscultatory and phonocardiographic studies revealed a decrease or abolition of the apical systolic murmur. These findings indicate that negative intrathoracic pressure reduced the left ventricular outflow tract gradient in muscular subaortic stenosis. We believe that negative intrathoracic pressure produced these changes by increasing left ventricular afterload through an increase in left ventricular transmural pressure, resulting in a decrease in the left ventricular outflow tract obstruction. These observations provide an explanation for the decrease in pressure gradient that occurs on inspiration in patients with muscular subaortic stenosis.

Adolescent↗
PubMed1996

[A successful staged complete repair in a neonate with coarctation of aorta, ventricular septal defect, and left ventricular outflow tract obstruction--a new palliative operation].

An eight day old neonate with coarctation of aorta (CoA), ventricular septal defect (VSD), and severe left ventricular outflow tract obstruction (LVOTO) underwent a successful staged repair following a new palliative operation, which comprised aortic arch reconstruction, PTFE bypass graft between main pulmonary artery and descending thoracic aorta, and pulmonary artery banding (PAB) distal to the graft. Insertion of the bypass graft was aimed to allow enough systemic blood flow and reduces after load of ventricles after PAB. The second staged definitive operation was performed 21 days after the first operation and the procedure comprised partial resection of posterioly deviated infundibular septum via VSD, patch closure of VSD, and division of the graft. No evidence of progression of LVOTO was noted until the second stage operation despite the tight PAB. This new palliative operation, which does not need aid of cardiopulmonary bypass, is particularly effective for those with LVOTO, and can be safely applied even to seriously ill neonate. Thus, for the staged repair in aortic arch obstructive disease with VSD and severe LVOTO, this procedure can be a good alternative for palliative operation.

Aortic Coarctation↗
PubMed1997

[Temporary use of left ventricle-to-pulmonary artery extracardiac conduit for the surgical repair of complete transposition of the great arteries with ventricular septal defect and left ventricular outflow tract obstruction].

A 1.8-year-old boy was first admitted to our hospital at 12 days of age with the diagnosis of transposition of the great arteries (TGA), ventricular septal defect (VSD), and left ventricular outflow tract obstruction (LVOTO). Echocardiography and catheter examination at 10 months of age disclosed severe organic stenosis of left ventricular outflow tract (LVOT) with its diameter of 5.6 mm (50% of N) and the left to right ventricular (LV/RV) pressure ratio of 0.6. At 1.8 years of age, he underwent complete correction which comprised intraatrial switch (Senning procedure), direct closure of VSD, and removal of thickened endocardium at LVOT. Because of the residual LVOTO, evidenced by postoperative LV/RV pressure ratio of 1.4, placement of 14 mm PTFE graft extracardiac conduit was concomitantly performed. The conduit from the left ventricular apex to the main pulmonary artery effectively lowered the left ventricular pressure with LV/RV pressure ratio of 0.68. Repeat catheter examination at 2.10 years of age revealed further descent of LV/RV pressure ratio to 0.32. Based on the findings that balloon occlusion of the conduit elicited only a minimal elevation of the left ventricular pressure (from 30 to 34 mmHg), the conduit was removed at 3.6 years of age. The third catheter examination at the age of 3.9 years confirmed LV/RV pressure ratio of 0.43. The patient is leading a normal life. without medication 3 years after the operation. This experience draws us to conclude that placement of left ventricle-to-pulmonary artery conduit concomitantly with the intraatrial switch is a useful adjunctive procedure for the complete correction of TGA, small VSD, and LVOTO, and that, in a subset of the patients, this procedure may allow amelioration of LVOTO and secondary removal of the conduit.

Blood Vessel Prosthesis↗
PubMed1987

Surgical anatomy of left ventricular outflow tract obstruction in complete atrioventricular septal defect. A concept for operative repair.

