Usefulness of preoperative echocardiography in predicting left ventricular outflow obstruction after primary repair of interrupted aortic arch with ventricular septal defect

OBJECTIVE: "Renal dose" dopamine is widely used in the perioperative period to provide renal protection. A comprehensive review of the literature was performed to determine whether dopamine does in fact confer protection on the kidneys of surgical patients. SUMMARY BACKGROUND DATA: Studies in healthy animals and human volunteers reveal that dopamine causes diuresis and natriuresis, as well as some degree of renal vasodilatation. RESULTS: Studies of the perioperative use of dopamine fail to demonstrate any benefit of dopamine in preventing renal failure. Studies in congestive heart failure, critical illness, and sepsis also fail to show any benefit of dopamine other than diuresis. Further, dopamine administration is not completely without risk, because of dopamine's catecholamine and neuroendocrine functions. CONCLUSIONS: Routine use of prophylactic "renal dose" dopamine in surgical patients is not recommended.     

Presentation of a müllerian anomaly with outflow obstruction after tubal ligation

OBJECTIVE: To report an unusual presentation of a patient with unicornuate uterus and a noncommunicating functional rudimentary horn and discuss related patient management issues. SETTING: University hospital. PATIENT: A 27-year-old woman who presented with cyclic abdominal pain after a postpartum tubal ligation. INTERVENTION: Diagnostic studies followed by a laparotomy and resection of the rudimentary horn. RESULTS: Resolution of patient's symptoms. CONCLUSIONS: Patients with a unicornuate uterus and a rudimentary horn recognized for the first time during a tubal ligation require individualized management depending in part on the precise nature of the horn.     

Early results of AV sequential pacing on left ventricular outflow obstruction after Senning procedure

Dual chamber pacing was shown to decrease left ventricular outflow tract (LVOT) obstruction in patients with hypertrophic cardiomyopathy 30 years ago. We report early results of AV sequential pacing from the LV apex in a patient with transposition of the great arteries who is post-Senning procedure. LVOT obstruction resulted from septal deviation and systolic anterior motion of the mitral valve. Pacing was indicated for sinus node dysfunction. AV sequential pacing with a short optimal AV interval of 60 ms demonstrated a 45% reduction in the degree of LVOT obstruction. This article suggests that LVOT obstruction after the Senning procedure can be palliated by asynchronous septal contraction induced by AV sequential pacing, even if the activation is from LV apex, and avoid or postpone surgery in selected situations.     

Changes in pulmonary physiology after lung volume reduction surgery in a rabbit model of emphysema

BACKGROUND: We administered a specific, nonselective matrix metalloproteinase (MMP) inhibitor (RS-113,456) to examine the effect of MMP inhibition on flow-mediated arterial enlargement in a rodent arteriovenous fistula (AVF) model. METHODS: Four groups of male Sprague-Dawley rats were created: sham (sham operated; n = 10), control (2.0 mm left common femoral AVF alone; n = 16), vehicle (AVF plus 0.5 mL vehicle orally twice a day; n = 20), and treatment (AVF plus 25 mg/kg RS-113,456 in 0.5 mL vehicle orally twice a day; n = 16). Heart rate, mean arterial pressure, and body weight were recorded on postoperative days 0, 7, 14, and 21. On day 21, AVF patency was confirmed, the infrarenal aorta and common iliac arteries were exposed, blood flow velocity and external diameter were measured, and wall shear stress (WSS) was calculated. Analysis was performed by paired, two-tailed Student t test, one-way analysis of variance, and the Bonferroni/Dunn procedure for post hoc testing. RESULTS: Heat rate, mean arterial pressure, and weight did not vary at any time between groups. Aortic and left iliac diameter was larger in the AVF groups than in sham groups (P < .001), and control and vehicle groups were larger than treatment groups (P < .0001). Changes in aortic and left iliac flow were also significant (AVF was more than sham and control, and vehicle was more than treatment). No difference in aortic and left iliac artery velocity and WSS or right iliac diameter, velocity, flow, or WSS was observed between groups. CONCLUSIONS: MMP inhibition diminishes flow-mediated arterial enlargement in the rat AVF model.     

