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1.
J Thromb Haemost ; 16(10): 1932-1940, 2018 10.
Article in English | MEDLINE | ID: mdl-29953716

ABSTRACT

Stroke is a major cause of disability worldwide, and is the second leading cause of death after ischemic heart disease. Until recently, tissue-type plasminogen activator (t-PA) was the only treatment for acute ischemic stroke. If administered within 4.5 h of symptom onset, t-PA improves the outcome in stroke patients. Mechanical thrombectomy is now the preferred treatment for patients with acute ischemic stroke resulting from a large-artery occlusion in the anterior circulation. However, the widespread use of mechanical thrombectomy is limited by two factors. First, only ⁓ 10% of patients with acute ischemic stroke have a proximal large-artery occlusion in the anterior circulation and present early enough to undergo mechanical thrombectomy within 6 h; an additional 9-10% of patients presenting within the 6-24-h time window may also qualify for the procedure. Second, not all stroke centers have the resources or expertise to perform mechanical thrombectomy. Nonetheless, patients who present to hospitals where thrombectomy is not an option can receive intravenous t-PA, and those with qualifying anterior circulation strokes can then be transferred to tertiary stroke centers where thrombectomy is available. Therefore, despite the advances afforded by mechanical thrombectomy, there remains a need for treatments that improve the efficacy and safety of thrombolytic therapy. In this review, we discuss: (i) current treatment options for acute ischemic stroke; (ii) the mechanism of action of fibrinolytic agents; and (iii) potential strategies to manipulate the fibrinolytic system to promote endogenous fibrinolysis or to enhance the efficacy of fibrinolytic therapy.


Subject(s)
Brain Ischemia/drug therapy , Fibrinolysis/drug effects , Fibrinolytic Agents/administration & dosage , Stroke/drug therapy , Thrombolytic Therapy , Brain Ischemia/blood , Brain Ischemia/diagnosis , Fibrinolytic Agents/adverse effects , Humans , Infusions, Intravenous , Stroke/blood , Stroke/diagnosis , Thrombectomy , Thrombolytic Therapy/adverse effects , Time-to-Treatment , Treatment Outcome
3.
J Thromb Haemost ; 14(2): 366-74, 2016 Feb.
Article in English | MEDLINE | ID: mdl-26663133

ABSTRACT

UNLABELLED: ESSENTIALS: It is unknown if thrombin activatable fibrinolysis inhibitor (TAFI) and protein C compete on cells. TAFI and protein C activation on endothelial cells was simultaneously quantified. TAFI and protein C do not compete for activation on endothelial cells. TAFI and protein C are independently recognized by the thrombin-thrombomodulin complex. BACKGROUND: When bound to thrombomodulin (TM), thrombin is a potent activator of protein C (PC) and thrombin activable fibrinolysis inhibitor (TAFI). By binding PC and presenting it to the thrombin-TM complex, endothelial cell PC receptor (EPCR) enhances PC activation. It is unknown whether PC and TAFI compete for the thrombin-TM complex on endothelial cells. OBJECTIVE: To compare PC and TAFI activation on the surface of cultured human endothelial cells in the absence or presence of JRK1535 and/or CTM1009, inhibitory antibodies directed against EPCR and TM, respectively, and to determine whether PC and TAFI compete with each other for activation. METHODS: PC and TAFI activation on endothelial cells were compared, and the effect of PC on TAFI activation and TAFI on PC activation was determined in the absence or presence of JRK1535 and/or CTM1009. RESULTS: In the absence of antibodies, activation of PC was four-fold faster than that of TAFI. Blocking EPCR with JRK1535 resulted in a 53-fold decrease in PC activation and no effect on TAFI activation. Blocking TM with CTM1009 inhibited both TAFI and PC activation. Neither TAFI nor PC competed with each other in the absence or presence of JRK1535. CONCLUSIONS: PC and TAFI are concurrently activated in a TM-dependent manner and do not compete for the thrombin-TM complex, raising the possibility that they interact with distinct activation complexes. EPCR selectively enhances PC activation so that PC and TAFI activation kinetics become comparable on endothelial cells.


