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Results for “Ventricular Outflow Obstruction”

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At least 19 recordsLinked to original sources
PubMed1973

Reflex vascular responses to left ventricular outflow obstruction and activation of ventricular baroreceptors in dogs.

Reflex vascular responses to acute left ventricular outflow obstruction were studied in anesthetized dogs. The studies were done to compare the effects of activation of ventricular baroreceptors on vascular resistance in skeletal muscle (gracilis muscle) and skin (hindpaw); to identify afferent and efferent pathways which mediate the reflex vasodilatation; and to assess the relative contribution of ventricular baroreceptors and baroreceptors in left atrium and pulmonary vessels in responses to left ventricular outflow obstruction. The gracilis artery and the cranial tibial artery to the paw were perfused separately at constant flow. Changes in perfusion pressure to each bed reflected changes in vascular resistance. Outflow obstruction was produced by inflating a balloon in the left ventricular outflow tract for 15 s while pressures in the left ventricle and aortic arch were measured. Inflation of the balloon increased left ventricular pressure and decreased pressure in the aortic arch. Low and high levels of obstruction produced dilator responses averaging -5+/-3 (SE) and -42+/-11 mm Hg in muscle and -1+/-1 and -3+/-2 mm Hg in paw. Denervation, phentolamine, and glyceryltrinitrate caused greater dilatation in paw than did left ventricular outflow obstruction. This indicates that dilator responses in the paw were not limited by a low level of resting neurogenic constrictor tone or by a negligible dilator capacity of these vessels. Obstruction to left ventricular inflow increased left atrial pressure, but did not cause reflex vasodilatation. This suggests that low pressure baroreceptors in atria or pulmonary vessels did not contribute to vasodilator responses to left ventricular outflow obstruction. Vasodilator responses to outflow obstruction were blocked by bilateral vagotomy, sectioning the sciatic and obturator nerves, and administration of phentolamine, but were not decreased by atropine or tripelennamine. The results indicate that activation of left ventricular baroreceptors produces striking vasodilatation in skeletal muscle, but only slight vasodilatation in skin. The data suggest that the difference in dilator responses in the two beds results from greater withdrawal of adrenergic constrictor tone to skeletal muscle than to skin. Activation of sympathetic cholinergic or histaminergic dilator pathways does not contribute to the dilatation.

Animals↗
PubMed1997

Right ventricular outflow obstruction with intact ventricular septum in adults.

Cardiothoracic surgeons whose practice is limited to adults rarely see patients with right ventricular outflow obstruction and an intact ventricular septum. Of more than 10,000 open-heart procedures performed at our institution from 1983 to 1993 (in patients 18 to 75 years old), only 5 procedures were for correction of this problem. Both the pulmonary valve and the subvalvular area were abnormal in these 5 patients, and 4 of the 5 had subvalvular stenosis. The gradient across the right ventricular outflow tract was measured by cardiac catheterization before repair in all patients and averaged 118 mmHg. Various surgical approaches were used for repair. In the 2 patients whose pressures were measured postoperatively, the gradients were 25 mmHg and 45 mmHg, respectively. There were no operative deaths. At follow-up (range, 2 months to 5 years after surgery), all patients were in New York Heart Association functional class I and all had murmurs. Those who underwent echocardiography were found to have minimal gradients across the right ventricular outflow tract.

Adult↗
PubMed1988

Effect of isolated right ventricular outflow obstruction on left ventricular function in infants.

