Obstruction To Right Ventricular Outflow Research Articles

Quantification of Pulmonary Regurgitation by Vector Flow Mapping in Congenital Heart Patients after Repair of Right Ventricular Outflow Obstruction: A Preliminary Study

Vector flow mapping (VFM) enables direct visualization of flow pattern and estimation of flow volume. The aim of this study was to determine its accuracy in the quantification of pulmonary regurgitation (PR) in congenital heart patients after repair of right ventricular (RV) outflow obstruction. This study comprised two parts: (1) validation of VFM in the quantification of PR in patients with repaired tetralogy of Fallot by cardiac magnetic resonance and (2) clinical application of VFM to determine PR in patients after biventricular repair of pulmonary atresia and stenosis with intact ventricular septum. PR was quantified by calculation of VFM-derived pulmonary regurgitant ratio (PRVFM), defined as ratio of backward to forward flow volume. Coefficients of variations for intra- and interobserver variability in the measurements of PRVFM were 7.0% and 10.4%, respectively. Fourteen patients with repaired tetralogy of Fallot aged 31.3±7.3years were studied. Their PRVFM correlated strongly with cardiac magnetic resonance-derived PR fraction (r=0.95, P<.001) and RV end-diastolic volume (r=0.84, P<.001). In the second part, 14 patients with pulmonary atresia with intact ventricular septum aged 25.6±6.0years, 14 patients with pulmonary stenosis aged 24.2±7.0years, and 14 healthy control subjects were studied. PRVFM was found to increase across groups of subjects with absent (4.6±3.3%), mild (11.1±7.1%), moderate (29.6±7.8%), and severe (50.1±8.2%) PR as defined semiquantitatively by color flow mapping. Furthermore, PRVFM correlated strongly with the ratio of PR color jet to width of RV outflow (r=0.92, P<.001). VFM is a reproducible technique for accurate quantification of PR in congenital heart patients after repair of RV outflow obstruction.

Outcome of the Repair of Double-Chambered Right Ventricle: A single centre experience

Background: The presence of anomalous muscle bundles may pro-duce a pressure gradient between the inflow and outflow portions of the right ventricle, resulting in double-chambered right ventricle. We reviewed the outcomes of double chambered right ventricle surgical repair.Methods: Between December 2012 and January 2014, 6 patients under went surgical repair of a double-chambered right ventricle. The patients ranged in age from 3 years to 20 years (mean 8.2±5.9 yrs). Right ventricular outflow tract pressure gradients were from 60 to 120 mm Hg (mean 63.3±40.3). An associated ventricular septal defect was present in 4 patients (66.66%).Results: There were no hospital or late deaths. Mean postsurgical follow up was 3.8±0.8 months). No patient required further surgery to relieve obstruction of right ventricular outflow tract.Conclusions: Surgical repair of a double chambered right ventricle yield excellent hemodynamic and functional results.Cardiovasc. j. 2016; 8(2): 165-168

Relation of right ventricular mechanics to exercise tolerance in children after tetralogy of Fallot repair

Progressive right ventricular (RV) dysfunction and exercise intolerance are common problems after tetralogy of Fallot (TOF) repair. We investigated RV myocardial deformation and dyssynchrony in children after TOF repair and their association with exercise capacity. Asymptomatic children after TOF repair were investigated by 2-dimensional speckle tracking echocardiography, magnetic resonance, and metabolic exercise study. Patients with RV outflow obstruction were excluded. Peak RV longitudinal strain and strain rate (SR) and dyssynchrony (RV intraventricular delay) were compared with healthy controls. Associations between RV strain, dyssynchrony, and exercise capacity were analyzed. Thirty-nine (81%) of 48 TOF patients and 40 healthy controls had adequate RV strain imaging. The TOF patients had moderately dilated RVs and normal RV ejection fraction. Right ventricular peak systolic strain (-23.2% ± 5.1% vs -28.5% ± 8.5%, P < .001) and SR (-1.46 ± 0.68 vs -2.1 ± 0.8, P < .001) were reduced in TOF patients compared with controls. Right ventricular intraventricular delay was higher in TOF patients (146.0 ± 159 vs 71.0 ± 92 milliseconds, P = .008). Decreased RV strain and SR were associated with increased RV dyssynchrony (strain parameter estimate [PE] 6.31 [2.30], P = .007; SR [PE] 11.32 [3.84], P = .004). Increased RV-left ventricular delay was associated with prolonged QRS duration (PE 0.13 [0.058], P = .03) and reduced RV ejection fraction (PE -2.95 [1.275], P = .02). Reduced RV peak SR was associated with decreased exercise peak oxygen uptake (PE 0.14 [0.07], P = .04). After repair of TOF, asymptomatic children have reduced RV deformation in association with RV dyssynchrony and reduced exercise tolerance.

