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Dive into the research topics where David L. Reich is active.

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Featured researches published by David L. Reich.


Circulation | 2010

2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease: Executive summary: A report of the american college of cardiology foundation/american heart association task force on practice guidelines, american association for thoracic surgery, american college of radiology, american stroke association

Loren F. Hiratzka; George L. Bakris; Joshua A. Beckman; Robert M. Bersin; Vincent F. Carr; Donald E. Casey; Kim A. Eagle; Luke K. Hermann; Eric M. Isselbacher; Ella A. Kazerooni; Nicholas T. Kouchoukos; Bruce W. Lytle; Dianna M. Milewicz; David L. Reich; Souvik Sen; Julie A. Shinn; Lars G. Svensson; David M. Williams; Alice K. Jacobs; Sidney C. Smith; Jeffery L. Anderson; Cynthia D. Adams; Christopher E. Buller; Mark A. Creager; Steven M. Ettinger; Robert A. Guyton; Jonathan L. Halperin; Sharon A. Hunt; Harlan M. Krumholz; Frederick G. Kushner

2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine


Journal of the American College of Cardiology | 2010

2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease

Loren F. Hiratzka; George L. Bakris; Joshua A. Beckman; Robert M. Bersin; Vincent F. Carr; Donald E. Casey; Kim A. Eagle; Luke K. Hermann; Eric M. Isselbacher; Ella A. Kazerooni; Nicholas T. Kouchoukos; Bruce W. Lytle; Dianna M. Milewicz; David L. Reich; Souvik Sen; Julie A. Shinn; Lars G. Svensson; David M. Williams

It is essential that the medical profession play a central role in critically evaluating the evidence related to drugs, devices, and procedures for the detection, management, or prevention of disease. Properly applied, rigorous, expert analysis of the available data documenting absolute and relative


Canadian Journal of Anaesthesia-journal Canadien D Anesthesie | 1989

Ketamine: an update on the first twenty-five years of clinical experience

David L. Reich; George Silvay

RésuméPendant presque 25 ans ďexpérience clinique, les bénéfices et les limitations de ľanesthésie à la kétamine ont été généralement bien définis. Les revues extensives de White et al.2 ainsi que celles de Reeves et al.43 ont énormément aidé à comprendre ľanesthésie dissociative. Néanmoins, des études récentes continuent à nous éclairer sur les différents aspects de la pharmacologie de la kétamine et suggèrent de nouvelles utilisations cliniques de cette drogue. Ľidentification du récepteur du N-M ethyl-Aspartate amène une preuve que ľanesthésie et ľanalgésie à la kétamine ont chacune un mécanisme ďaction différent. La liaison stéréospécifique de la (+) kétamine aux récepteurs opiacés in vitro, ľémergence plus rapide de ľanesthésie, et une incidence plus basse de séquelles lors de ľémergence, rend la (+) kétamine une drogue promettante pour des recherches futures. Les applications cliniques de la kétamine qui ressortent récemment, et qui probablement augmenteront dans le futur sont reliées é ľutilisation orale, rectale et intra-nasale de la kétamine pour des fins ďanalgésie, de sédation ou induction anesthésique. La kétamine est actuellement considérée comme une option raisonnable pour ľinduction anesthésique chez les nouveau-nés prématurés en hypotension. Ľexpérience initiale avec la kétamine en injection épidurale et intrathécale ne fut pas prometteuse et les données sont encore préliminaires dans ce domaine. Ľutilisation de la kétamine dans les catastrophes et les manoeuvres militaires va probablement être plus fréquente. La disponibilité clinique du midazolam va complementer ľanesthésie à la kétamine de plusieurs façons. Cette benzodiazépine est rapidement métabolisée. Elle réduit la stimulation cardiovasculaire de la kétamine ainsi que les phénomènes ďémergence sans avoir des métabolites actifs. Elle est disponible sous une forme aqueuse et n’est pas irritante lors de ľinjection intra-veineuse comme le diazépam. La combinaison de la kétamine et du midazolam sera bien acceptée par les patients contrairement à ce qui arrive quand on utilise la kétamine seule. Finalement, il est nécessaire de mentionner la possibilité ďabus de la kétamine.126 Alors que la kétamine n’est pas une substance contrôlée (aux États-Unis) la prudence suggère aux médecins de prendre des précautions appropriées contre son utilisation non-autorisée.


