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Olga Milo-Cotter,
Beth Cotter-Davison,
Carlo Lombardi,
Hengrui Sun,
Luca Bettari,
Silvia Bugatti,
Michele Rund,
Marco Metra,
Edo Kaluski, Isaac Kobrin,
Aline Frey,
Maurizio Rainisio,
John J V McMurray,
John R Teerlink,
Gad Cotter-Davison
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ABSTRACT: Recent heart failure studies have suggested that inflammatory and immune system activation are associated with increased levels of cytokines, chemokines and inflammatory proteins during acutely decompensated heart failure. The objectives of this substudy were to evaluate the role of neurohormonal and inflammatory activation in the pathogenesis and outcome of acute heart failure (AHF) and the correlation between biomarker levels and clinical outcomes.
Serum levels of B-type natriuretic peptide-32 (BNP-32), endothelin-1 (ET-1), norepinephrine, troponins I and T, C-reactive protein (CRP), von Willebrand factor, plasminogen activator inhibitor-1, interleukin-6 (IL-6) and tissue plasminogen activator (TPA) were measured at baseline, 24 and 48 h and 7 and 30 days in 112 patients with AHF recruited to the Value of Endothelin Receptor Inhibition with Tezosentan in Acute Heart Failure Study neurohormonal substudy.
On univariable analysis, CRP, BNP and ET-1 were predictive of worsening heart failure by day 30; when considered together, only CRP and BNP were significantly associated with this outcome. On adjustment for age, baseline blood pressure, serum sodium and serum creatinine, only age and BNP remained significant. CRP, IL-6 and TPA levels were significantly correlated with 180-day mortality on univariable analysis.
Circulating markers of inflammation may be useful in gauging prognosis in patients with AHF.
Cardiology 09/2011; 119(2):96-105. · 1.71 Impact Factor
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ABSTRACT: The most common outcome currently assessed in acute heart failure trials (AHF) is dyspnea improvement. Worsening hear failure (WHF) is a new outcome measure that incorporates failure to improve or recurrent symptoms of AHF requiring rescue intravenous therapy, mechanical circulatory or ventilatory support, or readmission because of AHF, occurring within 30 days of AHF admission.
Retrospective data analysis of 120 patients with AHF requiring hemodynamic monitoring who enrolled in the placebo arm of 2 prospective randomized studies. The incidence of WHF was 42% at 30 days from enrollment. Most WHF events occurred in-hospital during the first 7 days after admission (early WHF). Thirty-day readmission from AHF was an infrequent event in the present cohort (5.0%). The strongest hemodynamic predictors of WHF were cardiac power at baseline and its change during the initial 6 hours of monitoring. Other hemodynamic parameters associated with WHF events were blood pressure and its increase, cardiac output, and pulmonary wedge pressure change during the initial 6 hours of monitoring. WHF was found to be a strong predictor of 6-month mortality.
WHF is a common morbid event clustered mostly during the first week of AHF admission and is associated with higher 6-month mortality. The hemodynamic measurements associated with WHF are similar to those predicting adverse outcome in AHF and cardiogenic shock (low cardiac power, higher pulmonary capillary wedge pressure, and vascular resistance), emphasizing the notion that early WHF should become an important AHF-specific outcome measure.
Journal of cardiac failure 10/2009; 15(8):639-44. · 3.25 Impact Factor
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Edo Kaluski,
Gad Cotter,
Marina Leitman,
Olga Milo-Cotter,
Ricardo Krakover, Isaac Kobrin,
Tina Moriconi,
Maurizio Rainisio,
Avraham Caspi,
Leonardo Reizin,
Reuven Zimlichman,
Zvi Vered
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ABSTRACT: To evaluate the effects of bosentan on echo-derived hemodynamic measurements, and clinical variables in symptomatic heart failure (HF) patients.
Multi- center, double-blind, randomized (2:1), placebo-controlled study comparing bosentan (8-125 mg b.i.d.) to placebo in patients with New York Heart Association class IIIb-IV HF, left ventricular ejection fraction <35% and systolic pulmonary artery pressure (SPAP) >40 mm Hg. Primary and secondary endpoints were change from baseline to 20 weeks in SPAP and cardiac index, respectively. Safety endpoints were treatment emergent adverse events (AEs), change in body weight, hemoglobin, hematocrit, systolic blood pressure and diuretic use.
