|
| 1 |
TITLE: Leukocytes Can Enhance Platelet-mediated Aggregation and Thromboxane
Release via Interaction of P-selectin Glycoprotein Ligand 1 with
P-selectin.
AUTHORS: Faraday N; Scharpf RB; Dodd-O JM; Martinez EA
Rosenfeld BA; Dorman T
AUTHOR AFFILIATION:
Submitted for publication May 5, 2000.
PUBLICATION TYPES:
JOURNAL ARTICLE
LANGUAGES:
ENG
ABSTRACT:
BACKGROUND: Platelet-leukocyte conjugates have been observed in
patients with unstable coronary syndromes and after cardiopulmonary
bypass. In vitro, the binding of platelet P-selectin to leukocyte
P-selectin glycoprotein ligand-1 (PSGL1) mediates conjugate
formation; however, the hemostatic implications of these cell-cell
interactions are unknown. The aims of this study were to determine
the ability of leukocytes to modulate platelet agonist-induced
aggregation and secretion in the blood milieu, and to investigate the
role of P-selectin and PSGL-1 in mediating these responses. METHODS:
Blood was drawn from healthy volunteers for in vitro analysis of
platelet agonist-induced aggregation, secretion (adenosine
triphosphate, beta-thromboglobulin, and thromboxane), and
platelet-leukocyte conjugate formation. Experiments were performed on
live cells in whole blood or plasma to simulate physiologic
conditions. Whole-blood impedance and optical aggregometry, flow
cytometry, and enzyme-linked immunosorbent assays were performed in
the presence and absence of blocking antibodies to P-selectin and
PSGL1. The platelet-specific agonists, thrombin receptor activating
peptide and adenosine diphosphate, were used to elicit platelet
activation responses. RESULTS: Inhibition of platelet-leukocyte
adherence by P- selectin and PSGL1 antibodies decreased
agonist-induced aggregation in whole blood. The presence of
leukocytes in platelet-rich plasma increased aggregation, and this
increase was attenuated by P-selectin blocking antibodies. Data from
flow cytometry confirmed that platelet-leukocyte conjugate formation
contributed to aggregation responses. Blocking antibodies reduced
platelet agonist-induced thromboxane release but had no impact on
adenosine triphosphate and beta-thomboglobulin secretion.
CONCLUSIONS: Leukocytes can enhance platelet agonist- induced
aggregation and thromboxane release in whole blood and platelet-rich
plasma under shear conditions in vitro. Interaction of platelet
P-selectin with leukocyte PSGL1 contributes substantially to these
effects.
SOURCE: Anesthesiology 2001 Jan;94(1):145-151
|
| 2 |
TITLE: Tranexamic Acid Administration after Cardiac Surgery: A Prospective,
Randomized, Double-blind, Placebo-controlled Study.
AUTHORS: Casati V; Bellotti F; Gerli C; Franco A; Oppizzi M
Cossolini M; Calori G; Benussi S; Alfieri O; Torri G
AUTHOR AFFILIATION:
Submitted for publication December 1, 1999.
PUBLICATION TYPES:
JOURNAL ARTICLE
LANGUAGES:
ENG
ABSTRACT:
BACKGROUND: Many different doses and administration schemes have been
proposed for the use of the antifibrinolytic drug tranexamic acid
during cardiac surgery. This study evaluated the effects of the
treatment using tranexamic acid during the intraoperative period only
and compared the results with the effects of the treatment continued
into the postoperative period. METHODS: Patients undergoing elective
cardiac surgery with use of cardiopulmonary bypass (N = 510) were
treated intraoperatively with tranexamic acid and then were
randomized in a double-blind fashion to one of three postoperative
treatment groups: group A: 169 patients, infusion of saline for 12 h;
group B: 171 patients, infusion of tranexamic acid, 1 mg. kg-1. h-1
for 12 h; group C: 170 patients, infusion of tranexamic acid, 2 mg.
kg-1. h-1 for 12 h. Bleeding was considered to be a primary outcome
variable. Hematologic data, allogeneic transfusions, thrombotic
complications, intubation time, and intensive care unit and hospital
stay duration also were evaluated. RESULTS: No differences were found
among groups regarding postoperative bleeding and outcomes; however,
the group treated with 1 mg.kg-1.h-1 tranexamic acid required more
units of packed red blood cells because of a significantly lower
basal value of hematocrit, as shown by multivariate analysis.