Resting left ventricular (LV) function was evaluated in 29 infants with isolated right ventricular (RV) outflow obstruction. Age-corrected cardiac index was significantly inversely correlated with the degree of obstruction (r = 0.59, p = 0.0001). Right ventricular hypertension resulted in septal displacement and altered LV geometry. The magnitude of RV outflow obstruction related closely to the degree of LV distortion. Septal displacement toward the LV free wall was associated with lower values for cardiac index, indexed LV end-diastolic volume, ejection fraction, ratio of early to atrial LV diastolic inflow and with a higher RV ejection fraction. The LV end-diastolic volume index and the ratio of early to atrial LV diastolic inflow correlated with the degree of obstruction and amount of septal displacement. Four infants evaluated during the development of supravalvar pulmonary stenosis demonstrated decreasing cardiac index during development of obstruction and significant increase in cardiac index after surgical relief. These findings indicate that significant RV outflow obstruction in infants is associated with a reversible alteration in LV function related to abnormal LV geometry and impaired LV diastolic filling.

Cardiac Output↗
PubMed1991

Anomalous insertion of papillary muscle directly into anterior mitral leaflet in hypertrophic cardiomyopathy. Significance in producing left ventricular outflow obstruction.

BACKGROUND: Obstruction to left ventricular outflow in hypertrophic cardiomyopathy (HCM) is usually due to systolic anterior motion of the mitral valve. Occurrence of structural mitral valve abnormalities in HCM and their significance in producing outflow obstruction (even in the absence of typical systolic anterior motion) has not been fully appreciated. METHODS AND RESULTS: Analysis of 78 mitral valves excised from patients with obstructive HCM showed that 10 (13%) had anomalous insertion of one or both left ventricular papillary muscles directly into the anterior mitral leaflet. This malformation was identified by echocardiography, which demonstrated direct continuity between the hypertrophied papillary muscle and mitral leaflet, resulting in a long rigid area of midcavity narrowing that appeared to be solely or largely responsible for outflow obstruction. Basal subaortic pressure gradients were large (70-150 mm Hg). Mitral valve replacement reduced the outflow gradient substantially to 0-15 mm Hg in four patients with postoperative cardiac catheterization. However, two other patients who underwent septal myotomy/myectomy had persistent symptoms and incomplete relief of obstruction (gradients 60 and 70 mm Hg) because of continued midcavity apposition of papillary muscle and ventricular septum. CONCLUSIONS: Anomalous papillary muscle insertion into anterior mitral leaflet represents a mechanism of obstruction to left ventricular outflow in patients with HCM and differs considerably from typical dynamic obstruction caused by mitral valve systolic anterior motion that occurs in many other patients with HCM. Recognition of this malformation emphasizes the diverse morphological expression of HCM and also has important clinical implications for patients requiring operation because the gradient is likely to persist even after adequate myotomy/myectomy; consequently, mitral valve replacement would appear to be the operation of choice in most such patients.

Adult↗
PubMed1994

Systemic ventricular outflow obstruction progresses after the Fontan operation.

To evaluate the course of systemic ventricular outflow obstruction after the Fontan operation, the records of 57 hospital survivors of that procedure were reviewed. Ventricular outflow obstruction was identified in 7 patients (group 1) and was absent in 50 patients (group 2). Overall, the ventricular outflow gradient in group 1 was 6.3 +/- 2.9 mm Hg (mean +/- standard error) before the Fontan operation and 7.6 +/- 3.9 mm Hg at hospital discharge. Ventricular outflow obstruction subsequently progressed to 80.1 +/- 17.3 mm Hg (range, 33 to 165 mm Hg; p < 0.02) a mean of 28 months postoperatively. One patient died of severe progressive ventricular outflow obstruction. Group 1 did not differ from group 2 in age, ventricular morphology, presence of a subaortic outflow chamber, prior shunt, or length of follow-up. Compared with group 2, however, patients in group 1 more commonly had an aorta arising from a hypoplastic ventricle (p < 0.001) and had undergone prior pulmonary artery banding (p = 0.005). We conclude that systemic ventricular outflow obstruction occurs commonly after a Fontan procedure (incidence, 12%; 70% confidence interval, 9% to 18%) and is a progressive lesion.

Child, Preschool↗
PubMed1990

Isolated unruptured sinus of Valsalva aneurysm producing right ventricular outflow obstruction.

