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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↗
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↗
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↗
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↗
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↗
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↗
PubMed1977

Coexisting right and left hypertrophic subvalvular stenosis and fixed left ventricular outflow obstruction due to aortic valve stenosis.

A case of fixed left ventricular outflow tract obstruction due to aortic valve stenosis coexisting with right- and left-sided subvalvular hypertrophic stenosis is documented with hemodynamic data, angiograms, echocardiograms and findings at surgery. Histologic examination of the septal muscle with light and electron microscopy revealed hypertrophy of the muscle but none of the characteristics of idiopathic hypertrophic subaortic stenosis. Septal hypertrophy with subvalvular obstruction can occur secondary to left ventricular pressure overload due to fixed left ventricular outflow tract obstruction and is not always the chance occurrence of two separate diseases.

Aged↗
PubMed1991

[Right ventricular outflow obstruction due to accessory tricuspid valve tissue in corrected transposition of the great arteries with ventricular septal defect].

A 27-year-old man known to have corrected transposition of the great arteries (CTGA) associated with a ventricular septal defect (VSD) was admitted to our hospital with a suspected increase of the shunt volume. The patient is a first class bodybuilder. Heart catheterization confirmed the diagnosis of a "right-ventricular" mass obstructing the "right-ventricular" outflow tract, which had already been seen at echocardiography. The intraoperative finding showed the tumor to be accessory tissue of the anterior tricuspid leaflet prolapsing through the VSD into the subvalvular outflow tract of the right ventricle. The accessory tricuspid valve tissue was removed by transatrial access. The VSD was closed by a dacron patch using the same route. The postoperative course was uneventful.

Adult↗
PubMedDate not supplied

Relationship between mitral regurgitation and left ventricular outflow obstruction in hypertrophic cardiomyopathy.

To clarify the relationship between mitral regurgitation and left ventricular outflow obstruction, Doppler and two-dimensional echocardiographic studies were performed in 62 patients with hypertrophic cardiomyopathy (22 with and 40 without obstruction caused by mitral systolic anterior motion with septal contact). Pulsed Doppler echocardiography with color Doppler flow imaging demostrated that in 20 of the 22 patients with obstruction, mitral regurgitation occurred mainly during midsystole from the onset to the end of mitral-septal contact. Such midsystolic mitral regurgitation was not observed in patients without obstruction, except in three of 25 patients with mild mitral systolic anterior motion without septal contact. Furthermore, that regurgitation developed or disappeared together with the obstruction during follow-up periods or pharmacologic interventions. Two-dimensional echocardiography showed that in 21 of the 22 patients with obstruction, a distal residual portion of the "anterior" mitral leaflet moved anteriorly in early systole and protruded into the outflow tract during midsystole to cause the obstruction. In the other patient with obstruction, who had only early systolic mitral regurgitation, a distal residual "posterior" leaflet moved similary. These results may indicate that the midsystolic mitral regurgitation is hydrodynamically induced by the midsystolic pressure gradient across the protruding distal residual anterior mitral leaflet.

Adult↗
PubMed1975

The association of fixed and dynamic left ventricular outflow obstruction.

Twelve patients were investigated echocardiographically and angiographically and were shown to have severe fixed obstruction to the left ventricular outflow tract. Eight had valvular stenosis, and four had discrete subvalvular membranes. Two of the patients had additional dynamic obstruction of the left ventricular outflow tract. This was recognized preoperatively by echocardiography because of abnormal systolic motion of the mitral leaflet. At the time of definitive surgery for relief of the fixed obstruction, the additional dynamic obstruction was identified and treated, since persistent residual obstruction may lead to death in the immediate postoperative period or to long-term symptoms. The dynamic left ventricular outflow obstruction is probably a result of the hypertrophy produced by the fixed obstruction.

Adolescent↗
PubMed1985

[Marked right ventricular outflow obstruction in two children with hypertrophic cardiomyopathy].

Two children, aged one year and nine months, and six years, both with hypertrophic cardiomyopathy, presented as severe right ventricular outflow obstruction were presented. Initially, both of them were suspected of having heart disease because of precordial systolic murmurs. Their tentative diagnosis was pulmonary stenosis. Their apex cardiograms and carotid pulse waves were not diagnostic. Asymmetrical septal hypertrophy with systolic anterior motion of the mitral valve was identified by echocardiography in both cases. Cardiac catheterization revealed left ventricular outflow tract pressure gradients of 5 mmHg and 30 mmHg, respectively. The right ventricular peak systolic gradient was 100 mmHg and 82 mmHg and left ventricular end-diastolic pressure was 26 mmHg and 18 mmHg, respectively. Selective right and left ventricular angiocardiograms demonstrated severe right ventricular outflow obstruction, and hypertrophy of the interventricular septum. One of them underwent resection of the right ventricular outflow tract muscle, which showed histological findings characteristic of hypertrophic cardiomyopathy. This patient died suddenly at the age of 10 years. Infants or young children with hypertrophic cardiomyopathy often have associated predominant right ventricular outflow tract obstruction, progressive congestive heart failure, and death. Therefore, correct diagnosis and careful treatment are mandatory for proper management.

Cardiac Output↗
PubMed1975

Relief of sever left ventricular outflow obstruction in a case of hypertrophic obstructive cardiomyopathy treated with practolol.

The clinical and haemodynamic findings in a patient with hypertrophic obstructive cardiomyopathy and severe left ventricular outflow obstruction are presented. Treatment with an increasing dose of orally administered practolol up to a maximum of 1200 mg a day, resulted in symptomatic improvement, and abolition of the resting gradient when the patient was recatheterized six months later.

Administration, Oral↗