Subject(s)
Antigens, CD/metabolism , Carboxypeptidase B2/metabolism , Endothelial Cells/enzymology , Protein C/metabolism , Receptors, Cell Surface/metabolism , Binding, Competitive , Cells, Cultured , Endothelial Protein C Receptor , Enzyme Activation , Human Umbilical Vein Endothelial Cells/enzymology , Humans , Kinetics , Protein Binding , Thrombin/metabolism , Thrombomodulin/metabolism
5.
Thromb Haemost ; 112(2): 412-8, 2014 Aug.
Article in English | MEDLINE | ID: mdl-24696126

ABSTRACT

Haemostatic impairments are studied in vivo using one of several murine bleeding models. However it is not known whether these models are equally appropriate for assessing coagulation or platelet function defects. It was our study objective to assess the performance of arterial, venous and combined arterial and venous murine bleeding models towards impaired coagulation or platelet function. Unfractionated heparin (UFH) or αIIbß3inhibitory antibody (Leo.H4) were administered to mice, and their effects on bleeding in saphenous vein, artery, and tail tip transection models were quantified and correlated with their effects on plasma clotting and ADP-induced platelet aggregation, respectively. All models exhibited similar sensitivity with UFH (EC50 dose = 0.19, 0.13 and 0.07 U/g, respectively) (95% CI = 0.14 - 0.27, 0.08 - 0.20, and 0.03 - 0.16 U/g, respectively). Maximal inhibition of ex vivo plasma clotting could be achieved with UFH doses as low as 0.03 U/g. In contrast, the saphenous vein bleeding model was less sensitive to αIIbß3 inhibition (EC50 = 6.9 µg/ml) than tail transection or saphenous artery bleeding models (EC50 = 0.12 and 0.37 µg/ml, respectively) (95% CI = 2.4 - 20, 0.05 - 0.33, and 0.06 - 2.2 µg/ml, respectively). The EC50 of Leo.H4 for ADP-induced platelet aggregation in vitro (8.0 µg/ml) was at least 20-fold higher than that of the tail and arterial, but not the venous bleeding model. In conclusion, venous, arterial and tail bleeding models are similarly affected by impaired coagulation, while platelet function defects have a greater influence in models incorporating arterial injury.


Subject(s)
Blood Coagulation , Blood Platelets/metabolism , Hemorrhage/blood , Platelet Aggregation , Tail/blood supply , Adenosine Diphosphate , Animals , Antibodies/pharmacology , Anticoagulants/pharmacology , Arteries/surgery , Blood Coagulation/drug effects , Blood Coagulation Tests , Blood Platelets/drug effects , Disease Models, Animal , Dose-Response Relationship, Drug , Hemorrhage/drug therapy , Hemorrhage/etiology , Heparin/pharmacology , Male , Mice, Inbred C57BL , Platelet Aggregation/drug effects , Platelet Aggregation Inhibitors/pharmacology , Platelet Function Tests , Platelet Glycoprotein GPIIb-IIIa Complex/antagonists & inhibitors , Platelet Glycoprotein GPIIb-IIIa Complex/immunology , Platelet Glycoprotein GPIIb-IIIa Complex/metabolism , Saphenous Vein/surgery
6.
J Thromb Haemost ; 11 Suppl 1: 306-15, 2013 Jun.
Article in English | MEDLINE | ID: mdl-23809134

