Publications by authors named "Thourani V"

Background: Outcomes and resource utilization of patients undergoing mitral valve replacement (MVR) with or without concomitant coronary artery bypass grafting (CABG) were reviewed.

Methods: Data for 1,844 patients undergoing isolated primary MVR at Emory University Hospitals between 1980 and 1997 were recorded prospectively in a computerized database.

Results: The four groups included patients undergoing elective MVR with (n = 360) or without CABG (n = 1332) and urgent/emergent MVR with (n = 66) or without CABG (n = 86).

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Background: There has been increasing concern in recent years about the quality and cost of heart valvular replacement procedures. The purpose of this study is to examine the profile of patients undergoing valvular operations during the past decade, and to look at trends in outcome and resource utilization over that period.

Methods: Clinical and procedural data of 2,972 patients undergoing heart valve replacement at Emory University Hospitals between 1988 and 1997 were recorded prospectively on standardized forms by trained medical personnel and entered into a computerized database.

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The goals of myocardial protection during cardiac surgery are not only to facilitate the operation by providing a quiet bloodless field, thereby facilitating the precision of the operation, but also to avoid iatrogenic injury induced by cardiopulmonary bypass itself or by surgically imposed ischemia. In addition, myocardial protective strategies are geared to preventing reperfusion injury upon resolution of the coronary occlusion and the ultimate release of the aortic cross clamp. Cardioplegia plays a very important role in myocardial protection strategies.

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Objectives: This study tested the hypothesis that a recombinant human C5a antagonist, CGS 32359, attenuates neutrophil activation and reduces infarct size in a porcine model of surgical revascularization.

Methods: CGS 32359 (0.16-16 micromol/L) dose-dependently inhibited superoxide production by human C5a-activated porcine neutrophils (18 +/- 3.

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Heparin reduces ischemia-reperfusion injury to myocardium. This effect has been attributed to complement inhibition, but heparin also has other activities that might diminish ischemia-reperfusion. To further probe these mechanisms, we compared heparin or an o-desulfated nonanticoagulant heparin with greatly reduced anticomplement activity.

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Background: Multiple organ failure after deep hypothermic circulatory arrest (DHCA) may occur secondary to endothelial dysfunction and apoptosis. We sought to determine if DHCA causes endothelial dysfunction and apoptosis in brain, kidney, lungs, and other tissues.

Methods: Anesthetized pigs on cardiopulmonary bypass were: (1) cooled to 18 degrees C, and had their circulation arrested (60 minutes) and reperfused at 37 degrees C for 90 minutes (DHCA, n = 8); or (2) time-matched normothermic controls on bypass (CPB, n = 6).

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Objective: Recent studies suggest that ischemic preconditioning (IPC) inhibits myocardial apoptosis after ischemia and reperfusion. This study tested the hypothesis that IPC reduces ischemia/reperfusion-induced myocardial apoptosis by inhibiting neutrophil (PMN) accumulation and altering expression of Bcl-2 and Bax proteins.

Methods: Eighteen rats were subjected to 30 min of left coronary artery occlusion followed by 180 min of reperfusion with IPC (5 min ischemia and 10 min of reperfusion, n = 10) or without IPC (n = 8).

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Background: Hemodynamic instability during multivessel off-pump coronary artery bypass grafting can lead to hypotension, progressive myocardial ischemia, further hypotension, and the need for urgent cardiopulmonary bypass.

Methods: In 10 patients undergoing off-pump coronary artery bypass grafting, a novel technique of pressure-controlled blood delivery has been used that allows the immediate restoration of arterial blood to distal coronary beds after distal coronary anastomosis. This technique utilizes a servo-controlled pump to allow delivery of blood at systemic or suprasystemic pressures, and provides the option for infusion of supplemental additives for myocardial resuscitation, myocardial vasodilation, and enhancement of myocardial performance.