Biological Psychiatry | 2010

Safety and efficacy of repeated-dose intravenous ketamine for treatment-resistant depression.

Marije aan het Rot; Katherine A. Collins; James W. Murrough; Andrew M. Perez; David L. Reich; Dennis S. Charney; Sanjay J. Mathew

BACKGROUND A single subanesthetic (intravenous) IV dose of ketamine might have rapid but transient antidepressant effects in patients with treatment-resistant depression (TRD). Here we tested the tolerability, safety, and efficacy of repeated-dose open-label IV ketamine (six infusions over 12 days) in 10 medication-free symptomatic patients with TRD who had previously shown a meaningful antidepressant response to a single dose. METHODS On day 1, patients received a 40-min IV infusion of ketamine (.5 mg/kg) in an inpatient setting with continuous vital-sign monitoring. Psychotomimetic effects and adverse events were recorded repeatedly. The primary efficacy measure was change from baseline in the Montgomery-Asberg Depression Rating Scale (MADRS) score. If patients showed a > or =50% reduction in MADRS scores on day 2, they received five additional infusions on an outpatient basis (days 3, 5, 8, 10, and 12). Follow-up visits were conducted twice-weekly for > or =4 weeks or until relapse. RESULTS Ketamine elicited minimal positive psychotic symptoms. Three patients experienced significant but transient dissociative symptoms. Side effects during and after each ketamine infusion were generally mild. The response criterion was met by nine patients after the first infusion as well as after the sixth infusion. The mean (SD) reduction in MADRS scores after the sixth infusion was 85% (12%). Postketamine, eight of nine patients relapsed, on average, 19 days after the sixth infusion (range 6 days-45 days). One patient remained antidepressant-free with minimal depressive symptoms for >3 months. CONCLUSIONS These pilot findings suggest feasibility of repeated-dose IV ketamine for the acute treatment of TRD.


Anesthesia & Analgesia | 2005

Predictors of hypotension after induction of general anesthesia.

David L. Reich; Sabera Hossain; Marina Krol; Bernard Baez; Puja Patel; Ariel Bernstein; Carol Bodian

Hypotension after induction of general anesthesia is a common event. In the current investigation, we sought to identify the predictors of clinically significant hypotension after the induction of general anesthesia. Computerized anesthesia records of 4096 patients undergoing general anesthesia were queried for arterial blood pressure (BP), demographic information, preoperative drug history, and anesthetic induction regimen. The median BP was determined preinduction and for 0–5 and 5–10 min postinduction of anesthesia. Hypotension was defined as either: mean arterial blood pressure (MAP) decrease of >40% and MAP <70 mm Hg or MAP <60 mm Hg. Overall, 9% of patients experienced severe hypotension 0–10 min postinduction of general anesthesia. Hypotension was more prevalent in the second half of the 0–10 min interval after anesthetic induction (P < 0.001). In 2406 patients with retrievable outcome data, prolonged postoperative stay and/or death was more common in patients with versus those without postinduction hypotension (13.3% and 8.6%, respectively, multivariate P < 0.02). Statistically significant multivariate predictors of hypotension 0–10 min after anesthetic induction included: ASA III–V, baseline MAP <70 mm Hg, age ≥50 yr, the use of propofol for induction of anesthesia, and increasing induction dosage of fentanyl. Smaller doses of propofol, etomidate, and thiopental were not associated with less hypotension. To avoid severe hypotension, alternatives to propofol anesthetic induction (e.g., etomidate) should be considered in patients older than 50 yr of age with ASA physical status ≥3. We conclude that it is advisable to avoid propofol induction in patients who present with baseline MAP <70 mm Hg.


The Annals of Thoracic Surgery | 1999

Cerebral metabolic suppression during hypothermic circulatory arrest in humans.