Indolent cardiac angioma mimicking hypertrophic obstructive cardiomyopathy and causing right ventricular outflow tract obstruction

A 20-year-old female with a 12-year history of hypertrophic obstructive cardiomyopathy (HOCM) with progressive right ventricular outflow obstruction (RVOTO) and mild left ventricular outflow obstruction (LVOTO) was referred to our institution for consideration of septal myomectomy due to symptomatic outflow tract obstruction. The patient had New York Heart Association Class III dyspnoea, abdominal bloating, nausea, and vomiting with palpitations and presyncope on standing or walking up stairs. Examination revealed …

Right Ventricular Infundibulum Sparing (RVIS) Tetralogy of Fallot Repair

The natural history of standard (large, transmural right ventriculotomy) repair of tetralogy of Fallot (TOF) is associated with a concerning incidence of right ventricular (RV) failure and reoperation. We believe preserving the infundibulum using a TOF repair method with a mini-(<5 mm) or no ventricular incision optimizes RV function and confers long-term benefit. Over the past 13 years, we have uniformly applied this RV infundibulum sparing (RVIS) strategy. Using a retrospective cohort study design, 304 TOF patients who underwent the RVIS strategy (July 1995-June 2008) were reviewed. Median weight and age at repair: 8 kg (3-62 kg) and 9 months (2 days-23 years). Seventeen percent (51) of patients required a systemic-to-pulmonary artery shunt. Ninety-nine percent of patients had a mini- 73% (222) or no 26% (79) ventricular incision. Postoperative morbidity included arrhythmias 3% (10), postoperative bleeding 2% (7), temporary renal failure 1% (3), and neurologic injury <1% (2). Thirty-day survival was 99.7%. Overall 1 and 7-year Kaplan-Meier survivals were 97% and 96%. In nonsyndromic children, only 1 patient has died in the RVIS strategy. A total of 3.2% (10) of patients had reoperations. Twenty-one percent (65/304) of patients have been followed for >7 years (median: 8.5 years). None of them have severe dilation, > mild RV outflow obstruction, an arrhythmia, or a pacemaker/AICD. Ninety-five percent of these patients have normal RV function; 3 (4.6%) had mild dysfunction. This cohort has excellent exercise tolerance (MaxVO2 (mean): 41 ± 12 mL/kg/min). The RVIS strategy has allowed morbidity, mortality, and reoperation rates to be minimized. Midterm results suggest that RVIS does appear to preserve RV function. Longer term follow-up will be essential in establishing if the RVIS strategy can change the natural history of repaired TOF.