Ninety-four patients enrolled: 60 to bosentan, 34 to placebo. There was no significant difference between the 2 arms in SPAP change (0.1 +/- 11.5 mm Hg , 95% confidence limit (CL) -5.4 to 5.2, p = 0.97), cardiac index shift (0.12 +/- 0.45, 95% CL -0.09 to 0.33 , p = 0.24 ) or any of the other 22 echocardiographic measurements obtained. Therapy-duration was longer in the placebo arm, while more patients in the bosentan arm experienced adverse and serious AEs.
In HF patients with left ventricular dysfunction and secondary pulmonary hypertension, bosentan did not provide any measurable hemodynamic benefit, and was associated with more frequent AEs, requiring drug discontinuation.
Cardiology 01/2008; 109(4):273-80. · 1.71 Impact Factor
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John J V McMurray,
John R Teerlink,
Gadi Cotter,
Robert C Bourge,
John G F Cleland,
Guillaume Jondeau,
Henry Krum,
Marco Metra,
Christopher M O'Connor,
John D Parker,
Guillermo Torre-Amione,
Dirk J van Veldhuisen,
Jim Lewsey,
Aline Frey,
Maurizio Rainisio, Isaac Kobrin
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ABSTRACT: Plasma concentrations of the vasoconstrictor peptide endothelin-1 are increased in patients with heart failure, and higher concentrations are associated with worse outcomes. Tezosentan is an intravenous short-acting endothelin receptor antagonist that has favorable hemodynamic actions in heart failure.
To determine if tezosentan improves outcomes in patients with acute heart failure.
The Value of Endothelin Receptor Inhibition With Tezosentan in Acute Heart Failure Studies, 2 independent, identical, and concurrent randomized, double-blind, placebo-controlled, parallel-group trials conducted from April 2003 through January 2005 at sites in Australia, Europe, Israel, and North America. Patients admitted within the previous 24 hours with persisting dyspnea and a respiratory rate of 24/min or greater were eligible provided they fulfilled 2 of 4 criteria: (1) elevated plasma concentrations of B-type or N-terminal pro-B-type natriuretic peptide, (2) clinical pulmonary edema, (3) radiologic pulmonary congestion or edema, or (4) left ventricular systolic dysfunction.
Infusion of tezosentan (5 mg/h for 30 minutes, followed by 1 mg/h for 24 to 72 hours [n = 730]) or placebo (n = 718).
The coprimary end points were change in dyspnea (measured at 3, 6, and 24 hours using a visual analog scale from 0-100) over 24 hours (as area under the curve) in the individual trials and incidence of death or worsening heart failure at 7 days in both trials combined.
Of the 1435 patients who received treatment as assigned, 855 (60%) were men; mean age was 70 years. Mean left ventricular ejection fraction (measured in 779 patients [54%]) was 29% (SD, 11%). Baseline dyspnea scores were similar in the 2 treatment groups. Tezosentan did not improve dyspnea more than placebo in either trial, with a mean treatment difference of -12 (95% confidence interval [CI], -105 to 81) mm . h (P = .80) in the first trial and -25 (95% CI, -119 to 69) mm x h (P = .60) in the second. The incidence of death or worsening heart failure at 7 days in the combined trials was 26% in each treatment group (odds ratio, 0.99; 95% confidence interval, 0.82-1.21; P = .95).
The endothelin receptor antagonist tezosentan did not improve symptoms or clinical outcomes in patients with acute heart failure.
clinicaltrials.gov Identifiers: NCT00525707 (VERITAS-1) and NCT00524433 (VERITAS-2).
JAMA The Journal of the American Medical Association 12/2007; 298(17):2009-19. · 30.03 Impact Factor
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Nir Uriel,
Guillermo Torre-Amione,
Olga Milo,
Edo Kaluski,
Loïc Perchenet,
Alex Blatt, Isaac Kobrin,
Arkadi Turnovski,
Shoshana Kaplan,
Maurizio Rainisio,
Aline Frey,
Zvi Vered,
Gad Cotter
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ABSTRACT: Although echocardiographic ejection fraction (EF) is frequently used for the estimation of left ventricular contractility in patients with acute heart failure, its exact role and correlations with clinical, hemodynamic, and neurohormonal variables of cardiac contractility is not known.