Jock N McCullough; Ning Zhang; David L. Reich; Tatu S Juvonen; James J Klein; David Spielvogel; M. Arisan Ergin; Randall B. Griepp

BACKGROUND Hypothermic circulatory arrest (HCA) is used in surgery for aortic and congenital cardiac diseases. Although studies of the safety of HCA in animals have been carried out, the degree to which metabolism is suppressed in patients during hypothermia has been difficult to determine because of problems with serial measurements of cerebral blood flow in the clinical setting. METHODS To quantify the degree of metabolic suppression achieved by hypothermia, we studied 37 adults undergoing operations employing HCA. Cerebral blood flow was estimated using an ultrasonic flow probe on the left common carotid artery, and cerebral arteriovenous oxygen content differences were calculated from jugular venous bulb and arterial oxygen saturations. Cerebral metabolic rates while cooling were then ascertained. The temperature coefficient, Q10, which is the ratio of metabolic rates at temperatures 10 degrees C apart, was determined. RESULTS The human cerebral Q10 was found to be 2.3. The cerebral metabolic rate is still 17% of baseline at 15 degrees C. If one assumes that cerebral blood flow can safely be interrupted for 5 min at 37 degrees C, and that cerebral metabolic suppression accounts for the protective effects of hypothermia, the predicted safe duration of HCA at 15 degrees C is only 29 min. CONCLUSIONS The safe intervals calculated from measured cerebral oxygen consumption suggest that shorter intervals and lower temperatures than those currently used may be necessary to assure adequate cerebral protection during hypothermic circulatory arrest.


Anesthesiology | 1999

Beneficial effects from β-adrenergic blockade in elderly patients undergoing noncardiac surgery

Michael Zaugg; Thomas M. Tagliente; Eliana Lucchinetti; Ellis Jacobs; Marina Krol; Carol Bodian; David L. Reich; Jeffrey H. Silverstein

BackgroundPerioperative β-blockade has been shown to improve long-term cardiac outcome in noncardiac surgical patients. A possible mechanism for the reduced risk of perioperative myocardial infarction is the attenuation of the excitotoxic effects of catecholamine surges by β-blockade. It was hypothe


Anesthesia & Analgesia | 1999

Intraoperative hemodynamic predictors of mortality, stroke, and myocardial infarction after coronary artery bypass surgery.

David L. Reich; Carol Bodian; Marina Krol; Maxine M. Kuroda; Todd Osinski; Daniel M. Thys

UNLABELLED Evidence that intraoperative hemodynamic abnormalities influence outcome is limited. The purpose of this study was to determine whether intraoperative hemodynamic abnormalities were associated with mortality, stroke, or perioperative myocardial infarction (PMI) in a large cohort of patients undergoing coronary artery bypass grafting. Risk factors and outcomes were queried from a state-mandated cardiac surgery reporting system at two hospitals in New York, NY. Intraoperative hemodynamic abnormalities were derived from computerized anesthesia records by assessing the duration of exposure to moderate or severe extremes of hemodynamic variables. Multivariate logistic regression identified independent predictors of perioperative mortality, stroke, and PMI. Among 2149 patients, there were 50 mortalities, 51 strokes, and 85 PMIs. In the precardiopulmonary bypass (pre-CPB) period, pulmonary hypertension was a predictor of mortality (odds ratio [OR] 2.1, P = 0.029), and bradycardia and tachycardia were predictors of PMI (OR 2.9, P = 0.007 and OR 2.0, P = 0.028, respectively). During CPB, hypotension was a predictor of mortality (OR 1.3, P = 0.025). Post-CPB, tachycardia was a predictor of mortality (OR 3.1, P = 0.001), diastolic arterial hypertension was a predictor of stroke (OR 5.4, P = 0.012), and pulmonary hypertension was a predictor of PMI (OR 7.0, P < 0.001). Increased pulmonary arterial diastolic pressure post-CPB was a predictor of mortality (OR 1.2, P = 0.004), stroke (OR 3.9, P = 0.002), and PMI (OR 2.2, P = 0.001). Rapid intraoperative variations in blood pressure and heart rate were not independent predictors of these outcomes. These findings demonstrate the prognostic significance of intraoperative hemodynamic abnormalities, including data from pulmonary artery catheterization, to adverse postoperative outcomes. It is not known whether interventions to control these variables would improve outcome. IMPLICATIONS Intraoperative hemodynamic abnormalities, including pulmonary hypertension, hypotension during cardiopulmonary bypass, and postcardiopulmonary bypass pulmonary diastolic hypertension, were independently associated with mortality, stroke, and perioperative myocardial infarction over and above the effects of other preoperative risk factors.


The International Journal of Neuropsychopharmacology | 2010

Riluzole for relapse prevention following intravenous ketamine in treatment-resistant depression: a pilot randomized, placebo-controlled continuation trial.

