Peak Gradient (peak + gradient)

Distribution by Scientific Domains


Selected Abstracts


Reliability of Intraoperative Transesophageal Echocardiography During Tetralogy of Fallot Repair

ECHOCARDIOGRAPHY, Issue 4 2000
JAMES J. JOYCE M.D.
There is limited information available concerning the accuracy of intraoperative transesophageal echocardiography (TEE) in predicting the extent of residual abnormalities after recovery from surgical repair of tetralogy of Fallot. Therefore, we investigated differences between the results of final postbypass TEE and those of postrecovery (mean, 6 days after surgery) transthoracic echocardiography in a total of 28 consecutive pediatric patients who underwent repair of tetralogy of Fallot with biplane or multiplane TEE. Both postbypass and postrecovery echocardiographic examinations included measurements of the right ventricle (RV)-main pulmonary artery (PA) and the main PA-branch PA peak instantaneous gradients, the degree of pulmonary valvar insufficiency, and color Doppler interrogation of the ventricular septum for residual defects. The RV-main PA gradient did not change significantly: 15 ± 13 vs 18 ± 14 mmHg (postbypass versus postrecovery, mean ± SD). None of the patients had a decrease of , 10 mmHg; and only one patient had an increase of ,: 15 mmHg. There also was no change in the degree of pulmonary insufficiency (3.0 ±1.2 versus 3.1 ± 1.1, using a scale of 0 to 4). Only one of the seven very small (, 2 mm) residual ventricular septal defects was not discovered during postbypass TEE. However, postrecovery transthoracic echocardiography detected significant branch PA stenosis (peak gradient, , 15 mmHg) in five patients (18%) that was not detected during postbypass TEE (P < 0.03). Of the branch PA stenoses that were not detected during TEE, four were left and one was right. Conclusions: Postbypass TEE after tetralogy of Fallot repair reliably predicts residual postrecovery hemodynamic abnormalities, except for branch PA stenosis. [source]


Early Results of Balloon Dilatation of the Stenotic Bovine Jugular Vein Graft in the Right Ventricular Outflow Tract in Children

JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 3 2008
J. STEINBERG M.D.
The aim of this study was to evaluate the early results of interventional balloon dilatation of stenotic bovine jugular vein (BJV) grafts implanted for reconstruction of the right ventricular outflow tract (RVOT) in children. Methods: From May 2001 to December 2005, 153 BJV grafts were implanted in children in our institution. An average of 16.9 (7.6,41.1) months after implantation, 17 balloon dilatations in a significant stenosis proximal (n = 1), distal anastomosis (n = 8), BJV valve (n = 3), or at multiple sites (n = 5) were performed in 15 children (male:female = 9:6) with a mean age of 3.9 (0.8,13.0) years. Balloon diameter was 75,133.3% (mean 100.3) of the original BJV size. Mean follow-up was 8.8 (2 days to 22.8 months) months. Results: In 10 interventions (58.8%) the instantaneous peak gradient was reduced below 50 mmHg. A balloon diameter ,100% of the original BJV size correlated significantly with a successful intervention. No major complications, two minor (nonobstructive floating membranes at the dilatation site and one septicemia) occurred afterward. Freedom from reintervention after 6 months was 58.2% for all, 77.8% for dilatations of the proximal anastomosis and mixed stenotic lesions, and 33.3% for the distal anastomosis. Conclusion: Balloon dilatation of stenotic BJV grafts is safe and can significantly reduce the pressure gradient in two-thirds of interventions. Balloon diameters above the original graft size should be aimed for. The most frequent stenosis of the distal anastomosis tends to renarrow early after dilatation. Nevertheless, balloon dilatation should be considered in nearly every stenotic graft to gain time until a surgical or interventional graft exchange. [source]


The Effect of the Fiber Curvature Gradient on Break Excitation in Cardiac Tissue

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2006
DEBORAH LANGRILL BEAUDOIN
Background:Break excitation has been hypothesized as a mechanism for the initiation of reentry in cardiac tissue. One way break excitation can occur is by virtual electrodes formed due to a curving fiber geometry. In this article, we are concerned with the relationship between the peak gradient of fiber curvature and the threshold for break stimulation and the initiation of reentry. Methods: We calculate the maximum gradient of fiber curvature for different scales of fiber geometry in a constant tissue size (20 × 20 mm), and also examine the mechanisms by which reentry initiation fails. Results: For small peak gradients, reentry fails because break excitation does not occur. For larger peak gradients, reentry fails because break excitation fails to develop into full-scale reentry. For strong stimuli above the upper limit of vulnerability, reentry fails because the break excitation propagates through the hyperpolarized region and then encounters refractory tissue, causing the wave front to die. [source]


Treatment of severe valvular aortic stenosis and subvalvular discrete subaortic stenosis and septal hypertrophy with Percutaneous CoreValve Aortic Valve Implantation,

CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 5 2010
Ariel Finkelstein MD
Abstract Background: Percutaneous Aortic Valve Implantation (PAVI) is a procedure gaining popularity and becoming more widely used for the treatment of patients with severe aortic stenosis who are at high risk for surgery. Here we show, for the first time, that a successful and complete elimination of both valvular and subvalvular pressure gradients can be achieved with a slight modification of the valve implantation technique. Methods and Results: A 91-year-old woman presented with shortness of breath at rest, effort angina, and pulmonary congestion. Echocardiography revealed calcified aortic stenosis with a peak gradient of 75 mm Hg accros the valve, and discrete subaortic stenosis (DSS) and marked hypertrophy of the basal septum with systolic anterior motion of the mitral valve (SAM). The intra ventricular gradient had a dynamic pattern across the DSS and the septal hypertrophy and measured 75 mm Hg. The total gradient across the left ventricular outflow (valvular and subvalvular) was 125 mmHg. PAVI with a 23 mm CoreValve was performed with an intentional lower positioning of the valve towards the LV outflow tract; so that the valve struts cover the subaortic membrane and part of the thickened basal septum. At the end of the procedure, the SAM disappeared, and the left ventricular ouflow was widely open. At 1 month follow up the patient was asymptomatic, no pressure gradient was measured between the LV apex and the aorta. Conclusions: This is the first report of successful treatment of severe valvular aortic stenosis and combined subvalvular aortic stenosis due to DSS and septal hypertrophy with SAM with percutaneous aortic valve implantation. © 2010 Wiley-Liss, Inc. [source]


The Effect of the Fiber Curvature Gradient on Break Excitation in Cardiac Tissue

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2006
DEBORAH LANGRILL BEAUDOIN
Background:Break excitation has been hypothesized as a mechanism for the initiation of reentry in cardiac tissue. One way break excitation can occur is by virtual electrodes formed due to a curving fiber geometry. In this article, we are concerned with the relationship between the peak gradient of fiber curvature and the threshold for break stimulation and the initiation of reentry. Methods: We calculate the maximum gradient of fiber curvature for different scales of fiber geometry in a constant tissue size (20 × 20 mm), and also examine the mechanisms by which reentry initiation fails. Results: For small peak gradients, reentry fails because break excitation does not occur. For larger peak gradients, reentry fails because break excitation fails to develop into full-scale reentry. For strong stimuli above the upper limit of vulnerability, reentry fails because the break excitation propagates through the hyperpolarized region and then encounters refractory tissue, causing the wave front to die. [source]