CONCLUSIONS: Prolongation of treatment with tranexamic acid after
cardiac surgery is not advantageous with respect to intraoperative
administration alone in reducing bleeding and number of allogeneic
transfusions. Although the prevalence of postoperative complications
was similar among groups, there is an increased risk of procoagulant
response because of antifibrinolytic treatment. Therefore, the use of
tranexamic acid during the postoperative period should be limited to
patients with excessive bleeding as a result of primary fibrinolysis.
SOURCE: Anesthesiology 2001 Jan;94(1):8-14
|
| 3 |
TITLE: Similar neurobehavioral outcome after valve or coronary artery
operations despite differing carotid embolic counts.
AUTHORS: Neville MJ; Butterworth J; James RL; Hammon JW
Stump DA
AUTHOR AFFILIATION:
Departments of Anesthesiology and Cardiothoracic Surgery, Wake Forest
University School of Medicine, Winston-Salem, NC.
PUBLICATION TYPES:
JOURNAL ARTICLE
LANGUAGES:
ENG
ABSTRACT:
OBJECTIVES: The interrelationships among coronary and valvular
operations, microemboli, and neurobehavioral outcome are unclear. We
hypothesized that adult patients undergoing cardiac valve operations
would have more total emboli delivered to the brain than patients
undergoing coronary artery bypass grafting and that this would
associate with worse neurobehavioral outcomes. METHODS: One hundred
ninety-three patients undergoing coronary artery bypass grafting and
73 patients undergoing cardiac valve operations were compared.
Patients received neurologic, neuro-ophthalmologic, and 11
standardized neurobehavioral tests preoperatively and 5 to 7 days, 1
month, and 6 months postoperatively. Left common carotid Doppler
ultrasonographic embolus detection was performed intraoperatively.
Repeated measures and logistic regression analyses of outcome were
performed. RESULTS: Patients undergoing either coronary or valve
operations were well matched by age (61 +/- 10 and 59 +/- 12 years,
respectively), but a significantly greater fraction of patients
undergoing valve operations were female, diabetic, or had undergone
previous cardiac operations. Neurobehavioral scores of patients
undergoing either coronary artery bypass grafting or cardiac valve
operations did not differ significantly at any time. Total embolus
counts differed significantly: the median was 105 during coronary
artery bypass grafting and 479 during cardiac valve operations
(geometric means of 104 and 412, respectively; P =.0001).
Significantly more emboli were detected in the patients undergoing
cardiac valve operations after removal of the left ventricular vent
and after separation from cardiopulmonary bypass, but comparable
numbers of emboli were seen in the 2 groups before cardiopulmonary
bypass. In both groups decreased neurobehavioral performance was
apparent at 5 to 7 days, with improvement at 1 and 6 months.
Increasing numbers of carotid emboli significantly associated with
worse performance on the letter cancellation test. There were no
significant differences between patients undergoing valve and
coronary operations in neurobehavioral outcomes, strokes, transient
ischemic attacks, or deaths. CONCLUSIONS: The significantly greater
number of emboli in the group of patients undergoing cardiac valve
operations is likely the result of the entrainment of intracardiac
air. The greater numbers of emboli during cardiac valve operations do
not appear associated with a commensurately greater risk of adverse
neurologic or neurobehavioral outcome.
SOURCE: J Thorac Cardiovasc Surg 2001 Jan;121(1):125-136
|
| 4 |
TITLE: Low preoperative antithrombin activity causes reduced response to
heparin in adult but not in infant cardiac-surgical patients
AUTHORS: Dietrich W; Braun S; Spannagl M; Richter JA
AUTHOR AFFILIATION:
Department of Anesthesiology and Institute of Clinical Chemistry,
German Heart Center, Munich, Germany, and the Department of
Hematology, University Clinic, Munich, Germany.
LANGUAGES:
Eng
ABSTRACT:
We evaluated the interaction of preoperative antithrombin (AT)
activity and intraoperative response to heparin in cardiac surgery.