Sanjay J. Mathew; James W. Murrough; Marije aan het Rot; Katherine A. Collins; David L. Reich; Dennis S. Charney

The N-methyl-D-aspartate (NMDA) glutamate receptor antagonist ketamine may have rapid, albeit transient, antidepressant properties. This study in patients with treatment-resistant major depression (TRD) aimed to (1) replicate the acute efficacy of single-dose intravenous (i.v.) ketamine; (2) test the efficacy of the glutamate-modulating agent riluzole in preventing post-ketamine relapse; and (3) examine whether pretreatment with lamotrigine would attenuate ketamines psychotomimetic effects and enhance its antidepressant activity. Twenty-six medication-free patients received open-label i.v. ketamine (0.5 mg/kg over 40 min). Two hours prior to infusion, patients were randomized to lamotrigine (300 mg) or placebo. Seventeen patients (65%) met response criterion (50% reduction from baseline on the Montgomery-Asberg Depression Rating Scale) 24 h following ketamine. Lamotrigine failed to attenuate the mild, transient side-effects associated with ketamine and did not enhance its antidepressant effects. Fourteen patients (54%) met response criterion 72 h following ketamine and proceeded to participate in a 32-d, randomized, double-blind, placebo-controlled, flexible-dose continuation trial of riluzole (100-200 mg/d). The main outcome measure was time-to-relapse. An interim analysis found no significant differences in time-to-relapse between riluzole and placebo groups [log-rank chi(2) = 0.17, d.f. = 1, p = 0.68], with 80% of patients relapsing on riluzole vs. 50% on placebo. The trial was thus stopped for futility. This pilot study showed that a sub-anaesthetic dose of i.v. ketamine is well-tolerated in TRD, and may have rapid and sustained antidepressant properties. Riluzole did not prevent relapse in the first month following ketamine. Further investigation of relapse prevention strategies post-ketamine is necessary.


The Journal of Thoracic and Cardiovascular Surgery | 1999

Neuropsychologic outcome after deep hypothermic circulatory arrest in adults

David L. Reich; Suzan Uysal; Martin J. Sliwinski; M. Arisan Ergin; Ronald A. Kahn; Steven N. Konstadt; Jock N. McCullough; Mary R. Hibbard; Wayne Gordon; Rb Griepp

INTRODUCTION Pediatric patients undergoing prolonged periods of deep hypothermic circulatory arrest have been found to experience long-term deficits in cognitive function. However, there is limited information of this type in adult patients who are undergoing deep hypothermic circulatory arrest for thoracic aortic repairs. METHODS One hundred forty-nine patients undergoing elective cardiac or thoracic aortic operations were evaluated preoperatively; 106 patients were evaluated early in the postoperative period (EARLY), and 77 patients were evaluated late in the postoperative period (LATE) with a battery of neuropsychologic tests. Seventy-three patients had routine cardiac operations without deep hypothermic circulatory arrest, and 76 patients with deep hypothermic circulatory arrest were divided into 2 subgroups: those with 1 to 24 minutes of deep hypothermic circulatory arrest (n = 36 patients) and those with 25 minutes or more of deep hypothermic circulatory arrest (n = 40 patients). The neuropsychologic test battery consisted of 8 tests encompassing 5 domains: attention, processing speed, memory, executive function, and fine motor function. Data were normalized to baseline values, and changes from baseline were analyzed by analysis of covariance, multivariate logistic regression, and survival functions. RESULTS In all domains, poor performance or inability to be tested EARLY were significant predictors of poor performance LATE (odds ratio, 5.27; P <.01). Deep hypothermic circulatory arrest of 25 minutes or more and advanced age were significant predictors of poor performance LATE for the memory and fine motor domains. Deep hypothermic circulatory arrest of 25 minutes or more (odds ratio, 4. 0; P =.02) was a determinant of prolonged hospital stay (>21 days). CONCLUSION Deep hypothermic circulatory arrest of 25 minutes or more and advanced age were associated with memory and fine motor deficits and with prolonged hospital stay.

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Marina Krol

Icahn School of Medicine at Mount Sinai

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Steven N. Konstadt

Albert Einstein College of Medicine

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Carol Bodian

Icahn School of Medicine at Mount Sinai

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Suzan Uysal

Icahn School of Medicine at Mount Sinai

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Ronald A. Kahn

Icahn School of Medicine at Mount Sinai

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Daniel M. Thys

American Society of Echocardiography

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Gregory W. Fischer

Icahn School of Medicine at Mount Sinai

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Hung-Mo Lin

Icahn School of Medicine at Mount Sinai

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