ABSTRACT

Fibrinolysis is initiated when the zymogen plasminogen is converted to plasmin via the action of plasminogen activators. Proteolytic cleavage of fibrin by plasmin generates C-terminal lysine residues capable of binding both plasminogen and the plasminogen activator, thereby stimulating plasminogen activator-mediated plasminogen activation and propagating fibrinolysis. This positive feedback mechanism is regulated by activated thrombin activatable fibrinolysis inhibitor (TAFIa), which cleaves C-terminal lysine residues from the fibrin surface, thereby decreasing its cofactor activity. TAFI can be activated by thrombin alone, but the rate of activation is accelerated when in complex with thrombomodulin. Plasmin is also known to activate TAFI. TAFIa has no known physiologic inhibitors and consequently, its primary regulatory mechanism involves its intrinsic thermal instability. The rate of TAFI activation and stability of the active form, TAFIa, function in maintaining its concentration above the threshold value required to down-regulate fibrinolysis. Although all methods to quantify TAFI or TAFIa have their limitations, epidemiologic studies have indicated that elevated TAFI levels are correlated with an increased risk of venous thrombosis. Major efforts have been made to develop TAFI inhibitors that can either directly interfere with TAFIa activity or impair its activation. However, the anti-inflammatory properties of TAFIa might complicate the development and application of a TAFIa inhibitor that aims to increase the efficiency of thrombolytic therapy.


Subject(s)
Carboxypeptidase B2/physiology , Fibrinolysis , Humans
7.
Neurol Res ; 34(5): 447-54, 2012 Jun.
Article in English | MEDLINE | ID: mdl-22450252

ABSTRACT

OBJECTIVE: In addition to the mood-stabilizing effects of lithium in patients with bipolar disorder, recent in vitro and in vivo studies in rodents increasingly implicate that lithium may be useful for treating acute cerebral ischemia, neuroinflammatory conditions, and chronic neurodegenerative diseases. However, whether lithium has a protective effect against hemorrhagic stroke is yet unknown. To test this possibility, we attempted to determine lithium's effect on experimental intracerebral hemorrhage (ICH). METHODS: We treated adult rats with either lithium (2 mEq/kg) or saline for 3 days before inducing ICH via a stereotaxic infusion of collagenase into the left basal ganglia. Hematoma volumes, hemispheric swelling, long-term hemispheric atrophy, microglial activation, cell death, cyclooxygenase-2 expression, and behavioral outcomes were assessed. RESULTS: Per behavioral tests 2 days after ICH, the lithium-treated group recovered better than did the saline-treated group. Three days after ICH, the hematoma volumes did not differ between the groups, but hemispheric swelling was less in the lithium-treated group. Forty-two days after ICH, hemispheric atrophy was less in the lithium-treated group. Lithium reduced cell death, cyclooxygenase-2 expression, and reactive microglia in the perihematomal regions. CONCLUSION: The present study shows that lithium, via anti-inflammation, reduces the perihematomal cell death, which is associated with sensorimotor recovery after experimental ICH.


Subject(s)
Brain Injuries/etiology , Brain Injuries/prevention & control , Cerebral Hemorrhage/complications , Lithium/administration & dosage , Neuroprotective Agents/administration & dosage , Animals , Brain Edema/etiology , Brain Edema/prevention & control , Brain Injuries/pathology , Cell Death/drug effects , Cerebral Hemorrhage/chemically induced , Collagen Type IV/toxicity , Cyclooxygenase 2/metabolism , Disease Models, Animal , Hematoma/etiology , Hematoma/pathology , Male , Peroxidase/metabolism , Rats , Rats, Sprague-Dawley , Single-Blind Method
9.
J Thromb Haemost ; 5(6): 1250-6, 2007 Jun.
Article in English | MEDLINE | ID: mdl-17266698