Patients (343) with acute heart failure, enrolled into two prospective placebo-controlled hemodynamic studies of tezosentan, and in whom EF was available at baseline, were included. Outcome was evaluated in a subset of 94 patients who were enrolled in the placebo arms of the studies.
Higher echocardiographic EF was correlated with older age, increased incidence of hypertension and atrial fibrillation, and female gender. We observed weak correlation between EF and cardiac output or cardiac power and no correlation with wedge pressure, and the change in hemodynamic variables over time. Higher EF was correlated with more baseline leukocytosis and higher plasma levels of endothelin-1 and blood urea nitrogen, while lower EF was related to higher baseline B-type natriuretic peptide (BNP). We observed no overall correlations between EF and outcome.
In patients with acute heart failure, echocardiographic EF is weakly correlated with hemodynamic measures of left ventricular contractility and outcome; hence, it should be interpreted cautiously when evaluating patients admitted due to acute heart failure.
European Journal of Heart Failure 09/2005; 7(5):815-9. · 4.90 Impact Factor
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John R Teerlink,
John J V McMurray,
Robert C Bourge,
John G F Cleland,
Gadi Cotter,
Guillaume Jondeau,
Henry Krum,
Marco Metra,
Christopher M O'Connor,
John D Parker,
Guillermo Torre-Amione,
Dirk J Van Veldhuisen,
Aline Frey,
Maurizio Rainisio, Isaac Kobrin
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ABSTRACT: Endothelin 1 is a potent endogenous vasoconstrictor neurohormone, and endothelin 1 plasma concentrations predict adverse outcomes in patients with acute heart failure (AHF). Tezosentan, an intravenous endothelin receptor antagonist, improved hemodynamics in patients with AHF; however, its effects on morbidity and mortality have not been evaluated.
The VERITAS program consists of 2 identical, double-blind, randomized, placebo-controlled, concurrently conducted trials (VERITAS-1 and VERITAS-2), performed in 150 centers in Europe, Israel, Australia, and North America. The program is designed to enroll at least 1760 patients hospitalized with dyspnea at rest because of AHF requiring intravenous therapy. In addition to conventional therapy, patients are randomized to receive tezosentan (5 mg/h for 30 minutes, then 1 mg/h for 24-72 hours) or matching placebo. The 2 prespecified primary end points are the incidence of death or worsening heart failure at 7 days in the combined studies and the change from baseline in dyspnea over the first 24 hours of treatment, measured using a visual analog scale in VERITAS-1 and VERITAS-2, individually.
Enrollment started in April 2003, and the program was discontinued in November 2005 because of the low probability of achieving a significant treatment effect.
No currently available agents have been shown in a prospective, randomized, clinical trial to improve outcomes in patients with AHF. Thus, the VERITAS program will provide valuable insights into the effect of tezosentan on clinical outcomes in patients with AHF, as well as hemodynamics and clinical symptoms.
American heart journal 08/2005; 150(1):46-53. · 4.65 Impact Factor
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Gad Cotter,
Edo Kaluski,
Karl Stangl,
Richard Pacher,
Christoph Richter,
Olga Milo-Cotter,
Loïc Perchenet, Isaac Kobrin,
Shoshana Kaplan,
Maurizio Rainisio,
Aline Frey,
Eric Neuhart,
Zvi Vered,
Jasper Dingemanse,
Guillermo Torre-Amione
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ABSTRACT: In previous studies (the RITZ project), tezosentan, an intravenous (i.v.)-balanced dual endothelin (ET-A/B) antagonist, in doses of 50 and 100 mg/h, improved the hemodynamics but not the clinical outcome of patients with acute heart failure (AHF).
To evaluate the effect of lower doses of tezosentan in patients with AHF.
Included were 130 patients hospitalized due to AHF with dyspnea at rest, despite initial treatment, and were in need of hemodynamic monitoring with cardiac index (CI)<2.5 l/min/m(2) and wedge pressure > or = 20 mm Hg. Patients were randomized in a double-blind fashion to receive placebo or tezosentan: 0.2, 1, 5, or 25 mg/h for 24 h.