Left ventricular outflow obstruction as a result of external cardiac compression by a mediastinal tumor

A case of left ventricular outflow tract stenosis resulted from compression of the heart is presented. This symptomatic cardiovascular lesion was produced by extensive growth of mediastinal tumour. Numerous noninvasive methods were necessary to establish this difficult diagnosis. The patient underwent surgery that disclosed a benign process (of neurofibroma). After tumour's resection marked hemodynamic signs subsided.     

Myofibroblast-derived smooth muscle cells during remodelling of rabbit urinary bladder wall induced by partial outflow obstruction

BACKGROUND: Fibrosis of serosa, along with smooth muscle (SM) cell hypertrophy, has been shown to occur in the rabbit bladder after partial outflow obstruction. Identification of cells involved in the serosal thickening can be of primary interest to elucidate the functional changes that this organ undergoes. EXPERIMENTAL DESIGN: Cytoskeletal protein composition of cells present in the thickened serosa at different times from the onset of obstruction (7, 15, 30 and 60 days) was evaluated. This was accomplished by means of a panel of monoclonal antibodies specific for a number of differentiation markers of mesenchymal cells (vimentin, desmin, alpha-actin of SM type, nonmuscle (NM) and SM myosins), and by immunocytochemical and immunochemical techniques. RESULTS: The immunocytochemical study revealed that cells in serosal thickening follow a two-step maturation process from pre-existing vimentin-positive cells. In the first time period (7 to 15 days of obstruction), these cells predominantly achieved an immunophenotype corresponding to that of a specific myofibroblast subtype (i.e., containing vimentin, NM myosin, and SM alpha-actin). After 30 days from the onset of obstruction, the cytoskeletal protein content of serosal cells, as also revealed by Western blotting experiments, shifted towards that of fetal-type SM cells (i.e., presence of vimentin, NM myosin, SM alpha-actin, and SM myosin isoforms). Distribution of vimentin, desmin, SM alpha-actin, and SM myosin in tissue culture as well as the ultrastructure in vivo very closely resembled that of SM cells. Bromodeoxyuridine incorporation studies indicated that cells accumulated in the serosa of obstructed bladders did not derive, at least initially, from SM cells of the detrusor muscle. CONCLUSIONS: These findings are consistent with the existence of a differentiation process in which resident mesenchymal cells of bladder serosa may transform to myofibroblasts and, subsequently, in fetal-type SM cells during experimental outflow obstruction.     

Effect of hepatic venous outflow obstruction on pores and fenestration in sinusoidal endothelium

The ultrastructure of pores and fenestrations in hepatic sinusoidal endothelial cells was examined following partial surgical occlusion of the suprahepatic portion of the inferior vena cava. Within 12 h after partial obstruction of hepatic venous outflow, endothelial pores (less than 0-1 mum in diameter) and sieve plates in the distal halves of sinusoids were greatly reduced in number or were totally absent, and they were replaced by large fenestration (less than 1-0 mum in diameter). These results suggest that pores forming sieve plates may fuse to form large fenestrations. The findings also indicate that sinusoidal hypertension and hypoxia associated with obstruction of hepatic venous outflow alter the distribution of pores and fenestrations in sinusoidal endothelium     

Optimal size of outflow patch in total correction of tetralogy of Fallot

Hemodynamic and angiocardiographic studies were performed in postoperative patients with tetralogy of Fallot. Pressure gradient between the right ventricle and pulmonary artery was correlated with the narrowest area in the pulmonary arterial pathway. Regurgitant fraction was also correlated with regurgitant area which was determined by preoperative area of the pulmonic annulus and width of the outflow patch. Follow-up study of postoperative patients with tetralogy indicated that those with pressure gradient less than 20 mmHg and regurgitant fraction less than 15% could be considered ideally corrected. A table was constructed for determining the most appropriate width of the outflow patch for the ideal correction.     