An unusual case of right ventricular outflow obstruction and right heart failure due to an isolated unruptured congenital sinus of Valsalva aneurysm originating from the right coronary sinus in a 75-year-old-man is described. The diagnosis was made by two-dimensional echocardiography and cardiac catheterization. Successful surgical resection of the aneurysm resulted in dramatic symptomatic improvement.

Aged↗
PubMed1988

[Correlation of left ventricular outflow obstruction with mitral regurgitation].

Our previous study of mitral regurgitation in obstructive hypertrophic cardiomyopathy suggested that left ventricular outflow obstruction due to systolic anterior motion of the distal residual anterior mitral leaflet may hydrodynamically induce mid-systolic mitral regurgitation. To test this hypothesis, we examined whether drug-induced left ventricular outflow obstruction in dogs might cause mitral regurgitation. Dobutamine, 20-60 micrograms/kg/min, induced the obstruction due to mitral systolic anterior motion with mitral-septal contact in 11 of 18 dogs. Pulsed Doppler and contrast echocardiography demonstrated that mitral regurgitation was concomitantly induced in the 11 dogs. The regurgitation was prominent during mid-systole from the onset to the end of mitral-septal contact. Two-dimensional echocardiography showed reduction of the mitral annular dimension and anterior shifts of the mitral valve coaptation during drug infusion in the 11 dogs. Accordingly, the distal portion of the mitral valve, especially of its anterior leaflet, became residual, and moved anteriorly in early systole and protruded into the outflow tract during mid-systole. Catheter-tip pressure recordings simultaneous with two-dimensional echocardiographic observation revealed that the outflow pressure gradient occurred across the protruding distal residual mitral valve. The onset and the end of the pressure gradient were nearly simultaneous with those of the mitral-septal contact. After cessation of the infusion, the mid-systolic mitral regurgitation disappeared together with the obstruction. These results indicate a close relationship between left ventricular outflow obstruction and mid-systolic mitral regurgitation, and strongly support the hypothesis that the obstruction due to systolic anterior motion of the distal residual anterior mitral leaflet is responsible for mitral regurgitation.

Animals↗
PubMed2000

Predictors of left ventricular outflow obstruction following single-stage repair of interrupted aortic arch and ventricular septal defect.

This study looked at echocardiographic predictors of left ventricular outflow obstruction after primary neonatal repair of interrupted aortic arch and ventricular septal defect. Results of this study indicate that the only significant independent predictor of left ventricular outflow obstruction is aortic valve diameter; all patients with an aortic valve diameter <4.5 mm (Z score <-5) subsequently developed obstruction, whereas patients with annuli >4.5 mm (Z score >-5) remained free from obstruction.

Abnormalities, Multiple↗
PubMed1990

[A case of hypertrophic cardiomyopathy with right ventricular outflow obstruction manifested during three-year follow-up study].

A case is reported of a 55-year-old female with idiopathic hypertrophic cardiomyopathy, which was accompanied with outflow obstruction in the right ventricle developed during the previous 3 years without lesion of the left ventricle. In 1984, she was admitted to our hospital to be examined for cardiac murmurs and abnormal electrocardiogram including ST depression and inverted T. The findings of echocardiography and cardiac catheterization revealed non-obstructive hypertrophic cardiomyopathy. She had been treated with sympathetic beta-blockade and calcium antagonist for 3 years until she complained of dyspnea on exertion, and she was readmitted to our hospital in 1987. Echocardiographic findings showed protrusion of the ventricular septum toward the right ventricle and systolic turbulent flow along the right ventricular outflow tract (by pulsed Doppler technique). A pressure gradient of 20 mmHg across the protrusion was detected by the examination of the cardiac catheter. However, neither protrusion nor pressure gradient was observed in the left ventricular outflow tract as well as that in 1984. Idiopathic hypertrophic cardiomyopathy has been described as involving both ventricles, and outflow obstruction is the usual hemodynamic finding in the left ventricle. However, right ventricular outflow obstruction is the usual hemodynamic finding in the left ventricle. However, right ventricular outflow obstruction with the left ventricular outflow tract intact has been very rare. In addition, in this case, the change of hemodynamic characteristics from non-obstructive to obstructive hypertrophic cardiomyopathy, and the development of these changes only in the right ventricle were observed during the last 3 years.