The primary endpoint of the study, CI increase at 6 h of treatment, was significant in the 5 and 25 mg/h groups. Tezosentan induced a dose-dependent increase in CI and a decrease in wedge pressure, peaking after 3 h in the 5 and 25 mg/h groups. In the 1 mg/h group, this effect was smaller during the first 6 h and increased gradually, becoming significant at 24 h and beyond treatment discontinuation. There was no hemodynamic effect in the 0.2 mg/h arm. Type-B natriuretic peptide (BNP) decreased in the 1, 5, and 25 mg/h groups but not on placebo. Endothelin levels were significantly increased by the 5 and 25 mg/h groups but not in the lower (< or = 1 mg/h) tezosentan doses. Urine output decreased on the 25 mg/h dose. There was a trend towards improvement in patients' subjective dyspnea score and worsening heart failure events, mainly in the 1 mg/h group.
In patients admitted with AHF, tezosentan doses of 1-25 mg/h are efficacious in improving the hemodynamics and reducing BNP. Tezosentan doses beyond 1 mg/h increased plasma endothelin levels and reduced urine output, probably limiting their clinical efficacy, as compared to tezosentan 1 mg/h.
European Journal of Heart Failure 08/2004; 6(5):601-9. · 4.90 Impact Factor
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ABSTRACT: The relation of cardiac troponin-I (cTnI) to clinical outcomes was examined in patients with decompensated heart failure and concomitant acute coronary syndrome enrolled into the Randomized Intravenous TeZosentan 4 (RITZ-4) study. RITZ-4 was a multicenter, randomized, double-blind, placebo-controlled trial of the endothelin receptor antagonist tezosentan in patients admitted with acute heart failure and concomitant acute coronary syndrome. One hundred ninety-two patients were enrolled in this study. Patients with baseline cTnI values were included in this analysis, and the relation between cTnI and the composite clinical primary end point of RITZ-4 was evaluated.
The American Journal of Cardiology 07/2004; 93(11):1436-7, A10. · 3.37 Impact Factor
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ABSTRACT: The relation of cardiac troponin-I (cTnI) to clinical outcomes was examined in patients with decompensated heart failure and concomitant acute coronary syndrome enrolled into the Randomized Intravenous TeZosentan 4 (RITZ-4) study. RITZ-4 was a multicenter, randomized, double-blind, placebo-controlled trial of the endothelin receptor antagonist tezosentan in patients admitted with acute heart failure and concomitant acute coronary syndrome. One hundred ninety-two patients were enrolled in this study. Patients with baseline cTnI values were included in this analysis, and the relation between cTnI and the composite clinical primary end point of RITZ-4 was evaluated.
American Journal of Cardiology - AMER J CARDIOL. 01/2004; 93(11):1436-1437.
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Journal of Cardiac Failure - J CARD FAIL. 01/2004; 10(4).
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Journal of Cardiac Failure - J CARD FAIL. 01/2004; 10(4).
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Guillermo Torre-Amione,
James B Young,
Wilson S Colucci,
Basil S Lewis,
Craig Pratt,
Gad Cotter,
Karl Stangl,
Uri Elkayam,
John R Teerlink,
Aline Frey,
Maurizio Rainisio, Isaac Kobrin
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ABSTRACT: We sought to investigate the efficacy and safety of tezosentan, a dual endothelin receptor antagonist, in patients hospitalized for acute heart failure (HF).
Tezosentan has been previously shown to improve hemodynamics in patients with stable chronic HF.
In a double-blind fashion, 292 patients (cardiac index < or =2.5 l/min per m(2) and pulmonary capillary wedge pressure (PCWP) > or =15 mm Hg) who were admitted to the hospital and in need of intravenous treatment for acute HF and central hemodynamic monitoring were randomized to 24-h intravenous treatment with tezosentan (50 or 100 mg/h) or placebo. Central hemodynamic variables, the dyspnea score, and safety variables were measured.
After 6 h of treatment, significantly greater increases in the cardiac index and decreases in PCWP were observed with both tezosentan dosages than with placebo (mean treatment effects at 0.38 and 0.37 l/min per m(2) with 50 and 100 mg/h and -3.9 mm Hg for each dose, respectively; p < 0.0001). This effect was maintained during the remaining infusion and for > or =6 h after treatment cessation. A tendency for an improved dyspnea score and a decreased risk of clinical worsening was observed after 24 h of treatment with each tezosentan dose. Adverse events, more frequent with tezosentan than with placebo (headache, asymptomatic hypotension, early worsening of renal function, nausea, vomiting), were dose-related.