ABSTRACT

BACKGROUND: Elevated plasma fibrinogen is a well known risk factor for cardiovascular disease. The mechanistic rationale for this is not known. OBJECTIVES: These studies were carried out to determine the fibrinogen concentration dependencies of clotting and lysis times and thereby determine whether these times rationalize the correlation between an increased risk of cardiovascular disease and elevated plasma fibrinogen. METHODS: The time courses of clot formation and lysis were measured by turbidity in systems comprising a) fibrinogen, thrombin and plasmin, or b) fibrinogen, thrombin, plasminogen and t-PA, or c) plasma, thrombin and t-PA. From the lysis times, k(cat) and K(m) values for plasmin action on fibrin were determined. RESULTS: The time to clot increased linearly from 2.9 to 5.6 minutes as the fibrinogen concentration increased from 1 to 9 microM and did not increase further as the fibrinogen concentration was raised to 20 microM. In contrast, the clot lysis time increased linearly over the input fibrinogen concentration range of 2 to 20 microM. A similar linear trend was found in the two systems with t-PA and plasminogen. Apparent K(m) and k(cat) values for plasmin were 1.1 +/- 0.6 microM and 28 +/- 2 min(-1), respectively. K(m) values for plasmin in experiments initiated with t-PA and plasminogen were 1.6 +/- 0.2 microM in the purified system and 2.1 +/- 0.9 microM in plasma. CONCLUSION: As the concentration of fibrinogen increases, especially above physiologic level, the balance between fibrinolysis and clotting shifts toward the latter, providing a rationale for the increased risk of cardiovascular disease associated with elevated fibrinogen.


Subject(s)
Blood Coagulation/physiology , Cardiovascular Diseases/blood , Cardiovascular Diseases/etiology , Fibrinogen/metabolism , Hemolysis/physiology , Blood Coagulation/drug effects , Fibrin/metabolism , Fibrinogen/chemistry , Hemolysis/drug effects , Humans , In Vitro Techniques , Kinetics , Models, Cardiovascular , Nephelometry and Turbidimetry , Peptide Fragments/chemistry , Peptide Fragments/metabolism , Plasminogen/metabolism , Plasminogen/pharmacology , Recombinant Proteins/metabolism , Recombinant Proteins/pharmacology , Tissue Plasminogen Activator/metabolism , Tissue Plasminogen Activator/pharmacology , alpha-2-Antiplasmin/metabolism , alpha-2-Antiplasmin/pharmacology
10.
Brain Res ; 888(1): 11-18, 2001 Jan 05.
Article in English | MEDLINE | ID: mdl-11146047

ABSTRACT

Free radical-induced oxidative damages of macromolecules and cell death are important factors in the pathogenesis of ischemia/reperfusion brain injury. In the present study, an investigation as to whether green tea extract reduces ischemia/reperfusion-induced brain injury in Mongolian gerbils was conducted. The effect of green tea on the ischemia/reperfusion-induced production of hydrogen peroxide, lipid peroxidation and oxidative DNA damage (formation of 8-hydroxydeoxyguanosine), and cell death in addition to locomotor activity was studied. Two doses (0.5 or 2%) of green tea extract were added into the drinking water and to be accessed by animals ad libitum for 3 weeks prior to the induction of ischemia. A global ischemia was induced by the bilateral occlusion of the common carotid arteries for 5 min. Reperfusion was achieved by releasing the occlusion and restoring blood circulation for 48 h. The infarction volumes were 112+/-31 mm(3) and 76+/-11 mm(3) in the 0.5 and 2% green tea pretreated animals compared to 189+/-12 mm(3) in the ischemia/reperfusion animals. Green tea extract also reduced the levels of ischemia/reperfusion-induced hydrogen peroxide (from 1470+/-170 to 1034+/-46 and 555+/-30 nmole/mg protein), lipid peroxidation products (from 1410+/-210 to 930+/-40 and 330+/-20 nmole/mg protein) and 8-oxodG (from 3.9+/-0.1 to 2.8+/-0.3 and1.9+/-0.3 ng/microg DNA, x10(-2)) by pretreatment of 0.5 or 2% green tea for 3 weeks, respectively. Moreover, green tea also reduced the number of ischemia/reperfusion-induced apoptotic cells (from 59+/-12 to 37+/-8, 15+/-11 apoptotic cells/high power field in the striatum region) and locomotor activity (from 15140+/-2940 to 3900+/-600 and 4100+/-1200). This study therefore suggests that green tea may be a useful agent for the prevention of cerebral ischemia damage.