An integral part of the heart with an atrioventricular septal defect and a Rastelli type A valve configuration is left ventricular outflow tract obstruction. Current surgical techniques do not cater to this particular anatomic facet, and left ventricular outflow tract obstruction has been reported as a postoperative problem. The present study has focused on the surgical anatomy of the mode of attachment of the left superior atrioventricular valve and its relationship to the left ventricular outflow tract. It appeared that the anchoring of the superior leaflet was a major factor in limiting the excursions of the superior leaflet, contributing also to the tightness of the subaortic left ventricular outflow channel. On that basis a surgical repair is proposed in which the greater part of the tightly bound superior leaflet is detached from the septal crest, so that the left ventricular outflow tract is widened.

Chordae Tendineae↗
PubMed2001

[Reoperation for late postoperative right ventricular outflow tract obstruction].

Between February 1993 and July 2000, 18 patients with a mean age of 7.9 years underwent re-operation for critical stenosis of the right ventricular outflow tract. Their diagnoses of these patients included tetralogy of Fallot (n = 7), transposition of the great arteries (n = 6), truncus arteriosus communis (n = 3), and double outlet right ventricle with pulmonary stenosis (n = 2). The first operations were extracardiac conduit operations (n = 9), arterial switch operations (n = 6) and patch reconstruction of the right ventricular outflow tract (n = 3). At re-operation, the right ventricular outflow tract obstruction was released completely and reconstructed using a monocusp ventricular outflow patch (n = 14), valved pericardial roll (n = 2), or bovine pericardial patch sparing the native pulmonary valve annulus (n = 2). There were no early deaths, although one patient died of arrhythmia 2.6 years after re-operation. The pressure gradient across the right ventricular outflow tract, right ventricular systolic pressure, and right ventricle to systemic systolic pressure ratio were satisfactorily relieved (84.3 +/- 19.0 vs. 16.7 +/- 19.7 mmHg, 109.2 +/- 20.5 vs. 48.7 +/- 16.7 mmHg, 0.92 +/- 0.25 vs. 0.43 +/- 0.16; p < 0.001, p < 0.001, p < 0.001, respectively). The right ventricular end-diastolic volume index and right ventricular ejection fraction were also improved (166.3 +/- 85.2 vs. 105.6 +/- 28.8% of normal, 38.3 +/- 12.6 vs. 50.9 +/- 8.8%; p < 0.05, p < 0.005, respectively). Re-operation should be done before the development of marked right ventricular dysfunction, while it can still be performed at a low risk with satisfactory results.

Child↗
PubMed2003

Mid-systolic septal deceleration. A new sign of left ventricular outflow tract obstruction obtained by color-coded tissue Doppler echocardiography.

Hypertrophic obstructive cardiomyopathy (HOCM) is characterized by the presence of a dynamic left ventricular outflow tract gradient. We studied septal longitudinal motion by color coded tissue Doppler echocardiography in a 69-year old HOCM patient during and after catheter based treatment by trans coronary alcohol ablation of septal hypertrophy. The presence of dynamic left ventricular outflow tract obstruction was associated with a characteristic abrupt mid-systolic septal deceleration pattern in the tissue Doppler velocity trace. Five weeks after treatment, this pattern was no longer visible at rest.

Aged↗
PubMed1999

Left ventricular outflow tract obstruction after partial atrioventricular septal defect repair.

BACKGROUND: Narrowing of the left ventricular outflow tract has been associated with partial atrioventricular septal defect (PAVSD) in about 3% of patients. Because of the predisposing anatomy, hemodynamically significant obstruction in the subaortic area may appear after repair of ostium primum atrial septal defects. METHODS: From 1984 to 1998, 40 patients underwent surgical correction of PAVSD by patch closure. The mean age at the initial repair was 5.8 years (range 3 months to 22 years). RESULTS: Nine patients had 12 subsequent operations for hemodynamically significant subaortic obstruction. The mean age at PAVSD repair was 17 months (3 to 42 months) (p < 0.001 compared with others). Follow-up work-up was obtained due to symptoms in 5 patients and an abnormal echocardiogram in 4 asymptomatic patients. Subaortic stenosis developed at a mean of 5 years (range 4 months to 10 years), and 6 or more years in 4 patients. The mean age at subaortic stenosis repair was 6 years (range 2 to 12 years). Nine patients underwent subaortic fibromuscular resection. Of these, 4 developed recurrent stenosis and 2 have undergone additional operations. CONCLUSIONS: Left ventricular outflow tract obstruction after PAVSD repair may be more frequent than reported. Because of the progressive nature of the process, echocardiography should be utilized liberally on patients to uncover subclinical stenosis. Long-term follow-up is essential for diagnosis due to delayed appearance and lack of reliable clinical signs.