Responses of plasma norepinephrine and heart rate during exercise in patients after Fontan operation and patients with residual right ventricular outflow tract obstruction after definitive reconstruction

In a fetal autopsy series, we have explored the occurrence of renal tubular dysgenesis in twins. Renal tubular dysgenesis was found exclusively among those monozygotic twins with evidence of twin transfusion syndrome, particularly in those donor twins with oligohydramnios and growth restriction. We infer that hypotension in the donor twin of the twin transfusion syndrome pair is responsible for the failure of proximal convoluted tubule differentiation, and the disturbance of renal function is manifested as oligohydramnios prenatally, and either oliguria or tubular dysfunction postnatally.     

Acute endocarditis of the native aortic valve caused by Propionibacterium acnes

Propionibacterium acnes is often considered to be a contaminant but it has also been found to be the principal pathogen in serious infections. P. acnes is a rare cause of infective endocarditis. It has been suggested that aortic root abscesses are caused by bacteria that are particularly virulent. The strongest risk factor for serious infections by this bacteria is the presence of foreign bodies. A case is presented in which endocarditis of a native aortic valve caused by P. acnes was associated with an aortic root abscess. Transesophageal echocardiography is particularly helpful in the diagnosis of this severe complication of infective endocarditis. The literature for P. acnes endocarditis is reviewed.     

Acute thoracic inlet obstruction in achalasia of the oesophagus

Eleven women with fetal distress as manifested by a decrease of fetal movements up to cessation underwent amniocentesis for amniotic fluid evaluation under continuous FHR monitoring. All the fetuses showed abnormal heart rate response, manifested by absence of FHR acceleration or early or late deceleration. The pathologic response, or lack of response of fetal heart rate during amniocentesis is suggested as an additional test to evaluate the severity of fetal distress.     

Stress-induced left ventricular outflow tract obstruction: a potential cause of dyspnea in the elderly

OBJECTIVES: We sought to identify the pattern of disturbed left ventricular physiology associated with symptom development in elderly patients with effort-induced breathlessness. BACKGROUND: Limitation of exercise tolerance by dyspnea is common in the elderly and has been ascribed to diastolic dysfunction when left ventricular cavity size and systolic function appear normal. METHODS: Dobutamine stress echocardiography was used in 30 patients (mean [+/-SD] age 70 +/- 12 years; 21 women, 9 men) with exertional dyspnea and negative exercise test results, and the values were compared with those in 15 control subjects. RESULTS: Before stress, left ventricular end-diastolic and end-systolic dimensions were reduced, fractional shortening was increased, and the basal septum was thickened (2.3 +/- 0.5 vs. 1.4 +/- 0.2 cm, p < 0.001, vs. control subjects) in the patients, but posterior wall thickness did not differ from that in control subjects. Left ventricular outflow tract diameter, measured as systolic mitral leaflet septal distance, was significantly reduced (13 +/- 4.5 vs. 18 +/- 2 mm, p < 0.001). Isovolumetric relaxation time was prolonged, and peak left ventricular minor axis lengthening rate was reduced (8.1 +/- 3.5 vs. 10.4 +/- 2.6 cm/s, p < 0.05), suggesting diastolic dysfunction. Transmitral velocities and the E/A ratio did not differ significantly. At peak stress, heart rate increased from 66 +/- 8 to 115 +/- 20 beats/min in the control subjects, but blood pressure did not change. Transmitral A wave velocity increased, but the E/A ratio did not change. Left ventricular outflow tract velocity increased from 0.8 +/- 0.1 to 2.0 +/- 0.2 m/s, and mitral leaflet septal distance decreased from 18 +/- 2 to 14 +/- 3 mm, p < 0.001. In the patients, heart rate rose from 80 +/- 12 to 132 +/- 26 beats/min and systolic blood pressure from 143 +/- 22 to 170 +/- 14 mm Hg (p < 0.001 for each), but left ventricular dimensions did not change. Peak left ventricular outflow tract velocity increased from 1.5 +/- 0.5 m/s (at rest) to 4.2 +/- 1.2 m/s; mitral leaflet septal distance fell from 13 +/- 4.5 to 2.2 +/- 1.9 mm (p < 0.001); and systolic anterior motion of mitral valve appeared in 24 patients (80%) but in none of the control subjects (p < 0.001). Measurements of diastolic function did not change. All patients developed dyspnea at peak stress, but none developed a new wall motion abnormality or mitral regurgitation. CONCLUSIONS: Although our patients fulfilled the criteria for "diastolic heart failure," diastolic dysfunction was not aggravated by pharmacologic stress. Instead, high velocities appeared in the left ventricular outflow tract and were associated with basal septal hypertrophy and systolic anterior motion of the mitral valve. Their appearance correlated closely with the development of symptoms, suggesting a potential causative link.     