Heparin anticoagulation is essential during cardiopulmonary bypass
(CPB). Heparin itself has no anticoagulant properties, however it
causes a conformational change of the physiologic plasma inhibitor AT
that converts this slow-acting serine protease inhibitor into a fast
acting one. Thus, adequate AT activity is a prerequisite for
sufficient heparin anticoagulation. AT activity is reduced by
long-term heparin therapy. This prospective, observational study
investigated 1516 consecutive cardiac-surgical patients (1304
patients >1 yr (Group A) and 212 patients </=1 yr (Group I)).
AT activity was measured the day before surgery by a chromogenic
substrate assay. The celite-activated activated clotting time (ACT)
was used to guide intraoperative heparin administration. Heparin
sensitivity was calculated and the postoperative blood loss and
perioperative blood requirement was recorded. Infant patients had
significantly less preoperative AT activity compared with older
patients: 84 (33)% vs 97 (17)%, median (interquartile range) (P: <
0. 05). The subgroup of patients aged <1 mo (n = 64) demonstrated
a preoperative AT activity of 56 (27)% as compared with 90 (23)% in
infant patients between one month and one year (n = 148). In adult
patients, preoperative AT activity depended predominantly on
preoperative heparin treatment: 62% of the patients with an AT
activity <80% were pretreated with heparin. Five minutes after
heparin but before CPB the ACT was 587 (334) s in Group A patients
with AT activity >/=80%, and 516 (232) in patients with AT
activity </=80% (P: < 0.05). The target ACT of 480 s was
achieved in 70% of patients with normal AT activity in Group A
compared with only 54% of patients with AT activity <80% (P: <
0.05). In Group A patients with decreased AT activity, 18%
demonstrated an inadequate ACT response-defined as ACT <400 s-to
the first bolus injection of heparin. In Group I, preoperative AT
activity did not influence the ACT response (ACT 5 min after heparin:
846 [447] s in patients with AT activity >/= 80% vs 1000 [364] s
in patients with decreased AT activity). The heparin sensitivity was
2.4 (1.1) s/unit heparin/kg compared with 1.5 (0.8) s/unit heparin/KG
in group A (P: < 0.05). These results suggest that preoperative
diminished AT activity causes reduced response to heparin in adult
but not in infant patients. Infant patients demonstrate a higher
heparin sensitivity despite lower preoperative AT activity.
Measurement of preoperative AT activity identifies adult patients at
risk of reduced sensitivity to heparin. Implications: In patients
less than one year of age, low antithrombin (AT) activity is caused
by the immature coagulation system. Despite low AT activity, these
young patients demonstrate a normal or increased response to heparin
anticoagulation before cardiopulmonary bypass (CPB). In contrast, in
patients older than one year of age and adult patients decreased
preoperative AT activity is mainly caused by preoperative heparin
therapy and causes insufficient response to heparin anticoagulation
with a standard heparin dosage. Measurement of preoperative AT
activity identifies patients at risk of inadequate anticoagulation
during CPB.
SOURCE: Anesth Analg 2001 Jan;92(1):66-71
|
| 5 |
TITLE: Jejunal mucosal perfusion is well maintained during mild hypothermic
cardiopulmonary bypass in humans
AUTHORS: Thoren A; Elam M; Ricksten SE
AUTHOR AFFILIATION:
Departments of Cardiothoracic Anesthesia and Intensive Care and
Clinical Neurophysiology, Sahlgrenska University Hospital, Goteborg,
Sweden.
LANGUAGES:
Eng
ABSTRACT:
In the present study, the effects of mild hypothermic (34 degrees C)
cardiopulmonary bypass (CPB) on jejunal mucosal perfusion (JMP),
gastric tonometry, splanchnic lactate, and oxygen extraction were
studied in low-risk cardiac surgical patients (n = 10), anesthetized
and managed according to clinical routine. JMP was assessed by
endoluminal laser Doppler flowmetry. Patients were studied during
seven 10-min measurement periods before, during, and 1 h after the
end of CPB. Splanchnic oxygen extraction increased during hypothermia
and particularly during rewarming and warm CPB. JMP increased during
hypothermia (26%), rewarming (31%), and warm CPB (38%) and was higher
1 h after CPB (42%), compared with pre-CPB control. The
gastric-arterial PCO(2) difference was slightly increased (range
0.04-2.26 kPa) during rewarming and warm CPB as well as 1 h after
CPB, indicating a mismatch between gastric mucosal oxygen delivery
and demand. None of the patients produced lactate during CPB. We
conclude that jejunal mucosal perfusion appears well preserved during
CPB and moderate (34 degrees C) hypothermia; this finding is in
contrast to previous studies showing gastric mucosal hypoperfusion
during CPB. Implications: Jejunal mucosal perfusion increases during
mild hypothermic cardiopulmonary bypass (CPB). Intestinal laser
Doppler flowmetry, gastric tonometry, and measurements of splanchnic
lactate extraction could not reveal a local or global splanchnic
ischemia during or after CPB. A mismatch between splanchnic oxygen
delivery and demand was seen, particularly during rewarming and warm
CPB.