Subject(s)
Beverages , Brain/metabolism , Deoxyguanosine/analogs & derivatives , Ischemic Attack, Transient/drug therapy , Plant Extracts/pharmacology , Reperfusion Injury/drug therapy , 8-Hydroxy-2'-Deoxyguanosine , Aldehydes/metabolism , Animals , Apoptosis/drug effects , Brain/blood supply , Brain/cytology , Brain Infarction/drug therapy , Cerebrovascular Circulation/drug effects , Cysteine Proteinase Inhibitors/metabolism , DNA/metabolism , Deoxyguanosine/metabolism , Female , Gerbillinae , Hydrogen Peroxide/metabolism , Lipid Peroxidation/drug effects , Malondialdehyde/metabolism , Motor Activity/drug effects , Neurons/cytology , Neurons/metabolism , Oxidative Stress/drug effects
11.
Arch Pharm Res ; 23(4): 413-7, 2000 Aug.
Article in English | MEDLINE | ID: mdl-10976593

ABSTRACT

The effect of ischemia/reperfusion-induced neuronal damage on the memory impairment were investigated using active avoidance and Morris water maze tasks in Wistar rats. Focal ischemia was induced by 1 h occlusion of the right middle cerebral artery (MCA) of Wistar male rats. Reperfusion was induced by releasing the occlusion and restoring the blood circulation for 24 h. The acquisition and preservation memory tested by active avoidance showed a significant difference between the sham and ischemia/reperfusion group. The water maze acquisition performance was also significant difference between sham and ischemia/reperfusion groups in both latency and moving distance. The infarction volume was increased by the ischemia/reperfusion. Furthermore, the cresyl violet staining of the ischemia/reperfusion brain showed severe neuronal damage (pyramidal cell loss) in the cortex in addition to the striatum lesion of brain. This study shows that pyramidal cell damage in the cortex lesion may be partially related to memorial disturbance in the ischemia/reperfusion brain injury.


Subject(s)
Brain Ischemia/complications , Cerebral Cortex/pathology , Memory Disorders/etiology , Animals , Avoidance Learning , Corpus Striatum/pathology , Male , Maze Learning , Rats , Rats, Wistar , Reaction Time , Reperfusion
12.
Toxicol In Vitro ; 14(4): 345-9, 2000 Aug.
Article in English | MEDLINE | ID: mdl-10906441

ABSTRACT

Cultured human skin cells are a potentially useful model for skin irritancy testing. We have investigated the use of human skin fibroblasts for in vitro screening for skin toxicity. To assess the cytotoxic effects of surfactants, cell viability was measured by the NRU (neutral red uptake) assay and AB (Alamar blue) assay as in vitro methods. The skin irritation potential of surfactants by human skin patch test was assessed as in vivo methods. The close relationship was found between AB assay with human skin fibroblasts and human patch test (r=0.867). There was a relatively good agreement between the NRU and in vivo patch test (r=0.648). These results suggest that AB and NRU assay using cultured human fibroblast could be predictable methods for the irritancy of various surfactants in human.


Subject(s)
Animal Testing Alternatives , Irritants/toxicity , Skin/drug effects , Surface-Active Agents/toxicity , Adult , Cell Survival/drug effects , Cells, Cultured , Fibroblasts/cytology , Fibroblasts/drug effects , Fibroblasts/metabolism , Humans , Infant, Newborn , Irritants/classification , Neutral Red/metabolism , Patch Tests , Predictive Value of Tests , Reproducibility of Results , Skin/cytology , Skin/metabolism , Toxicity Tests
13.
Ann Thorac Surg ; 69(4): 1276-7, 2000 Apr.
Article in English | MEDLINE | ID: mdl-10800844

ABSTRACT

The number of off-pump coronary artery bypass grafting procedures without cardiopulmonary bypass is steadily increasing. We report on a new, minimally invasive surgical approach for off-pump coronary revascularization in multivessel disease. A distal sternotomy is performed to gain access to the left and right internal thoracic arteries and to reach the left anterior descending coronary artery, diagonal branches, and right coronary artery for off-pump revascularization.