Thrombosis with outflow obstruction delays thrombolysis and results in chronic wall thickening of rat veins

PURPOSE: An in vivo model of acute deep venous thrombosis was developed in rats to assess the role of venous thrombosis and outflow obstruction in recanalization and development of secondary wall changes. METHODS: The left femoral veins of male Sprague-Dawley rats were thrombosed either by means of proximal ligation (obstruction, group A, n = 38) or by means of temporary 24-hour occlusion with a microvascular clamp (unobstructed, group B, n = 20). Right femoral veins served as controls. The rats were killed at intervals over 5 weeks. Wall thickness was compared among groups by means of counting of cells on representative sections through the midvein area. Thrombi were indirectly quantitated with a radiolabeled fibrinogen assay in a parallel series of rats. RESULTS: Control veins showed no evidence of cellular or structural changes. Early thrombus extension was seen in group A (peak at day 4) followed by recanalization after 2 weeks. Group A veins had marked wall thickening (27 +/- 7 vs 6 +/- 2 cells, p < 0.01, peak at 10 days) consisting of smooth muscle-type, neointimal, and medial cellular proliferations. Within 2 to 3 weeks, local neovascular channels had grown to bypass the outflow obstruction, and resumption of normal cephalad flow was seen. At the same time neointimal proliferation regressed, but medial cellular growth persisted, resulting in chronic wall thickening (11 +/- 3 vs 5 +/- 1 cells, p < 0.01, after 21 days). In contrast, group B veins exhibited no thrombus extension, had significantly less wall thickening (13 +/- 2 vs 5 +/- 1 cells, p < 0.01, peak at 4 days), and did not induce growth of local collateral blood vessels. Within 2 weeks, group B veins regained normal appearance and resumed normal flow. CONCLUSIONS: Thrombosis of rat femoral veins without chronic obstruction results in rapid lysis of thrombus and transient proliferative changes. In contrast, thrombosis with chronic outflow obstruction results in delayed recanalization, early extension of thrombus, and development of vigorous and persistent proliferative cellular responses. Thrombus-induced chronic wall thickening may be an important factor in development of postthrombotic venous insufficiency.     

Right ventricular obstruction in aortic dissection: a mechanism of hemodynamic collapse

The main and right pulmonary arteries may be compressed by the false lumen of a type I aortic dissection. We report a 73-year-old women with a dissection of the aorta in whom echocardiographic examination revealed acute pulmonary arterial compression causing right ventricular failure and hemodynamic collapse.     

