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Results for “Ventricular Outflow Obstruction”

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PubMedDate not supplied

Two dimensional and Doppler echocardiographic evaluation of double chambered right ventricle.

Two-dimensional and Doppler echocardiographic findings in 20 patients with double chambered right ventricle are described. All patients had the diagnosis established by cardiac catheterisation and confirmed at operation. Echocardiographic evaluation was done prior to surgical correction. Anomalous muscle bands in right ventricular cavity were detected in 16 patients. Doppler flow velocities in the right ventricular cavity suggested infundibular obstruction to blood flow at a low level in all 17 patients studied by Doppler echocardiography. Ventricular septal defects (11 patients), pulmonary stenosis (3 patients), and aortic regurgitation (3 patients) were detected accurately before operation by echocardiographic examination. Failure to detect the anomalous muscles in right ventricular cavity may occur in adult patients with poor anterior resolution and in those with severe right ventricular outflow obstruction and myocardial hypertrophy. Two dimensional echocardiography with Doppler flow analysis is useful in the evaluation and differential diagnosis of right ventricular outflow obstructions prior to invasive studies and surgical intervention.

Adolescent↗
PubMed2005

Implantation of endovascular stents for the obstructive right ventricular outflow tract.

OBJECTIVES: To evaluate the effectiveness and long term outcomes of catheter intervention for obstructive conduits between the right ventricle and pulmonary arteries. DESIGN: Retrospective chart review. SETTING: Tertiary care paediatric cardiology unit. PATIENTS AND INTERVENTIONS: 70 procedures in 68 children (median age at intervention 6 years, median interval after conduit insertion 3.4 years) were analysed. All children had haemodynamic indications for conduit replacement. Twenty four children underwent a second intervention (stent dilatation in 17, second stent implantation in seven). RESULTS: Mean (SD) conduit pressure gradient decreased from 44 (18) mm Hg to 18 (12) mm Hg at the initial intervention (n = 62, p < 0.001) and from 39 (15) mm Hg to 23 (10) mm Hg at the second intervention (n = 16, p < 0.001). The percentage of the predicted right ventricular outflow area increased from 17 (9)% to 44 (22)% at the initial intervention (n = 62, p < 0.001) and from 24 (8)% to 29 (11)% at the second intervention (n = 21, p < 0.001). The conduit was subsequently replaced in 33 children. Freedom from conduit replacement from the time of stent implantation was 83%, 75%, and 47% at one, two, and five years, respectively, and from the time of the initial conduit surgery it was 87%, 64%, and 42% at five, eight, and 10 years, respectively. Body growth was maintained, no deaths were reported during follow up, and pulmonary insufficiency was well tolerated. CONCLUSION: A catheter treatment strategy for obstructive conduits is safe and effective in prolonging conduit function.

Adolescent↗
PubMed2005

Aortic hypoplasia and right ventricular outflow tract obstruction in a young man with uncontrolled hypertension.

We report the case of a 35-year-old man who presented to hospital with symptomatic uncontrolled hypertension. He had no other conventional cardiovascular risk factors, but did have previous cataract surgery and patent ductus arteriosus repair. Echocardiography revealed normal valves, right ventricular outflow tract obstruction, and heavy calcification of the aortic root compromising luminal diameter. Pulmonary angiography confirmed supravalvular and subvalvular pulmonary stenosis. Aortography showed hypoplasia of the entire aortic trunk extending into the iliac arteries, but without involvement of other major branches. A possible unifying diagnosis, with the combination of aortic hypoplasia, pulmonary artery stenosis, patent ductus arteriosus, and cataracts, was believed to have been congenital rubella syndrome. Although associated with numerous cardiovascular abnormalities, aortic hypoplasia is an extremely rare manifestation of congenital rubella that, to our knowledge, has been reported in only two cases in the literature to date.

Adult↗
PubMed1991

Left ventricular outflow tract obstruction in atrioventricular septal defects: a pathologic and morphometric evaluation.