Cardiomyopathy, Hypertrophic↗
PubMed1983

Management of infants with left ventricular outflow obstruction by conduit interposition between the ventricular apex and thoracic aorta.

On the basis of experience with older children, creation of a double-outlet ventricle by interposition of a valved conduit between the apex of the left ventricle and the thoracic aorta appeared to be an option for treating life-threatening left ventricular outflow tract obstruction even in the small heart of the infant. Over the recent 3 year period, nine infants ranging in age from 3 days to 13 months with various forms of left ventricular outflow tract obstruction underwent placement of an apical-aortic conduit to decompress the hypertensive left ventricle. There were two early and two late deaths. Five patients are clinically well and developing normally 5 to 23 months following the operation. This series demonstrates that this operation permits normal growth and development in infants previously failing to thrive. Echocardiographic and cardiac catheterization data suggest that left ventricular function need not be adversely affected by placement of a stent in the small infant ventricle; rather, ventricular function can be markedly improved. Although the mortality in this series is appreciable, it appears that apical-aortic conduit interposition can provide significant palliation for infants with otherwise lethal left ventricular outflow tract obstruction.

Aorta, Thoracic↗
PubMed1989

Balloon dilation of postoperative right ventricular outflow obstructions.

Balloon dilation was attempted in 16 patients, aged 5 months to 19.5 years, with right ventricular outflow obstruction after repair of congenital heart defects. Stenosis of a valved conduit between the pulmonary ventricle and pulmonary artery was present in nine patients with a mean transvalvular peak systolic ejection gradient of 61.6 +/- 21.0 mm Hg and a mean right ventricle to aorta pressure ratio of 0.9 +/- 0.2. Supravalvular pulmonary stenosis was present in seven patients; in five, stenosis was at the anastomotic site after the arterial switch operation with a mean peak systolic ejection gradient of 72.2 +/- 10.6 mm Hg and mean right ventricle to aorta pressure ratio of 0.93 +/- 0.05. The other two patients had stenosis at a previous pulmonary artery band site with a peak systolic ejection gradient of 60 and 65 mm Hg and right ventricle to aorta pressure ratio of 0.75 and 0.72, respectively. Balloon dilation was successful in three of nine patients with a valved conduit; two of them had additional successful balloon dilation of the right pulmonary artery. In five of the nine patients (including one with successful dilation) the conduit was replaced 5.7 +/- 4.5 months after balloon dilation. Balloon dilation was successful in only one of the five patients with supravalvular pulmonary stenosis after the arterial switch operation and partially successful in the two patients with supravalvular pulmonary stenosis at a previous band site. The success rate of balloon dilation of postoperative right ventricular outflow obstruction is much lower than that for other right heart obstructions.

Bioprosthesis↗
PubMed1992

Dynamic left ventricular outflow obstruction related to atrial fibrillation.

A 48-year-old male patient underwent mitral annuloplasty for severe mitral regurgitation secondary to myxomatous degeneration of the mitral valve, with ruptured chordae. Intraoperative transesophageal echocardiography showed satisfactory repair. The patient developed postoperative atrial fibrillation and clinical and echocardiographic evidence of left ventricular outflow obstruction. Following conversion to sinus rhythm, the evidence for left ventricular outflow obstruction markedly improved. We suggest that postoperative atrial fibrillation may precipitate dynamic left ventricular outflow obstruction following mitral annuloplasty.

Atrial Fibrillation↗
PubMed1979

Nongenetically transmitted disproportionate ventricular septal thickening associated with left ventricular outflow obstruction.