Subject(s)
Coronary Artery Bypass/methods , Humans , Minimally Invasive Surgical Procedures , Sternum/surgery
14.
Brain Res Bull ; 53(6): 743-9, 2000 Dec.
Article in English | MEDLINE | ID: mdl-11179838

ABSTRACT

Eicosanoids accumulation and formation of oxygen free radicals have been implicated in the pathogenesis of ischemia/reperfusion brain injury. In the present study, we examined whether green tea extract protects against ischemia/reperfusion-induced brain injury by minimizing eicosanoid accumulation and oxygen radical-induced oxidative damage in the brain. Green tea extract (0.5%) was orally administered to Wistar rats for 3 weeks before induction of ischemia. Ischemia was induced by the occlusion of middle cerebral arteries for 60 min and reperfusion was achieved for 24 h. Infarction volume in the ipsilateral hemisphere of ischemia/reperfusion animals was 114 +/- 16 mm(3) in the 0.5% green tea pretreated animals compared to 180 +/- 54 mm(3) in left hemisphere of nontreated animals. Green tea extract (0.5%) also reduced ischemia/reperfusion-induced eicosanoid concentration: Leukotriene C(4) (from 245 +/- 51 to186 +/- 22), prostoglandin E(2) (from 306 +/- 71 to 212 +/- 43) and thromboxane A(2) (327 +/- 69 to 251 +/- 87 ng/mg protein). Ischemia/reperfusion-induced increases of hydrogen peroxide level (from 688 +/- 76 to 501 +/- 99 nmole/mg protein), lipid peroxidation products (from 1010 +/- 110 to 820 +/- 70 nmole/mg protein) and 8-oxodG formation (from 1.3 +/- 0.3 to 0.8 +/- 0.2 ng/microg DNA, x10(-2)) were also reduced. Moreover, 0.5% green tea extract also reduced the apoptotic cell number (from 44 +/- 11 to 29 +/- 1 in the striatum, and from 72 +/- 11 to 42 +/- 5 apoptotic cells/high power field in the cortex region). Green tea extract pretreatment also promoted recovery from the ischemia/reperfusion-induced inhibition of active avoidance. The present study shows that the minimizing effect of green tea extract on the eicosanoid accumulation and oxidative damage in addition to the reduction of neuronal cell death could eventually result in protective effect on the ischemia/reperfusion-induced brain injury and behavior deficit.


Subject(s)
Brain Ischemia/drug therapy , Brain/drug effects , Deoxyguanosine/analogs & derivatives , Neuroprotective Agents/pharmacology , Plant Extracts/pharmacology , Reperfusion Injury/drug therapy , Tea/chemistry , 8-Hydroxy-2'-Deoxyguanosine , Animals , Antioxidants/pharmacology , Apoptosis/drug effects , Apoptosis/physiology , Avoidance Learning/drug effects , Avoidance Learning/physiology , Brain/metabolism , Brain/physiopathology , Brain Infarction/drug therapy , Brain Infarction/physiopathology , Brain Ischemia/metabolism , Brain Ischemia/physiopathology , Deoxyguanosine/metabolism , Eicosanoids/metabolism , Hydrogen Peroxide/metabolism , Lipid Peroxidation/drug effects , Lipid Peroxidation/physiology , Neurons/drug effects , Neurons/physiology , Rats , Rats, Wistar , Reperfusion Injury/metabolism , Reperfusion Injury/physiopathology
15.
Int J Radiat Oncol Biol Phys ; 45(4): 835-40, 1999 Nov 01.
Article in English | MEDLINE | ID: mdl-10571186