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Ischemia-reperfusion results in contractile dysfunction, necrosis, and vascular injury. This postischemic injury is mediated in part by superoxide radical production, neutrophils, dysfunction to ionic pumps, and edema formation. Adenosine is an autacoid released tonically by myocytes, endothelium, and neutrophils; the release of adenosine from the myocyte compartment into the interstitium is increased during ischemia.

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Background: Peroxynitrite (ONOO(-)) has been implicated as a primary mediator in the deleterious effects of nitric oxide (NO) in crystalloid solutions, possibly due to a lack of detoxification mechanisms, leading to the formation of.OH. In contrast, ONOO(-) may exert cardioprotective effects in blood environments secondary to detoxification and the subsequent formation of NO-donating nitrosothiols.

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Background: Various studies have reported that the administration of adenosine (ADO) in cardioplegia reduces myocardial ischemic injury, but this timing may not utilize ADO's potential against myocardial reperfusion injury. This study tested the hypothesis that ADO-supplemented blood cardioplegia (BCP) or ADO administered during reperfusion reduces postischemic dysfunction after severe regional ischemia.

Methods And Results: After 75 minutes of left anterior descending coronary artery occlusion, total cardiopulmonary bypass was initiated; cold (4 degrees C) antegrade BCP (8:1 blood:crystalloid) was delivered every 20 minutes for the first 3 doses, and 27 degrees C BCP was delivered for the terminal infusion.

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This study tested the hypothesis that A(3) adenosine receptors inhibit neutrophil (PMN) function and PMN-mediated reperfusion injury. 2-Chloro-N(6)-(3-iodobenzyl)adenosine-5'-N-methyluronamide (Cl-IB-MECA), an A(3) agonist, did not attenuate superoxide production or myeloperoxidase release from stimulated PMNs. However, Cl-IB-MECA reduced platelet-activating factor-stimulated PMN adherence to coronary endothelium at low concentrations: 52 +/- 27, 45 +/- 10, and 87 +/- 23 PMNs/mm(2) at 0.

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Background: A screening and treatment protocol was implemented to extend the benefit of prophylactic carotid endarterectomy to patients who had open heart operations.

Methods: Patients aged 65 or older or who at any age had left main coronary disease, transient ischemic attack, or stroke were eligible for preoperative carotid duplex screening. Carotid endarterectomies and open heart operations were planned as a staged (n = 59) or combined procedure (n = 55) for angiographically confirmed carotid stenosis of at least 80%.

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This is a report of a 22-year experience with penetrating cardiac trauma at a single urban Level I trauma center. We conducted a retrospective chart review supplemented by computerized patient log. Comparisons of mortality between Period 1 (1975-1985; 113 patients) and Period 2 (1986-1996; 79 patients) were by chi2 or Fisher's exact tests.

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The normal coronary vascular endothelium (VE) tonically releases nitric oxide (NO) by converting L-arginine to citrulline by a constitutive NO synthase. Reperfusion after myocardial ischemia reduces basal and stimulated release of NO. This "vascular reperfusion injury" is mediated largely by neutrophils (PMN) through specific interactions between adhesion molecules on the endothelium and the PMN, an interaction that precedes myocyte injury.

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We tested the hypothesis that selective adenosine A(3)-receptor stimulation reduces postischemic contractile dysfunction through activation of ATP-sensitive potassium (K(ATP)) channels. Isolated, buffer-perfused rat hearts (n = 8/group) were not drug pretreated (control) or were pretreated with adenosine (20 microM), 2-chloro-N(6)-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (Cl-IB-MECA; A(3) agonist, 100 nM), Cl-IB-MECA + 8-(3-noradamantyl)-1,3-dipropylxanthine (KW-3902; A(1) antagonist, 5 microM), Cl-IB-MECA + glibenclamide (Glib; K(ATP)-channel blocker, 0. 3 microM), or Glib alone for 12 min before 30 min of global normothermic ischemia followed by 2 h of reperfusion.