Clinical, haemodynamic, and morphological features are described in 2 patients with disproportionate ventricular septal thickening, left ventricular outflow obstruction with systolic anterior motion of the anterior mitral leaflet, and either acquired or congenital heart disease. The disproportionate septal thickening in these patients appeared to be secondary to their underlying cardiac disease rather than a manifestation of genetically transmitted hypertrophic cardiomyopathy. One patient with combined aortic and mitral stenosis had severe systolic anterior motion of the anterior mitral leaflet and a residual large systolic pressure gradient between left ventricle and systemic artery after aortic valve replacement. In this patient the systolic anterior motion was evident in the presence of mitral valve stenosis. The other patient with mild aortic stenosis and a previously repaired coarctation of the aorta also had mild systolic anterior motion and a small subaortic systolic pressure gradient. Hence, these 2 patients demonstrate that disproportionate septal thickening secondary to acquired or congenital heart disease may be associated with left ventricular outflow obstruction and systolic anterior motion of the anterior mitral leaflet.

Adolescent↗
PubMed1980

Accessory flaplike tissue causing ventricular outflow obstruction.

In three cases, two in children and one in a young adult, ventricular outflow obstruction was caused by a valvelike flap of accessory endocardial tissue. The angiocardiographic feature was that of a narrow radiolucent, crescent-shaped or linear filling defect corresponding to the site of obstruction. Resection of the accessory tissue was performed in each case at the time of correction of associated conditions. In one case (a woman 20 years of age) the obstructing membrane was in the outflow tract of the right ventricle, and a ventricular septal defect was associated. In each of the other two cases the outflow tract of the left ventricle was the site of obstruction. In one (a 14-month-old boy), an ostium primum type of atrial septal defect and cleft mitral valve were associated; in the remaining case (a 7-year-old boy) complete transposition and ventricular septal defect were also present. In the latter case a Mustard procedure was performed and was followed by death. Successful results were obtained in the first two patients.

Adult↗
PubMed1990

Use of Doppler echocardiography and amyl nitrite inhalation to characterize left ventricular outflow obstruction in hypertrophic cardiomyopathy.

The presence of left ventricular outflow tract obstruction (LVOTO) of either a resting or dynamic nature may have important therapeutic and prognostic implications in patients with hypertrophic cardiomyopathy (HCM). Doppler echocardiograms combined with amyl nitrite (Amyl) inhalation were performed in 333 consecutive patients referred for suspected HCM to diagnose and categorize the nature and severity of LVOTO. Hypertrophic cardiomyopathy was present by 2-D and M-mode criteria in 145/333 (44 percent) patients. Normal limits of resting and post-Amyl continuous wave Doppler peak left ventricular outflow tract velocities were established in 15 subjects with completely normal 2-D and Doppler echocardiograms. Based on these criteria, of the 145 patients with HCM, 63 (43 percent) were classified as having resting LVOTO, peak velocity 4.2 +/- 1.3 m/s. Among 82 patients with HCM without resting LVOTO, 47 (57 percent) received Amyl. Latent LVOTO was provoked in 25/47 (53 percent), peak post-Amyl velocity 4.5 +/- 1.2 m/s. The remaining 22 (47 percent) had nonobstructive HCM, as indicated by no significant increase in post-Amyl velocity. Among a total 62 subjects receiving Amyl, none experienced serious morbidity or mortality. Doppler echocardiography, in conjunction with Amyl inhalation in selected patients, is a useful noninvasive method to diagnose and categorize patients with HCM according to the nature and severity of LVOTO.

Aged↗
PubMed1981

Right ventricular outflow obstruction from thrombus with small peripheral pulmonary emboli.

A patient is described with clinical features of massive pulmonary embolism and a normal pulmonary angiogram. At necropsy, a large thrombus obstructed right ventricular outflow. A right atrial or right ventricular angiogram is suggested in patients suspected of having pulmonary embolism when a pulmonary angiogram shows the pulmonary trunk and main right and left pulmonary arteries to be normal.

Adult↗