SOURCE: Anesth Analg 2001 Jan;92(1):5-11
|
| 6 |
TITLE: Gene therapy with vascular endothelial growth factor for inoperable
coronary artery disease: anesthetic management and results
AUTHORS: Lathi KG; Vale PR; Losordo DW; Cespedes RM; Symes JF
Esakof DD; Maysky M; Isner JM
AUTHOR AFFILIATION:
Departments of Anesthesiology, Surgery, and Medicine, St. Elizabeth's
Medical Center and Tufts University School of Medicine, Boston,
Massachusetts.
LANGUAGES:
Eng
ABSTRACT:
Gene transfer for therapeutic angiogenesis represents a novel
treatment for medically intractable angina in patients judged not
amenable to further conventional revascularization. We describe the
anesthetic management of 30 patients with class 3 or 4 angina,
enrolled in a Phase 1 clinical trial to assess the safety and
bioactivity of direct myocardial gene transfer of naked DNA-encoding
vascular endothelial growth factor (phVEGF(165)), as sole therapy for
refractory angina. The phVEGF(165) was injected directly into the
myocardium through a mini-thoracotomy. All patients had major
clinical predictors for adverse perioperative cardiac complications.
Fast-track anesthetic management with remifentanil and desflurane,
multimodal analgesia, and aggressive hemodynamic control with
nitroglycerin and esmolol were used. All patients tolerated
anesthesia and surgery without problems. No perioperative myocardial
infarction, hemodynamic instability, or ventricular failure occurred.
VEGF injections caused no clinically significant changes in
cardiovascular function. Mean hospital stay was 3.8 days. There was
one late death (5 months postoperative). Twenty-nine of 30 patients
experienced reduced angina (56.2 +/- 4.1 episodes/week preoperatively
versus 3.8 +/- 1.6 postoperatively, P: < 0.0001) and reduced
sublingual nitroglycerin consumption (60.1 +/- 4.4 tablets/week
preoperatively versus 2.9 +/- 1.1 postoperatively, P: < 0.0001).
Implications: Previously revascularized patients now judged
"inoperable," continue to present with chronic, recurrent
angina. Our study describes the anesthetic considerations and
management of such patients treated with a novel approach by using
gene therapy to stimulate angiogenesis and improve perfusion to
ischemic myocardium.
SOURCE: Anesth Analg 2001 Jan;92(1):19-25
|
| 7 |
TITLE: Coronary artery bypass grafting in patients with mild renal
insufficiency.
AUTHORS: Hayashida N; Chihara S; Tayama E; Takaseya T
Yokose S; Hiratsuka R; Enomoto N; Kawara T; Aoyagi S
AUTHOR AFFILIATION:
Department of Surgery, Kurume University, Fukuoka, Japan.
nobuhiko@med.kurume-u.ac.jp
PUBLICATION TYPES:
Journal Article
LANGUAGES:
eng
ABSTRACT:
It is well known that dialysis-dependent renal failure increases the
likelihood of a poor outcome following cardiac surgery. However, it
is not known whether non-dialysis-dependent mild renal insufficiency
also influences clinical outcome. Fifty-five patients with
non-dialysis-dependent renal insufficiency undergoing coronary artery
bypass grafting (CABG) (Renal group: serum creatinine level >1.5
mg/dl) were enrolled. These patients were then matched on prognostic
variables to 148 patients with normal renal function (Control group:
serum creatinine level <1.5 mg/dl). The early postoperative
clinical results showed that patients in the Renal group were more
likely to develop postoperative renal failure (18% vs 1%: p=0.0002)
and hemorrhage requiring re-exploration (11% vs 2%; p=0.01). Total
morbidity was significantly higher in the Renal group (40% vs 22%;
p=0.01). Multivariate analysis revealed that the Renal group was the
second most important predictor of morbidity (odds ratio (OR) =2.2)
behind left ventricular dysfunction (OR=2.9). The Renal group was
also the second most important predictor of postoperative renal
failure (OR=12.5). Therefore, non-dialysis-dependent mild renal
insufficiency also increases the risk of morbidity following CABG.