Evaluation of the role of neurolinins and urecholine hypersensitivity in an animal model of infravesical outflow obstruction

OBJECTIVES: To determine whether detrusor muscle strips from a male rat with infravesical outflow obstruction model demonstrate supersensitivity to parasympathomimetic and neurokinin NK-1 and NK-2 selective agonists. METHODS: Bladder instability developed after 6 weeks of partial urethral obstruction. The micturition frequency and voided volume were determined in unanesthetized animals. Detrusor hypertrophy was confirmed by evaluation of bladder weight. In vitro organ bath was used to compare the affinity and maximal activity of bethanechol and neurokinin NK-1 and NK-2 selective agonists on strips from the detrusor muscle of sham and obstructed rats. Bethanechol, N-Ac[Arg6, Sar9, Met(O2)]-SP(6-11), and [beta-Ala8]-NKA(4-10) were used to characterize cholinergic muscarinic, neurokinin NK-1 and NK-2 receptors. Results. No significant differences in affinities and maximal responses were found using 10-mg detrusor muscle strips with each of the three agonists. CONCLUSIONS: Bladder instability produced by outlet obstruction does not involve changes in the affinity or maximal activity of cholinergic muscarinic, neurokinin NK-1 and NK-2 receptors. Furthermore, detrusor supersensitivity to neurokinins or bethanechol was not seen. This suggests that bladder instability is not due to an increased affinity or maximal response to neurokinins or parasympathomimetics.     

The effect of the ingestion of ethanol on obstruction of the left ventricular outflow tract in hypertrophic cardiomyopathy

BACKGROUND: Ethanol causes vasodilation, which might have an adverse effect, due to increased obstruction of the left ventricular outflow tract, in patients with hypertrophic obstructive cardiomyopathy. We assessed the hemodynamic effects of the ingestion of ethanol, in an amount commonly consumed socially, in patients with hypertrophic cardiomyopathy. METHODS: We performed echocardiography in 36 patients before and several times after the ingestion of either 50 ml of 40 percent ethanol or an isocaloric placebo with the aroma of rum. Each patient received both ethanol and placebo, on different days. The patients, but not the physicians, were blinded to the content of the drink. We measured the sizes of the left atrium and left ventricle, the left-ventricular-wall thickness, blood pressure, heart rate, the degree of systolic anterior motion of the mitral valve, and the pressure gradient across the left ventricular outflow tract. RESULTS: The ingestion of ethanol regulated in a significant drop in the mean (+/- SD) systolic blood pressure (from 130.5 +/- 18.6 to 122.5 +/- 20.3 mm Hg, P<0.001), a significant increase in systolic anterior motion of the mitral valve (from a grade of 2.1 to a grade of 2.5, P<0.001), and a 63 percent increase in the mean gradient across the left ventricular outflow tract (from 38.1 +/- 26.5 to 62.2 +/- 42.4 mm Hg, P<0.001). These changes, which were not associated with symptoms, did not occur after the ingestion of placebo. CONCLUSION: The ingestion of a small amount of ethanol caused an increase in the gradient across the left ventricular outflow tract in patients with hypertrophic obstructive cardiomyopathy, which could have and adverse clinical effect.     

Murine strain differences in the volume effect and incidence of radiation-induced colorectal obstruction

We have previously reported high levels of the coagulation inhibitor TFPI in the blood of patients with gastrointestinal cancer. TFPI is not an acute-phase reactant, but high levels have also been reported in patients with septicaemia and disseminated intravascular coagulation (DIC). To study its relationship with other types of malignancy, TFPI activity was first determined in plasma samples from 214 patients with various malignancies. In a second cohort of 83 patients, total and free TFPI antigen, protein C, antithrombin, fibrin monomer and D-dimer were also measured. Elevated TFPI activity and antigens were found in about half of the patients with solid tumours. In contrast, elevated TFPI was rare in haematological malignancies (12%). In the 18 patients with acute nonlymphocytic leukaemia (ANLL), elevated free TFPI was found only in patients who also had DIC. No correlation was found between TFPI levels and fibrin monomer or D-dimer levels. Only four out of 20 patients with solid tumours had normal levels of fibrin monomer and D-dimer, yet three out of these four had elevated TFPI. In conclusion, elevated TFPI in ANLL is related to the coexistence of DIC. In solid tumour disease increased TFPI may reduce protective fibrin formation, but the pathogenic mechanism is as yet unknown.