Intravenous tezosentan rapidly and effectively improved hemodynamics in these patients. The similar beneficial effects of the two dosages and the increased dose-related adverse events with the higher dosage suggest that the optimal dosing regimen is <50 mg/h.
Journal of the American College of Cardiology 08/2003; 42(1):140-7. · 14.16 Impact Factor
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Christopher M O'Connor,
Wendy A Gattis,
Kirkwood F Adams,
Vic Hasselblad,
Bleakley Chandler,
Aline Frey, Isaac Kobrin,
Maurizio Rainisio,
Monica R Shah,
John Teerlink,
Mihai Gheorghiade
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ABSTRACT: We sought to determine the effect of tezosentan in patients with acute decompensated heart failure (HF) associated with acute coronary syndrome (ACS).
Tezosentan is a dual endothelin receptor antagonist that has been shown to improve cardiac output, decrease pulmonary capillary wedge pressure, and reduce pulmonary and systemic vascular resistance in initial clinical studies in acute decompensated HF.
The Randomized Intravenous TeZosentan (RITZ)-4 study was a multicenter, randomized, double-blinded, placebo-controlled study of tezosentan in patients with acute decompensated HF associated with ACS. A total of 193 patients were randomized to receive tezosentan (25 mg/h for 1 h, then 50 mg/h for 23 to 47 h) or placebo. Patients with evidence of acute decompensated HF and ACS were eligible to participate. The primary end point was the composite of death, worsening HF, recurrent ischemia, and recurrent or new myocardial infarction within 72 h.
No significant differences were observed between placebo and 50 mg/h tezosentan in the composite primary end point: 24.2% (95% confidence interval [CI] 16.0% to 34.1%) and 28.9% (95% CI 20.1% to 39.0%), respectively (p = 0.5152). Symptomatic hypotension was more frequent in the treatment group.
At the doses studied, tezosentan did not result in a significant improvement in the composite primary clinical end point in the RITZ-4 trial. Tezosentan did not demonstrate pro-ischemic effects in this population. Symptomatic hypotension may have resulted in an increased number of adverse events in the treatment group. Further studies with lower tezosentan doses are warranted.
Journal of the American College of Cardiology 06/2003; 41(9):1452-7. · 14.16 Impact Factor
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Edo Kaluski, Isaac Kobrin,
Reuven Zimlichman,
Alon Marmor,
Oscar Krakov,
Olga Milo,
Aline Frey,
Shoshana Kaplan,
Rikardo Krakover,
Avi Caspi,
Zvi Vered,
Gad Cotter
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ABSTRACT: The objective of this study was to evaluate the addition of intravenous (IV) tezosentan to standard therapy for patients with pulmonary edema.
Tezosentan is an IV nonselective endothelin (ET)-1 antagonist that yields favorable hemodynamic effects in patients with acute congestive heart failure (CHF).
Pulmonary edema was defined as acute CHF leading to respiratory failure, as evidenced by an oxygen saturation (SO(2)) <90% by pulse oxymeter despite oxygen treatment. All patients received oxygen 8 l/min through a face mask, 3 mg of IV morphine, 80 mg of furosemide, and 1 to 3 mg/h continuous drip isosorbide-dinitrate according to their blood pressure level and were randomized to receive a placebo or tezosentan (50 or 100 mg/h) for up to 24 h.
Eighty-four patients were randomized. The primary end point, the change in SO(2) from baseline to 1 h, was 9.1 +/- 6.3% in the placebo arm versus 7.6 +/- 10% in the tezosentan group (p = NS). The incidence of death, recurrent pulmonary edema, mechanical ventilation, and myocardial infarction during the first 24 h of treatment was 19% in both groups. Reduced baseline SO(2), lower echocardiographic ejection fraction, high baseline mean arterial blood pressure (MAP), and inappropriate vasodilation (MAP reduction at 30 min of <5% or >30%) correlated with worse outcomes. A post-hoc analysis revealed that the outcome of patients who received only 50 mg/h tezosentan was better than patients in the placebo group whereas patients receiving 100 mg/h had the worst outcomes.