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Background: The cardioprotective effects of the adenosine A3 receptor in a cardioplegia model have not been described. We tested the hypothesis that infusion of the A3 receptor agonist, Cl-IB-MECA (100 nM), as a pretreatment (PTx) and/or as a cardioplegic (CP) additive reduces postischemic myocardial injury.

Methods: Isolated perfused rat hearts underwent 30 minutes of normothermic ischemia, 60 minutes of intermittent hypothermic cardioplegia (10 degrees C), followed by 2 hours of reperfusion.

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Background: Diabetes mellitus is an established independent risk factor for significant morbidity and mortality after coronary artery bypass grafting.

Methods: The impact of diabetes on short- and longterm follow-up after coronary artery bypass grafting was studied by comparing the outcomes between 9,920 patients without diabetes mellitus and 2,278 patients with diabetes from 1978 to 1993.

Results: Compared with nondiabetic patients, the group with diabetes was older (62+/-10 years versus 60+/-10 years), comprised more women (31% versus 19%), had a greater incidence of hypertension (61% versus 44%) and previous myocardial infarction (51% versus 48%), had class III-IV angina more commonly (69% versus 63%), showed a higher incidence of congestive heart failure (11% versus 5%) or triple-vessel or left main disease (60% versus 50%), and had lower ejection fractions (0.

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Objective: Unmodified reperfusion without cardioplegia in minimally invasive direct coronary artery bypass grafting procedures causes endothelial dysfunction that may predispose to polymorphonuclear neutrophil-mediated myocardial injury. This study tested the hypothesis that ischemic preconditioning in a minimally invasive direct coronary artery bypass grafting model attenuates postischemic endothelial dysfunction in coronary vessels.

Methods: In anesthetized dogs, the left anterior descending coronary artery was occluded for 30 minutes and reperfused for 3 hours without ischemic preconditioning (no-ischemic preconditioning; n = 7); in 7 dogs, the left anterior descending occlusion was preceded by 5 minutes occlusion followed by 5 minutes of reperfusion.

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Background: Empyema thoracis is treated with a multitude of therapeutic options. Optimal therapy and cost-containment requires selection of the most appropriate initial intervention.

Methods: A retrospective review of treatment modalities was performed on 77 patients diagnosed with empyema thoracis from 1990 to 1997 at one institution.

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Background: Ischemic preconditioning (IP) may be cardioprotective in minimally invasive direct coronary artery bypass where cardioplegia is not used. This study tested the hypothesis that IP of the area at risk (AAR) would attenuate postischemic injury from transient coronary artery occlusion.

Methods: In 19 anesthetized dogs, the left anterior descending coronary artery was occluded for 30 minutes (simulating coronary occlusion during anastomosis) followed by 3 hours of reperfusion.

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Background/purpose: The focused assessment for the sonographic evaluation of trauma patients (FAST) in adults is effective in detecting intraperitoneal and intrapericardial fluid and can be performed quickly by surgeons in the emergency department (ED). The authors sought to validate the accuracy of FAST performed by surgeons during ED resuscitation of pediatric trauma patients.

Methods: Patients were assigned to one of three groups based on standard clinical criteria: immediate surgery, abdominal computed tomography (CT), or observation alone.

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Background: Reconstruction of the complex pharyngeal wound after radiotherapy presents a surgical challenge.

Methods: Evaluation of the gastro-omental flap in the reconstruction of the pharynx and overlying soft tissue after local flap failure.

Results: A 70-year-old patient underwent a total laryngectomy and radical neck dissection after 70 Gy of external beam radiotherapy for an advanced squamous cell carcinoma of the pyriform sinus.

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Angiotensin converting enzyme (ACE) activity contributes to the vascular response to injury because ACE inhibition limits neointima formation in rat carotid arteries after balloon injury. To investigate the mechanisms by which ACE may contribute to vascular smooth muscle cell (VSMC) proliferation, we studied expression of ACE in vivo after injury and in vitro after growth factor stimulation. ACE activity 14 d after injury was increased 3.

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