Subaortic stenosis has been described with increasing frequency as an ominous feature of atrioventricular septal defect (AVSD), especially following surgical correction of the anomaly in non-Down's syndrome patients. In order to study the surgical anatomy of the left ventricular outflow tract in this malformation, 48 hearts featuring AVSD were examined. Obstructive lesions were classified into unequivocal forms (class A, 13.5%) and potential ones (class B, 10.8%). In the remaining hearts (class C, 75.7%) no obstruction was noted. In class A, subaortic stenosis was due to exaggeration of the anticipated anomalous arrangement of atrioventricular valve tensor apparatus, to the persistence of a subaortic muscular infundibulum, and to a discrete fibrous diaphragm. A potential for subaortic stenosis is provided by the unwedged position of the aortic valve. The left ventricular outflow tract is transformed into a long, forward-displaced fibromuscular channel. Morphometric analysis showed in AVSD (with both common annulus and separate orifices) a significantly (p less than 0.01) lower inflow/outflow tract ratio, and a significantly (p less than 0.01) lower right ventricular/left ventricular outflow length ratio than normal hearts. These results suggest that AVSD is characterized not only, as commonly stated, by inflow tract shortening, but by outflow tract lengthening as well. On these anatomical grounds, nearly all cases of AVSD could harbor the potential for subaortic stenosis; however, this becomes a real hazard (class B) only when associated with forward displacement of the left anterior papillary muscle, or direct insertion on the ventricular septum of the anterior bridging leaflet, and it may be converted to an actual obstruction by the effects of surgery.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve Stenosis↗
PubMed2006

Relationship between outflow obstruction and left ventricular functional impairment in hypertrophic cardiomyopathy: a Doppler echocardiographic study.

Left ventricular outflow tract (LVOT) obstruction is predictive of a worse outcome in hypertrophic cardiomyopathy (HCM). In a detailed Doppler echocardiographic study of 178 selected HCM patients, the group of patients (n = 73) with the obstructive form (resting peak gradient > or = 30 mmHg) presented more hypertrophy and poorer systolic and diastolic left ventricular (LV) functions than the HCM group (n = 105) without obstruction. LVOT peak gradient was positively correlated with hypertrophy (P < 0.0001) and negatively to tissue Doppler mitral annulus systolic (P = 0.0001) and early diastolic (P < 0.0001) velocities. The gradient significantly correlated with E/Ea ratio (r = 0.67; P < 0.0001). By multiple regression, LVOT gradient was related to E/Ea, LV maximal thickness and left atrial size. In comparison with patients without obstruction, patients with obstruction presented greater hypertrophy (P < 0.0001), lower systolic and early diastolic mitral annulus velocities (both P < 0.0001), higher E/Ea ratio (P < 0.0001) and higher global function index (P < 0.0001). In HCM, beyond the effects on hypertrophy, LVOT obstruction is an independent determinant of LV functional abnormalities.

Adolescent↗
PubMed1993

Morphologic basis for obstruction to right ventricular outflow in hypertrophic cardiomyopathy.

The mechanism by which obstruction to right ventricular (RV) outflow occurs in patients with hypertrophic cardiomyopathy (HC) is not well understood. To clarify this issue, 5 severely symptomatic patients (aged 18 to 55 years, mean 30) with HC and marked subpulmonic obstruction (basal peak systolic pressure gradients 60 to 118 mm Hg) were studied. Four patients also had obstruction to left ventricular outflow (maximal basal or provocable pressure gradient 12 to 110 mm Hg). The RV outflow obstruction in each patient resulted from greatly hypertrophied musculature comprised of crista supraventricularis, moderator band or trabeculae. Operative resection of portions of this muscle resulted in abolition or substantial reduction of the RV outflow gradient (to 0 to 11 mm Hg) in the 3 patients with both pre- and postoperative hemodynamic studies. The left ventricular wall and ventricular septum also were massively thickened (32 to 40 mm) in each patient. These findings support the view that marked RV outflow tract obstruction in patients with HC is due to greatly hypertrophied RV muscle, and that operative resection will relieve the outflow gradients and normalize RV systolic pressure. The muscular RV hypertrophy causing obstruction appeared to constitute a primary and excessive hypertrophic process involving both ventricles.

Adolescent↗
PubMed1983

Fate of dynamic left ventricular outflow tract obstruction after anatomic correction of transposition of the great arteries.

Fourteen patients undergoing successful anatomic correction for transposition of the great arteries had subpulmonary gradients of 20 to 120 mm Hg (mean 40) across the left ventricular outflow tract before surgery. Ten patients had an intact ventricular septum, and four had an additional ventricular septal defect. In one patient obstruction was due to ballooning of the septal leaflet of the tricuspid valve through the ventricular septal defect. In the remaining patients obstruction was due to bulging of the interventricular septum plus or minus septal hypertrophy and with or without a fibromuscular shelf. At operation the pulmonary valve was normal and the left ventricular outflow tract was of adequate dimension with no organic obstruction. No attempt at surgical widening was made. After surgery abnormalities revealed by echocardiography were immediately reversed. Routine reinvestigation 6 to 26 months after surgery in 10 patients showed no gradient across the left ventricular outflow tract and normal development of this region.

Child↗