In the present study, tezosentan (an ET-1 antagonist) did not affect the outcome of pulmonary edema, possibly because of the high dose used.
Journal of the American College of Cardiology 01/2003; 41(2):204-10. · 14.16 Impact Factor
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ABSTRACT: Endothelin-1 is the most potent known endogenous vasoconstrictor. It is released during ischemia, and elevated levels have been demonstrated in hypertension, myocardial infarction, and heart failure. Tezosentan is a dual endothelin receptor antagonist, and it has improved cardiac output and reduced pulmonary and systemic vascular resistance in experimental animal models and in initial human acute decompensated heart failure studies.
The Randomized Intravenous TeZosentan (RITZ-4) study was a multicenter, randomized, double-blind, placebo-controlled trial of tezosentan in patients with acute heart failure associated with acute coronary syndrome. The estimated sample size was 200 patients. Patients with evidence of acute heart failure and acute coronary syndrome were eligible for the study. Eligible patients were randomly assigned to tezosentan or matching placebo. The primary end point was the composite of death, worsening heart failure, recurrent ischemia, and recurrent or new myocardial infarction within 72 hours after the start of study drug treatment. Secondary end points included all-cause death and hospitalization at 30 days, and length of initial hospital stay.
Enrollment was completed in February 2001, with 193 patients enrolled.
The RITZ-4 study evaluated an important population in which few data are available to guide medical management. RITZ-4 will provide valuable safety and efficacy data with the novel compound tezosentan in patients with acute heart failure and acute coronary syndrome.
American heart journal 11/2002; 144(4):583-8. · 4.65 Impact Factor
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Christopher M O’Connor,
Wendy A Gattis,
Kirkwood F Adams,
Vic Hasselblad,
Bleakley Chandler,
Aline Frey, Isaac Kobrin,
Maurizio Rainisio,
Monica R Shah,
John Teerlink,
Mihai Gheorghiade
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ABSTRACT: ObjectivesWe sought to determine the effect of tezosentan in patients with acute decompensated heart failure (HF) associated with acute coronary syndrome (ACS).BackgroundTezosentan is a dual endothelin receptor antagonist that has been shown to improve cardiac output, decrease pulmonary capillary wedge pressure, and reduce pulmonary and systemic vascular resistance in initial clinical studies in acute decompensated HF.MethodsThe Randomized Intravenous TeZosentan (RITZ)-4 study was a multicenter, randomized, double-blinded, placebo-controlled study of tezosentan in patients with acute decompensated HF associated with ACS. A total of 193 patients were randomized to receive tezosentan (25 mg/h for 1 h, then 50 mg/h for 23 to 47 h) or placebo. Patients with evidence of acute decompensated HF and ACS were eligible to participate. The primary end point was the composite of death, worsening HF, recurrent ischemia, and recurrent or new myocardial infarction within 72 h.ResultsNo significant differences were observed between placebo and 50 mg/h tezosentan in the composite primary end point: 24.2% (95% confidence interval [CI] 16.0% to 34.1%) and 28.9% (95% CI 20.1% to 39.0%), respectively (p = 0.5152). Symptomatic hypotension was more frequent in the treatment group.ConclusionsAt the doses studied, tezosentan did not result in a significant improvement in the composite primary clinical end point in the RITZ-4 trial. Tezosentan did not demonstrate pro-ischemic effects in this population. Symptomatic hypotension may have resulted in an increased number of adverse events in the treatment group. Further studies with lower tezosentan doses are warranted.
Journal of the American College of Cardiology.
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Christopher M. O'Connor,
Wendy A. Gattis,
Kirkwood F. Adams,
Vic Hasselblad,
Bleakley Chandler,
Aline Frey, Isaac Kobrin,
Maurizio Rainisio,
Monica R. Shah,
John Teerlink,
Mihai Gheorghiade
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Maurizio Rainisio, Isaac Kobrin,
Craig Pratt,
Gad Cotter,
Karl Stangl,
Uri Elkayam,
John R. Teerlink,
Aline Frey,
Guillermo Torre-Amione,
James B. Young,
Wilson S. Colucci,
Basil S. Lewis