ABSTRACT

PURPOSE: To determine if there is a racial difference in prostate cancer related to loss of heterozygosity (LOH) on chromosome 8p12-23, the region most frequently altered in prostate cancer. METHODS AND MATERIALS: A total of 51 prostate cancer patients, consisting of 23 African Americans and 28 Caucasians, were included in this study. All patients underwent radical prostatectomy, and patients in the two racial subgroups were matched for median serum PSA, Gleason score, and pathological stage of cancer. Paired normal prostate and cancer tissue DNA was isolated and amplified with 13 polymorphic markers mapped to 8p12-23 by radiolabeled polymerase chain reaction. The amplified products were resolved by polyacrylamide gel electrophoresis, autoradiographed, and analyzed for allelic losses. RESULTS: The overall incidence of LOH at 8p12-23 was 53%, and 16% showed homozygous deletions. The incidence of LOH in Caucasians was 68% compared to 35% in African Americans. On univariate (p = 0.02) and multivariate logistic regression analysis (p = 0.02), only Caucasian race was a significant predictor for LOH. The other clinicopathologic parameters did not have any significant effect on incidence of LOH. CONCLUSION: These results highlight the independent influence of Caucasian race on incidence of LOH at 8p12-23, and suggest that genetic differences at specific tumor suppressor loci may be a factor responsible for racial variations observed in prostate cancer.


Subject(s)
Black People/genetics , Chromosomes, Human, Pair 8/genetics , Loss of Heterozygosity , Prostatic Neoplasms/genetics , White People/genetics , Aged , Analysis of Variance , Genetic Markers , Humans , Male , Middle Aged , Prostate-Specific Antigen/blood , Prostatic Neoplasms/blood
16.
Ann Thorac Surg ; 68(2): 470-2, 1999 Aug.
Article in English | MEDLINE | ID: mdl-10475414

ABSTRACT

BACKGROUND: Coronary revascularization in patients with pectus excavatum is technically difficult through a median sternotomy secondary to the posterior displacement of the sternum and the asymmetric angulation that it produces. The role of minimally invasive coronary artery bypass grafting (MIDCABG) in this subset of patients was evaluated. METHODS: In 1998, four patients with pectus excavatum underwent revascularization of the left anterior descending artery without cardiopulmonary bypass through a left anterior minithoracotomy. RESULTS: All patients underwent the procedure without intraoperative complications and postoperative angiography demonstrated adequate graft patency. CONCLUSIONS: The advantages of MIDCABG in patients with pectus excavatum is the superior exposure to the LAD and LIMA and avoidance of a median sternotomy and cardiopulmonary bypass. This procedure is deemed safe and effective in patients with such deformities of the chest wall.


Subject(s)
Coronary Disease/surgery , Funnel Chest/surgery , Minimally Invasive Surgical Procedures , Myocardial Revascularization , Cardiopulmonary Bypass , Coronary Disease/diagnostic imaging , Funnel Chest/diagnostic imaging , Humans , Internal Mammary-Coronary Artery Anastomosis , Male , Middle Aged , Thoracotomy , Tomography, X-Ray Computed
17.
Ann Thorac Surg ; 67(6): 1648-52, 1999 Jun.
Article in English | MEDLINE | ID: mdl-10391269

ABSTRACT

BACKGROUND: To improve the acceptance of cosmetic results after closure of atrial septal defects, anterior or lateral thoracotomies are preferred rather than median sternotomies. Along with the availability of minimally invasive techniques, a further reduction in incision length appeared feasible while preserving thoracic stability. METHODS: Various minimally invasive approaches differing in the type of incision and mode of cannulation have been applied under conditions of normothermic ventricular fibrillation. In technique 1 (n = 5), a right parasternal mini-incision was combined with a central aortic and bicaval cannulation. Technique 2 (n = 2) was composed of an anterior submammary mini-incision with femoral arterial and central bicaval cannulation. To optimize the surgical access, the transincisional cannulation of the superior vena cava was replaced by a percutaneous cervical cannulation (technique 3, n = 17). RESULTS: Effective atrial septal defect closure assessed by intraoperative echocardiography was achieved in all patients. Central neurologic complications were completely absent. Besides temporary atrial fibrillation in one case, no other cardiac complications occurred. There were no cases with complicated wound healing. CONCLUSIONS: Along with modified cannulation techniques and intraoperative echocardiography, minimally invasive techniques can be safely applied for atrial septal defect closure. Submammary incisions were highly accepted and allowed for adequate surgical exposure.


