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At least 55 records · Page 3Linked to original sources
PubMed1975

Effects of systemic-pulmonary shunts on regional myocardial blood flow in experimental pulmonary stenosis.

The pulmonary artery of anesthetized dogs was constricted until right ventricular failure occurred (decreased cardiac output and aortic blood pressure; elevated right ventricular end-diastolic pressure). Coronary blood flow distribution was measured by means of an electromagnetic flowmeter and radioactive microspheres. With moderate levels of pulmonary stenosis (right ventricular pressure to 60 per cent of systemic pressure), right ventricular coronary flow increased (30 per cent, p smaller than 0.01) despite a significant fall in right ventricular driving pressure (aorto-right atrial pressure). Right ventricular failure occurred when right ventricular coronary flow did not increase sufficiently to meet raised oxygen requirements. Opening a pulmonary-systemic shunt during right ventricular failure increased pulmonary blood flow but lowered coronary driving pressure further, as blood was diverted into the lungs through the low-resistance fistula. Consequently, right ventricular coronary flow fell 50 per cent (p smaller than 0.01) and right ventricular failure with pulmonary stenosis resulted in a 362 per cent (p smaller than 0.01) increase in right coronary flow plus improved cardiac output. We made the following conclusions: (1) Right ventricular failure with pulmonary stenosis and intact ventricular septum is due to inadequate right ventricular blood flow to meet raised oxygen demands; (2) opening a pulmonary-systemic shunt may potentiate this failure and exaggerate ischemia by lowering coronary driving pressure and reducing right ventricular coronary flow.

Animals↗
PubMed1993

Concurrence of supravalvular aortic stenosis and peripheral pulmonary stenosis in three generations of a family: a form of arterial dysplasia.

Isolated supravalvular aortic stenosis (SVAS) commonly is an autosomal dominant trait; it may also occur in the Williams syndrome (WS). While peripheral pulmonary stenosis (PPS) can occur in the same individual with familial isolated SVAS, concurrence of these lesions in different relatives of a family is uncommon. We describe five affected individuals in one family; three had isolated SVAS, one had isolated PPS, and one had SVAS and PPS. Based on this family and review of literature, we suggest that SVAS is a form of arterial dysplasia encompassing PPS in its spectrum. It is developmentally distinct from other left heart obstructive lesions that are hypothesized to be related to blood flow abnormalities in the developing embryo. We also conclude that the clinical disorder in this family represents one that is distinct from WS.

Abnormalities, Multiple↗
PubMed2002

Supravalvular aortic stenosis and peripheral pulmonary stenosis coexisting with a straight thoracic spine.

Supravalvular aortic stenosis (SVAS) is recognized in cases of Williams syndrome and in sporadic cases not associated with other features of the syndrome. It is also well recognized as associated with peripheral pulmonary stenosis (PPS). A male patient was diagnosed as having PPS at the age of 1 year and 8 months, and was found at the age of 18 years to have SVAS. Cardiac catheterization showed that he had a localized type of SVAS and regression of the PPS. Chest X-ray showed that he did not have the normal thoracic curvature. His 19-year-old sister had also been diagnosed with PPS, and his 43-year-old mother was known to have a harsh systolic cardiac murmur of unknown etiology. Cardiac magnetic resonance imaging showed a localized type of SVAS in his mother also, though not in his sister, both of whom had a somewhat straight thoracic spine, most noticeably in the mother, though not to the degree observed in the patient. This case appears to be familial, though it is not clear whether this skeletal abnormality is an unknown phenotypic feature of this cardiovascular disease.

Adult↗
PubMed1994

Successful repair of the right atrial isomerism, double outlet right ventricle, common atrioventricular canal, pulmonary stenosis, and total anomalous pulmonary venous connection.

A 6-year-old boy was successfully operated on for double outlet ventricle, common atrioventricular canal with severe valvular regurgitation, right atrial isomerism, L-loop ventricles, total anomalous pulmonary venous connection, and pulmonary stenosis with hypoplastic left pulmonary artery. The interventricular rerouting from the left ventricle to the ascending aorta was performed with a spiral patch, the interatrial switching was performed by a Mustard patch, the common atrioventricular orifice was partitioned and valve repair was performed, and an 18-mm valved conduit was inserted between the right ventricle and the pulmonary artery. Although the patient had a small residual ventricular septal defect and pulmonary stenosis, the patient is alive and well.

Abnormalities, Multiple↗
PubMed2002

An infant with subvalvar and valvar aortic stenosis, subvalvar and valvar pulmonary stenosis, severe biventricular hypertrophy and pulmonary hemorrhage.

An infant with subvalvar and valvar pulmonary stenosis, subvalvar, and valvar aortic stenosis and hypertrophic cardiomyopathy, who presented with pulmonary hemorrhage, is reported. He had right ventricular hypertrophy, thickened pulmonary valve leaflets, severe asymmetric left ventricular hypertrophy with outflow tract obstruction, and a thickened and dysplastic aortic valve.

Abnormalities, Multiple↗
PubMed2001

Critical pulmonary stenosis.

Critical pulmonary stenosis causes cyanosis and can be potentially lethal in the neonate. Initial treatment includes general resuscitation and infusion of prostaglandin E1 to dilate the ductus. The diagnosis is usually made echocardiographically, but a right ventriculogram in the outflow tract may be necessary in some patients with only a tiny valve opening. Preformed catheters may aid in the passage of an appropriate guidewire. Valvuloplasty should be performed with a balloon approximately 1.2 times the annulus diameter. Most patients remain mildly to moderately cyanotic immediately after the procedure. With right ventricular (RV) growth and improved RV compliance, the cyanosis eventually resolves. Some patients may require prolonged prostaglandin infusion, a surgical shunt, or other mechanical means of maintaining systemic-to-pulmonary artery flow. Intermediate--to long-term results are excellent. However, only 5%-10% of patients may require surgical relief of residual valve or subvalvular stenosis. Very long-term follow-up raises concern about the significance of induced pulmonary insufficiency. Up to 30% of patients may require repeat balloon valvuloplasty.