Adolescent↗
PubMed1976

Cross-sectional echocardiographic localization of sites of left ventricular outflow tract obstruction.

Real time two-dimensional echocardiographic studies of left ventricular outflow tract cross-sectional anatomy were obtained by the multicrystal echocardiographic method (Bom system) in 35 patients with various types of outflow obstruction as delineated by clinical, hemodynamic and angiographic studies. In each patient the noninvasive test allowed prediction of the site of obstruction. In valvular aortic stenosis, echocardiographic diagnostic findings included poststenotic dilatation of the ascending aorta, thickened aortic cusp tissue and increased superior-inferior cusp excursion (doming). The site of supravalvular aortic stenosis was readily observed although echocardiographic findings often underestimated the degree of obstruction recorded at cardiac catheterization. In patients with discrete subvalvular aortic stenosis, the major finding was a localized thickening of the septum and anterior mitral anulus producing a narrowing of the left ventricular outflow tract that was present in diastole and persisted throughout the cardiac cycle.

Adolescent↗
PubMed1986

Septal origin of sustained ventricular tachycardia in a patient with right ventricular outflow tract obstruction after correction of tetralogy of Fallot.

Right ventricular hypertension and ventricular arrhythmias are risk factors for sudden death after correction of tetralogy of Fallot, but sustained ventricular tachycardia has been reported only in patients without residual hemodynamic abnormalities. A patient with right ventricular hypertension and hypotensive ventricular tachycardia tolerated the arrhythmia better after relief of right ventricular outflow tract obstruction. This case provides insight into the relationship between hemodynamic abnormalities and the clinical consequences of arrhythmias. To our knowledge, it is the first report of ventricular tachycardia originating in scar adjacent to the ventricular septal defect patch after correction of tetralogy of Fallot.

Adolescent↗
PubMed2001

[Evaluation of dynamic left ventricular outflow tract obstruction by dobutamine stress echocardiography].

OBJECTIVE: This study was planned to evaluate the dynamic left ventricular outflow tract (LVOT) obstruction by using dobutamine stress echocardiography (DSE) in patients with asymmetric septal hypertrophy and/or septal bulging, who have no signs of LVOT gradient detected by conventional echocardiography, with symptoms mimicking hypertrophic obstructive cardiomyopathy (HOCM). METHODS: In sixty-one consecutive patients referred to our echocardiography laboratory with HOCM pre-diagnosis, exercise dyspnea and limitation of exercise capacity were evaluated. DSE was performed in 31 patients who fulfilled the inclusion criteria. Patients were divided into two groups according to the degree of dynamic gradient increase above baseline values during stress-test (Group 1 < 30 mmHg, Group 2 > 30 mmHg). Left ventricular diameters, septum and posterior wall thicknesses, ejection fraction, LVOT and aortic root diameters, presence of septal bulging and systolic anterior motion (SAM) and degree of septal angulation were sought. RESULTS: There were no significant differences between groups by means of LV diameters, septum and posterior wall thicknesses, EF, LVOT and aortic root diameters, presence of septal bulging (p > 0.05); whereas there were significant differences in SAM and degree of septal angulation (p < 0.05 and p < 0.0001, respectively). Systolic anterior motion (r = 0.61, p < 0.0001) and degree of septal angulation (r = -0.71, p < 0.001) correlated significantly with the dynamic gradient increase. CONCLUSION: Presence of SAM and degree of septal angulation obtained by DSE are reliable parameters to determine dynamic LVOT obstruction in patients who have asymmetric septal hypertrophy and septal bulging with no gradient on LVOT by conventional echocardiography.

Cardiotonic Agents↗
PubMed2001

Accessory mitral valve tissue causing left ventricular outflow tract obstruction: case reports and literature review.