Subject(s)
Heart Septal Defects, Atrial/surgery , Adolescent , Adult , Cardiac Surgical Procedures/methods , Catheterization , Catheterization, Central Venous , Female , Femoral Artery , Humans , Male , Middle Aged , Minimally Invasive Surgical Procedures , Sternum/surgery , Thoracotomy/methods
19.
Gynecol Oncol ; 69(3): 243-7, 1998 Jun.
Article in English | MEDLINE | ID: mdl-9648595

ABSTRACT

Cervical carcinoma frequently metastasizes to the paraaortic region, necessitating extended field radiotherapy to effect a cure. As imaging modalities are unreliable in identifying all cases of paraaortic nodal metastases (PAN), surgical staging is often utilized prior to radiotherapy. This study was aimed at identifying factors predictive of survival in women with cervical carcinoma and paraaortic metastases. In particular, survival based on extent of paraaortic disease was examined. The study group consisted of 43 women (stages IB-IVB) identified between 1982 and 1993 who were treated with extended field radiation for cervical carcinoma with histologically confirmed paraaortic metastases. The estimated 5-year survival for the study population was 24% with a median survival of 18 months. Pelvic tumor size had a significant impact on survival with the median survival being 34 months if the primary lesion was < 6 cm compared to 14 months if > or = 6 cm (P = 0.01). Eight of the 26 (31%) women without residual PAN disease after surgical staging remain alive and disease free (mean follow-up, 74 months). In contrast, only 1 of the 17 (6%) women with gross residual PAN is alive 71 months after treatment (P = 0.05). However, a comparison of Kaplan-Meier survival curves did not show a statistically significant advantage to the surgical excision of grossly involved PAN (P = 0.98). Although long-term survival among women with grossly involved, unresected paraaortic metastases is uncommon, further study is necessary to elucidate the role of surgical excision of bulky aortic disease in women with cervical cancer.


Subject(s)
Carcinoma, Squamous Cell/secondary , Lymph Node Excision , Lymph Nodes/pathology , Uterine Cervical Neoplasms/pathology , Adenocarcinoma/secondary , Adenocarcinoma/surgery , Adult , Aged , Aged, 80 and over , Aorta , Carcinoma, Adenosquamous/secondary , Carcinoma, Adenosquamous/surgery , Carcinoma, Squamous Cell/surgery , Female , Humans , Lymphatic Metastasis , Middle Aged , Neoplasm Staging , Prognosis , Retrospective Studies , Survival Analysis , Uterine Cervical Neoplasms/surgery
20.
Ann Surg Oncol ; 5(3): 261-4, 1998.
Article in English | MEDLINE | ID: mdl-9607629

ABSTRACT

BACKGROUND: Carcinoid tumors of the breast have been described in the literature. The diagnosis is made by identification of typical histologic features and confirmed by a positive argyrophilic reaction or the presence of neurosecretory granules. There are several theories of the pathogenesis of carcinoid tumors in the breast and controversy as to whether these tumors actually originate in the breast ducts or are tumors that arise from neuroectodermal cells that have migrated to the breast ducts. Historically, treatment of carcinoid of the breast has been by mastectomy. METHODS: We report three cases of primary carcinoid tumor of the breast treated with lumpectomy and axillary node dissection. No adjuvant radiation or systemic treatment was administered. RESULTS: In all three cases, no metastases were identified in lymph nodes sampled and all patients have remained clinically free of recurrent disease. CONCLUSIONS: Decisions about the need for radiation or systemic treatment of breast carcinoid tumors depend on one's interpretation of the pathogenesis of this disease. Breast conservation is a surgical option that has not been previously reported. Larger series of carcinoid tumors of the breast, their treatment, and their follow-up are needed.


Subject(s)
Breast Neoplasms/pathology , Breast Neoplasms/surgery , Carcinoid Tumor/pathology , Carcinoid Tumor/surgery , Mastectomy, Segmental , Aged , Biopsy, Needle , Breast Neoplasms/etiology , Carcinoid Tumor/etiology , Female , Humans , Lymph Node Excision , Middle Aged , Neurosecretory Systems/pathology , Patient Selection , Silver Staining
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