Catheterization↗
PubMed1990

Regression of infundibular pulmonary stenosis after successful balloon pulmonary valvuloplasty in adults.

Between July 1985 and March 1988, 22 adult patients with congenital pulmonary stenosis underwent balloon pulmonary valvuloplasty. There were 10 males and 12 females aged 16-45 (average 25 +/- 9.9) years. All patients had additional mild to severe infundibular stenosis; 16 were restudied 6-36 (mean 12.6) months later by repeat catheterization. Student's t-test was used for comparison of data. Right ventricular (RV) systolic pressure before dilatation was 84-196 (mean 129 +/- 32.3) mm Hg, and the peak pulmonary gradient (PPG) was 60-176 (mean 111 +/- 33.2) mm Hg immediately after dilatation. The RV systolic pressure dropped to 32-140 (mean 59.2 +/- 27) (P less than 0.001); and PPG dropped to 10-113 (mean 37.8 +/- 26.4) (P less than 0.001), and the infundibular gradient ranged from 8 to 113 (mean 35.1 +/- 25.8) mm Hg. The infundibular diameter, before dilatation, ranged from 2 to 15 (mean 9.5 +/- 4) mm Hg. At repeat catheterization, the RV systolic pressure dropped further to 33-66 (mean 42.8 +/- 9.7) mm Hg and the PPG was reduced to 0-48 (mean 18.4 +/- 10.9) mm Hg (P less than 0.001). The infundibular gradient regressed to 0-34 (mean 15 +/- 8.8) mm Hg (P less than 0.001). The infundibular diameter increased to 8-25 (mean 15.8 +/- 5.4) (P less than 0.001). It is concluded that moderate to severe infundibular stenosis, in adults, can regress after successful pulmonary valvuloplasty.

Adult↗
PubMed1975

Echocardiographic differentiation of infundibular from valvular pulmonary stenosis.

Echocardiographic tracings of the pulmonary valve were examined in 24 normal subjects, 16 patients with valvular pulmonary stenosis and 3 patients with infundibular pulmonary stenosis. In normal subjects, atrial contraction produced a slight posterior opening motion of the pulmonary valve leaflet (a wave). This presystolic opening motion (a wave) varied with respiration, and maximal a wave depth recorded during quiet inspiration (Amax) averaged 3.7 plus or minus 1.2 (standard error of the mean) mm (range 2 to 7 mm). In the 10 cases with moderate or severe valvular pulmonary stenosis, increased force of right atrial contraction and elevated right ventricular end-diastolic pressure resulted in an increased posterior or opening motion of the pulmonary valve leaflet, and Amax averaged 9.6 plus or minus 2.0 mm (range 8 to 13 mm, P less than 0.001 versus normal). When both anterior and posterior leaflets were recorded, presystolic opening or doming of the valve was observed. In six cases of mild valvular pulmonary stenosis, Amax averaged 4 plus or minus 2.5 mm (not significant). In patients with infundibular pulmonary stenosis, marked chaotic systolic fluttering of the valve leaflet, which lies in the turbulent stream of blood distal to the obstruction, was recorded. This finding was never seen with valvular pulmonary stenosis. In two cases of mild infundibular pulmonary stenosis, the amplitude of presystolic opening motion was within the normal range of 3 and 7 mm. In one case of severe infundibular pulmonary stenosis, no presystolic opening motion was recorded, thus suggesting that the small pressure changes produced by atrial systole failed to reach the valve leaflets. Echocardiography, therefore, should be of use in differentiating valvular from infundibular pulmonary stenosis.

Adolescent↗
PubMed2006

Surgical management of infants with isolated supravalvular pulmonary stenosis: case reports.

Pulmonary stenosis (PS) can be seen from the right ventricular outflow tract to the peripheral pulmonary arteries. Most frequently, the obstruction occurs at the level of the pulmonary valve; however, it occurs less frequently at the infindibular level within the trabecular component of the right ventricle or within the pulmonary arterial pathways. Lesions at any of these levels can occur as part of more congenital cardiac malformations such as tetralogy of Fallot, complete transposition of great arteries, or atrial septal defect. Isolated supravalvular pulmonary stenosis (iSPS) is less common than other types of PS. In this study, we present our experience with 4 patients who underwent cardiopulmonary bypass operation for iSPS. In one patient, the circular stenotic area was noted on the touch point of the pulmonary valve. Right ventricular pressures ranged from 70 to 90 mmHg, and the pulmonary artery mean pressures ranged from 14 to 17 mmHg. In all patients, the left ventricular and aortic systolic, diastolic, and mean pressures were moderately increased. Pulmonary artery stenosis was treated successfully using a pericardial or Dacron patch on cardiopulmonary bypass. Various techniques such as balloon dilation have been proposed to deal with this problem, but these may often be unsuccessful because of the elasticity and recoil of the pulmonary artery constrictive ring. Even though endovascular stenting and/or balloon angioplasty have been recently proposed as an initial treatment strategy, they may be associated with some severe complications including pulmonary artery thrombosis or stent migration. Our study, even though it consists of a limited number of cases, suggests that open heart surgery using an oval-shaped patch may be a used as the other main choice for the treatment of iSPS.

Cardiopulmonary Bypass↗