Accessory mitral valve (AMV) tissue is a rare congenital malformation causing left ventricular outflow tract obstruction (LVOTO). We present three patients with AMV tissue undergoing surgery. A 60-year old man presented with an AMV leaflet, mild LVOTO and coronary artery disease and underwent accessory leaflet excision and coronary revascularization. A 24-year old man presented with an AMV leaflet, LVOTO and interatrial septal defect and underwent defect closure and accessory leaflet resection. An 8-month-old girl underwent interventricular septal closure and AMV leaflet resection but died on postoperative day 5 from progressive heart failure. Another 87 cases with AMV tissue were identified in the literature The anomaly was classified as: Type I (fixed: A = nodular, B = Membranous), and type II (mobile: A = pedunculated, B = leaflet like). Type IIB was further subdivided as rudimentary chordae and developed chordae. Patients with AMV tissue causing LVOTO may undergo mass removal with acceptable postoperative outcome. Prophylactic removal of AMV tissue should not be attempted in patients with no or mild LVOTO and no other associated heart defects. These patients should be followed and observed periodically by Doppler echocardiography to identify any progression in LVOTO.

Adult↗
PubMed2000

Congenital Heart Surgery Nomenclature and Database Project: right ventricular outflow tract obstruction-intact ventricular septum.

The extant nomenclature for pulmonary atresia/stenosis with intact ventricular septum, pulmonary artery and/or pulmonary branch stenosis, double chambered right ventricle, absent pulmonary valve with intact ventricular septum, and ventricular to pulmonary artery conduit failure is reviewed for the purpose of establishing a unified reporting system. The subject was debated and reviewed by members of the STS-Congenital Heart Surgery Database Committee and representatives from the European Association for Cardiothoracic Surgery. All efforts were made to include all relevant nomenclature categories using synonyms where appropriate. Multiple risk factors were considered such as coronary artery fistulas/sinusoids, tricuspid annular size and location of peripheral pulmonary artery stenoses. A comprehensive database set is presented which is based on a hierarchical scheme. Data are entered at various levels of complexity and detail which can be determined by the clinician. These data can lay the foundation for comprehensive risk stratification analyses. A minimum database set is also presented which will allow for data sharing and would lend itself to basic interpretation of trends. Potential diagnostic related risk factors for each lesion are presented.

Databases, Factual↗
PubMed1992

Impact of surgical relief of outflow obstruction on thallium perfusion abnormalities in hypertrophic cardiomyopathy.

BACKGROUND: To assess the impact of surgical relief of left ventricular outflow obstruction on myocardial perfusion abnormalities in patients with obstructive hypertrophic cardiomyopathy, 20 symptomatic patients who underwent a septal myectomy or mitral valve replacement were studied with assessment of myocardial perfusion during exercise by 201Tl emission computed tomography before and 6 months after surgery. METHODS AND RESULTS: Before surgery, 15 patients had myocardial perfusion defects during exercise that completely normalized at rest, one patient had both reversible and fixed perfusion defects, two patients had fixed defects only, and two patients had normal exercise and rest thallium scans. After surgical relief of left ventricular outflow obstruction (basal gradient reduced from 62 +/- 40 to 7 +/- 12 mm Hg, p less than 0.001; peak provokable gradient reduced from 131 +/- 27 to 49 +/- 36 mm Hg, p less than 0.001), repeat exercise thallium studies showed complete normalization of perfusion defects in 11 patients, including the two patients with fixed defects alone before surgery, and improvement in the magnitude and distribution of perfusion defects in five additional patients. This was associated with a significant reduction in the number of patients with reversible regional defects (five patients compared with 13 patients before surgery, p = 0.026) and of patients with endocardial hypoperfusion (four patients compared with 12 patients before surgery, p = 0.024). Furthermore, increased lung uptake of thallium was noted in five patients after surgery, compared with 12 patients before surgery (p = 0.055). Only two patients with reversible perfusion defects before surgery had unchanged postoperative studies. However, four patients acquired new fixed defects as a consequence of surgery, and two of these four had the greatest severity and distribution of left ventricular hypertrophy by echocardiography. These four patients experienced a substantially greater decrease in ejection fraction (-26 +/- 15%) after surgery than the remaining patients (-3 +/- 14%, p less than 0.01). CONCLUSIONS: Surgical relief of left ventricular outflow obstruction results in normalization or improvement of myocardial perfusion in the majority of patients with reversible and fixed perfusion defects by 201Tl scintigraphy. However, surgery may result in myocardial injury and scarring, with consequent decreased left ventricular ejection fraction in some patients.