Right and left ventricular systolic function late after repair of tetralogy of Fallot

Right ventricular (RV) dysfunction has adverse effects on long-term outcome in patients with repaired tetralogy of Fallot (TOF). We employed serial radionuclide angiography (RNA) to examine RV and left ventricular (LV) systolic function in adults late after TOF repair and its relation to clinical outcome. We reviewed 10-year records of 95 patients (53 men) with TOF followed in our clinic (mean age at repair 12.6 ± 10.5 years, mean age at last follow-up 37.7 ± 9.8 years) who underwent at least 2 RNAs between 1987 and 1997. Most patients were well by the end of the study (80% were New York Heart Association class I, 17% were class II, and 3% were in class III). Sixteen patients experienced sustained tachyarrhythmias (8 had atrial; 8 patients had ventricular). One patient died suddenly. Fifteen patients underwent RV outflow reoperations (15 underwent pulmonary valve replacement; 7 had relief of RV outflow obstruction); RV systolic function during exercise in these 15 patients was significantly impaired before and returned to similar levels after surgery, compared with the rest of the patients. Overall, RV and LV function remained stable in the whole group at a mean interval of 5.7 ± 2.2 years between first and last RNA. This group of closely followed adults with TOF remained well over 10 years with a low incidence of sudden death and stable RV and LV systolic function, despite a relatively large number of RV outflow reoperations. Aggressive intervention for right-sided hemodynamic abnormalities may have contributed to this outcome. Preserved ventricular function may herald a favorable long-term outlook in this group.

82-Year-Old Man With Recurrent Syncope

82-Year-Old Man With Recurrent Syncope

Effect of Body Repositioning After Venous Air Embolism

BACKGROUND: Current therapy for massive venous air embolism (VAE) may include the use of the left lateral recumbent (LLR) position, although its effectiveness has been questioned. This study used transesophageal echocardiography to evaluate the effect of body repositioning on intracardiac air and acute cardiac dimension changes. METHODS: Eighteen anesthetized dogs in the supine position received a venous air injection of 2.5 ml/kg at a rate of 5 ml/ s. After 1 min the dogs were repositioned into either the LLR, LLR 10 degrees head down (LLR-10 degrees), right lateral recumbence, or remained in the supine position. RESULTS: Repositioning after VAE resulted in relocation of intracardiac air to nondependent areas of the right heart. Peak right ventricular (RV) diameter increase and mean arterial pressure decrease were greater in the repositioned animals compared with those in the supine position (P < 0.05). Right ventricular diameter and mean arterial pressure showed an inverse correlation (r = 0.81). Peak left atrial diameter decrease was greater in the LLR and LLR-10 degrees positions compared with the supine position (P < 0.05). Repositioning did not influence peak pulmonary artery pressure increase, and no correlation was found between RV diameter and pulmonary artery pressure. All animals showed electrocardiogram and echocardiographic changes reconcilable with myocardial ischemia. CONCLUSIONS: In dogs, body repositioning after VAE provided no benefit in hemodynamic performance or cardiac dimension changes, although relocation of intracardiac air was demonstrated. Right ventricular air did not appear to result in significant RV outflow obstruction, as pulmonary artery pressure increased uniformly in all groups and was not influenced by the relocation of intracardiac air. The combination of increased RV afterload and arterial hypotension, possibly with subsequent RV ischemia rather than RV outflow obstruction by an airlock appeared to be the primary mechanism for cardiac dysfunction after VAE.

Effect of Body Repositioning after Venous Air Embolism

Current therapy for massive venous air embolism (VAE) may include the use of the left lateral recumbent (LLR) position, although its effectiveness has been questioned. This study used transesophageal echocardiography to evaluate the effect of body repositioning on intracardiac air and acute cardiac dimension changes. Eighteen anesthetized dogs in the supine position received a venous air injection of 2.5 ml/kg at a rate of 5 ml/ s. After 1 min the dogs were repositioned into either the LLR, LLR 10 degrees head down (LLR-10 degrees), right lateral recumbence, or remained in the supine position. Repositioning after VAE resulted in relocation of intracardiac air to nondependent areas of the right heart. Peak right ventricular (RV) diameter increase and mean arterial pressure decrease were greater in the repositioned animals compared with those in the supine position (P < 0.05). Right ventricular diameter and mean arterial pressure showed an inverse correlation (r = 0.81). Peak left atrial diameter decrease was greater in the LLR and LLR-10 degrees positions compared with the supine position (P < 0.05). Repositioning did not influence peak pulmonary artery pressure increase, and no correlation was found between RV diameter and pulmonary artery pressure. All animals showed electrocardiogram and echocardiographic changes reconcilable with myocardial ischemia. In dogs, body repositioning after VAE provided no benefit in hemodynamic performance or cardiac dimension changes, although relocation of intracardiac air was demonstrated. Right ventricular air did not appear to result in significant RV outflow obstruction, as pulmonary artery pressure increased uniformly in all groups and was not influenced by the relocation of intracardiac air. The combination of increased RV afterload and arterial hypotension, possibly with subsequent RV ischemia rather than RV outflow obstruction by an airlock appeared to be the primary mechanism for cardiac dysfunction after VAE.

Reoperation for residual defects following intracardiac repair for tetralogy of Fallot

Reoperation was carried out in two patients who had previously undergone correction for tetralogy of Fallot and presented with severe pulmonary hypertension. One patient who had undergone intracardiac repair five years earlier had a residual ventricular septal defect (VSD), right ventricular outflow (RVOT) obstruction, patent ductus arteriosus and severe pulmonary hypertension. The second patient, who had undergone intracardiac repair four years earlier, also had a residual VSD and RVOT obstruction. Both underwent VSD closure, RVOT resection and pulmonary valve replacement and did well postoperatively. We recommend aggressive surgical treatment in such patients even in the presence of pulmonary hypertension.

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 appearedto constitute a primary and excessive hypertrophic process involving both ventricles.

HEMANGIOSARCOMA IN THE MAIN PULMONARY ARTERY OF A DOG

The clinical, radiological and necropsy findings in a five‐year old dog with a hemangiosarcoma in the main pulmonary artery are described. Hemangiosarcoma in this location has not been previously described in the dog, the typical location in the heart being the right atrium and auricle. The tumor in this dog caused both a perfusion deficit to the right lung and obstruction of right ventricular outflow, which eventually caused right heart failure.

Pulsed doppler evaluation of right ventricular diastolic filling in children with pulmonary valve stenosis before and after balloon valvuloplasty

To assess right ventricular (RV) diastolic filling in children with pulmonary stenosis (PS), 14 patients (mean age 5.1 years) were examined immediately before and after pulmonary balloon valvuloplasty. Fourteen normal children (mean age 4.8 years) were also studied. From the tricuspid valve inflow Doppler study, the following measurements were made at peak inspiration: peak velocities at rapid filling (peak E) and during atrial contraction (peak A), ratio of peak E to peak A velocities, RV peak filling rate normalized for stroke volume, total area under the Doppler curve, percent of the total Doppler area occurring in the first third of diastole (0.33 area fraction), percent of the total area occurring under the E wave (E area fraction), percent of the total area occurring under the A wave (A area fraction) and the ratio of E area to A area. Before balloon valvuloplasty, the patients with PS had higher peak A velocity (0.64 ± 0.28 vs 0.39 ± 0.08 m/s), lower E A velocity ratio (1.11 ± 0.52 vs 1.76 ± 0.45), lower 0.33 area fraction (0.34 ± 0.14 vs 0.49 ± 0.08), higher A area fraction (0.45 ± 0.21 vs 0.27 ± 0.09) and lower E A area ratio (1.73 ± 1.05 vs 2.96 ± 1.14) than the normal subjects (p < 0.01). In patients before and after balloon valvuloplasty, there was a significant difference in RV outflow gradient (71 ± 35 vs 28 ± 15 mm Hg), but there was no change in any Doppler index. Thus, patients with PS have abnormal diastolic filling with decreased filling in early diastole and increased filling during atrial contraction. These abnormalities are unchanged immediately after successful relief of RV outflow obstruction, suggesting that hypertrophy rather than afterload mismatch is the primary determinant of the impaired relaxation.

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.