Cardiac Catheterization↗
PubMed2000

[Modified Konno procedure for a child with left ventricular outflow tract obstruction after repair of atrioventricular septal defect: a transaortic transpulmonary approach].

A one-year-old infant underwent repair of atrioventricular septal defect with common orifice. About 2 years later, echocardiography revealed a left ventricular outflow tract obstruction for the first time. Because of progression of the obstructive lesion, a modified Konno procedure through a transaortic transpulmonary approach was later performed at 8 years old, and the postoperative course was uneventful. This is a useful procedure for left ventricular outflow tract obstruction with normal aortic valve and aortic annulus, because it can both preserve a native aortic valve and dose not necessitate right ventriculotomy in resection of hypertrophied muscle and patch enlargement of interventricular septum.

Aorta↗
PubMed1994

Left ventricular outflow tract obstruction and hemolytic anemia after mitral valve repair with a Duran ring.

We report a case of mitral valve repair with a Duran ring that was complicated by left ventricular outflow tract obstruction, mitral regurgitation, and hemolytic anemia. A 59-year-old man with severe mitral valve regurgitation underwent mitral valve repair, including a Duran ring annuloplasty. Postoperatively, left ventricular outflow tract obstruction developed and echocardiography revealed severe systolic anterior motion of the mitral valve. The patient then underwent mitral valve replacement with a 29-mm St. Jude valve.

Adult↗
PubMed1985

Secondary left atrioventricular valve replacement in atrioventricular septal (AV canal) defect: a method to avoid left ventricular outflow tract obstruction.

Patients with atrioventricular septal defects are morphologically predisposed to subaortic obstruction. Some individuals require secondary left atrioventricular valve replacement for severe incompetence persisting after repair, and they are especially susceptible to left ventricular outflow tract obstruction. A surgical technique is described for replacement of the atrioventricular valve which seems to avoid the complication of left ventricular outflow tract obstruction by the prosthesis.

Adolescent↗
PubMed2006

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

This report describes the echocardiographic diagnosis of accessory mitral valve tissue causing left ventricular outflow tract obstruction in a symptomatic man. The accessory tissue was surgically removed and the mitral valve replaced with complete resolution of left ventricular outflow tract gradient and symptoms. The case illustrates the importance of transthoracic and transesophageal echocardiography in the diagnosis and preoperative evaluation of this rare but treatable cause of subaortic valve obstruction.

Humans↗
PubMed1975

Mechanism of left ventricular outlfow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis).

Left ventricular outflow obstruction in patients with idiopathic hypertrophic subaortic stenosis or obstructive asymmetric septal hypertrophy is due to abnormal forward motion during systole of the anterior mitral leaflet. To determine why some patients with this disease hav left ventricular outflow obstruction whereas others do not, we studied a large number of patiens with assymetric septal hypertrophy using both one- and two-dimensional echocardiography. In 100 patients with asymmetric septal hypertrophy and 22 normal subjects, mitral valve position at the onset of systole was quantitated by measuring the distance from the ventricular septum to the mitral valve and the distance from the mitral valve to the posterior left ventricular wall. None of the normal subjects and only 3 (6 percent) of 51 patients with nonobstructive asymmetric septal hypertrophy had a septal-mitral valve distance of less than 20 mm compared with 23 (66 percent) of 35 patients with obstructive asymmetric septal hypertrophy. Moreover, the mitral valve at the onset of systole was actually positioned forward in the left ventricular activity. Two-dimensional studies in 11 patients with obstructive asymmetric septal hypertrophy revealed that contraction of the malaligned papillary muscles did not cause the abnormal forward mitral valve motion. We propose that the left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy occurs as a result of two factors: (1) narrowing of the left ventricular outflow tract at the onset of systole, and (2) hydrodynamic forces generated by contraction on the left ventricle.

Aortic Stenosis, Subvalvular↗