Canine biventricular performance during acute progressive pulmonary microembolization: Regional myocardial perfusion and fatty acid uptake

The cardiac output during acute pulmonary artery hypertension (PAH) may be compromised by right ventricular (RV) outflow obstruction, myocardial ischemia, or adverse ventricular interactions. To study the relative contributions of these mechanisms to impaired biventricular function during PAH, we injected 75 to 105-μm glass beads into the pulmonary vasculature of 11 dogs and correlated the hemodynamic alterations with changes in biventricular function. Biventricular ejection fractions and interventricular septal motion were evaluated by gated blood pool angiocardiograms. Regional myocardial blood flow (n = 8 dogs) was measured with microspheres, and regional myocardial fatty acid metabolism during PAH (n = 8 dogs) was assessed by measuring the regional myocardial extraction of the radioiodinated fatty acid analog, 15-(p-iodophenyl)-3-methylpentadecanoic acid (3m-PIP/PDA). Following microembolization, the mean pulmonary artery pressure increased from 14 ± 1 to 48 ± 2 mm Hg ( P < .001) and cardiac output decreased from 3.5 ± 0.3 to 2.6 ± 0.3 1 /min ( P < .05). Right ventricular volume increased and RV ejection fraction decreased progressively. Abnormal septal motion during PAH occurred in 5 of 11 dogs and was associated with decreased LV diastolic compliance. Right ventricular myocardial blood flow remained increased during PAH while the regional extraction of 3m-PIP/PDA was uniform throughout the heart. These findings suggest that during moderate PAH the canine cardiac output is limited by RV outflow obstruction and decreased LV diastolic compliance rather than by ischemia.

Ventricular pump performance in patients with obstructed right ventricular-pulmonary artery conduits

Postoperative data were obtained from 18 patients with partially obstructed right ventricular (RV) to pulmonary artery (PA) conduits, who were studied 1 to 9 years following a Rastelli operation. Age at operation was 1 to 8 months in seven patients (group I: infant group) and 2 to 9 years in the remaining 11 patients (group II: childhood group). The diagnosis was pulmonary atresia in eight patients, truncus arteriosus in seven, and transposition of the great arteries with ventricular septal defect and pulmonary stenosis in three. Porcine-valved conduits were inserted in 17 patients and an aortic homograft in one. All but seven patients were free of symptoms at the time of postoperative study. Neither peak RV pressures nor RV to PA gradients were different between groups. RV ejection fraction (EF) was decreased in group II (0.43 ± 0.11) but was normal (0.60 ± 0.10) in group I. In addition, there was a significant inverse relationship between RVEF and age at repair ( r = 0.714; p < 0.005). RV end-diastolic volume (EDV) was normal or increased in all patients and did not differ between the two groups. Left ventricular (LV) ejection fraction was also decreased in the older group (0.56 ± 0.10 vs 0.68 ± 0.08; p < 0.05), and there was a decrease in RVEF and/or LVEF from pre- to postoperative studies in one of six group I patients compared with four of five group II patients. Radionuclide ventriculography with exercise was performed in eight patients (seven in group II) and RVEF responses were abnormal in all of them, whereas LVEF responses were abnormal in seven of eight. A decrease in RVEF of > 5 EF units with exercise was associated with a resting gradient from the right ventricle to the pulmonary artery of > 50 mm Hg. These data indicate that RVEF is usually abnormal in patients with obstructed RV to PA conduits, who are operated upon after infancy. The progressive decrease in RVEF with age indicates the inadequacy of hypertrophy to normalize RV pump function with time. Further data after relief of RV outflow obstruction are needed to discern risk factors for permanent RV dysfunction in this clinical setting.

Complete transposition of the great arteries: Visualization of left and right outflow tract obstruction by oblique subcostal two-dimensional echocardiography

Subcostal oblique 2-dimensional echocardiography was performed in 64 infants younger than 2 years with complete transposition of the great arteries (TGA) (situs solitus, concordant atrioventricular and discordant ventriculoarterial connections). All patients examined before cardiac catheterization had a correct diagnosis by 2-dimensional echocardiography using the subcostal oblique views. Twelve patients had associated left ventricular (LV) outflow tract obstruction and 7 had right ventricular (RV) outflow obstruction. The standard parasternal views failed to diagnose obstruction in 1 patient with LV outflow obstruction and 5 with RV outflow obstruction; the subcostal left oblique cut and long axis of the left ventricle visualized all left-sided obstructions, and right-sided obstructions were correctly displayed in 5 of 7 cases using a combination of left oblique and right oblique cuts. Two-dimensional echocardiographic subcostal oblique views allow an excellent definition of the morphologic characteristics of RV and LV outflow tracts in patients with TGA and improve the diagnosis of the outflow obstruction in these malformations.

Right ventricular outflow obstruction secondary to nonpenetrating blunt trauma to the canine myocardium.

The purpose of this study was to investigate the development of a right ventricular (RV) outflow tract obstruction of sufficient severity to produce a systolic murmur following blunt cardiac trauma. A nonpenetrating impact directly on the anterior surface of the heart was produced in 34 open chest anesthetized dogs. Impact velocity was 12 m/sec in 15 dogs and 18 m/sec in 19 dogs. Seventeen dogs died immediately following impact. Pressures in the pulmonary artery and RV were measured during the control period in all dogs, and intermittently for 90 minutes following impact in ten of the 17 surviving dogs. At 90 minutes following impact a systolic pressure gradient of 9 +/- 2 mm Hg (range, 3 to 22 mm Hg) developed across the RV outflow tract and was associated with a prominent ejection murmur. At autopsy, RV wall thickness measured at the midventricular level was 13.5 +/- 1 mm (mean +/- SEM) which was thicker than in dogs that died immediately following impact, 6 +/- 1 mm (p less than 0.001). Microscopy of the RV myocardium of dogs that survived impact showed interstitial bleeding with prominent accumulations of blood between muscle bundles, whereas dogs that died immediately after impact showed no interstitial bleeding. The obstruction seems to have resulted from the increased RV wall thickness due to interstitial bleeding. In the absence, therefore, of other evidence to explain a new systolic murmur in patients following nonpenetrating cardiac trauma, the possibility of RV outflow obstruction might be considered.

Cardiac output as a controller of ventilation through changes in right ventricular load

Ventilatory responses to changes in right ventricular (RV) load were studied in spontaneous breathing anesthetized dogs. Moving average RV pressure leads to (PRV) was used as an index of the RV strain. RV load was changed in two ways: 1) cardiac output (Q) was increased by infusion of isoproterenol (0.7-1.2 micrograms/min) and reduced by infusion of vasopressin (0.3-0.5 U/min); and 2) RV pressure was increased independently on Q by partial balloon obstruction of the RV outflow. When Q was changed by drug infusion there was a linear correlation between leads to PRV and Q (avg r = 0.04). Well-correlated linear relationships were found between expired minute ventilation (VE) and leads to PRV (avg r greater than 0.03), the slopes and intercepts of which were not significantly different whether leads to PRV was changed by altering Q, partial obstruction of RV outflow, or combining both procedures. Bilateral vagotomy did not alter the VE/leads to PRV slope resulting from RV balloon inflations. It is suggested that the RV strain may act as a controller of ventilation and provide a link between Q and VE.

Right-to-Left Atrial Shunt in Cardiac Dislocation Following Extensive Pneumonectomy

Previous reports dealing with cardiac herniation following intrapericardial pneumonectomy illustrate the critical and often lethal hemodynamic sequelae of this complication. In the case presented here, the first and nearly exclusive sign of cardiac herniation after left-sided pneumonectomy with extensive resection of the pericardium was systemic arterial hypoxemia. Subsequent investigations suggested inter-atrial right-to-left shunt in the presence of a patent foramen ovale, caused by slight right-ventricular outflow obstruction with consecutively reversed pressure relationships at atrial level. This explanation was supported by the operative findings, and reversibility was achieved by pericardial reconstruction with parietal pleura. When the patient died 8 months later due to general progression of a mucoepidermoid carcinoma, autopsy confirmed a large patent foramen ovale.