SOURCE: Jpn Circ J 2001 Jan;65(1):28-32
|
| 8 |
TITLE: Interaction between paracrine tumor necrosis factor-alpha and
paracrine angiotensin II during myocardial ischemia.
AUTHORS: Frolkis I; Gurevitch J; Yuhas Y; Iaina A; Wollman Y
Chernichovski T; Paz Y; Matsa M; Pevni D; Kramer A; Shapira I; Mohr R
AUTHOR AFFILIATION:
Department of Thoracic and Cardiovascular Surgery, Tel Aviv Medical
Center, Israel.
PUBLICATION TYPES:
Journal Article
LANGUAGES:
eng
ABSTRACT:
OBJECTIVES: The purpose of this study was to explore interactions
between paracrine angiotensin II (Ang-II) and tumor necrosis
factor-alpha (TNF-alpha) during myocardial ischemia. BACKGROUND:
Ischemic myocardium releases significant amounts of TNF-alpha. This
paracrine release correlated with postischemic myocardial injury.
Other studies showed myocardial protection obtained by the use of
angiotensin-converting enzyme inhibitors (i.e., captopril) and the
Ang-II type 1 receptor antagonist losartan after ischemia. The
possibility that these agents decrease TNF-alpha synthesis has not
yet been investigated. METHODS: Using the modified Langendorff model,
isolated rat hearts underwent either 90 min of nonischemic perfusion
(control group) or 1 h of global cardioplegic ischemia. In both
groups, either captopril (360 micromol/liter) or losartan (182.2
micromol/liter) was added before ischemia. The hearts were assayed
for messenger ribonucleic acid (mRNA) expression and effluent
TNF-alpha levels. In addition, cardiac myocytes were incubated in
cell culture with Ang-II. RESULTS: After ischemia, TNF-alpha mRNA
expression intensified from 0.63 +/- 0.06 (control group) to 0.92 +/-
0.12 (p < 0.03), and effluent TNF-alpha levels were 711 +/- 154
pg/ml. The TNF-alpha mRNA expression declined to 0.46 +/- 0.07 (p
< 0.01) and 0.65 +/- 0.08 (p < 0.02) in captopril- and
losartan-treated hearts, respectively. Effluent TNF-alpha was below
detectable levels. Concentrations of TNF-alpha in supernatants of
incubated cardiac myocytes treated with 10 and 50 nmol/liter of
Ang-II were 206.0 +/- 47.0 pg/ml and 810 +/- 130 pg/ml, respectively
(p < 0.004). When pretreated with 700 micromol/liter of losartan,
TNF-alpha was below detectable levels. CONCLUSIONS: This study
presents an original explanation for previously reported myocardial
protection after ischemia, obtained by the use of captopril and
losartan. These drugs reduce TNF-alpha synthesis, providing strong
evidence of active interactions between paracrine TNF-alpha and
Ang-II in the evolution of the ischemic cascade.
SOURCE: J Am Coll Cardiol 2001 Jan;37(1):316-22
|
| 9 |
TITLE: Protein kinase C isoform-dependent myocardial protection by ischemic
preconditioning and potassium cardioplegia.
AUTHORS: Lu K; Otani H; Yamamura T; Nakao Y; Hattori R
Ninomiya H; Osako M; Imamura H
AUTHOR AFFILIATION:
Department of Thoracic and Cardiovascular Surgery, Kansai Medical
University, Moriguchi City, Osaka, Japan.
PUBLICATION TYPES:
JOURNAL ARTICLE
LANGUAGES:
ENG
ABSTRACT:
OBJECTIVE: Ischemic preconditioning combined with potassium
cardioplegia does not always confer additive myocardial protection.
This study tested the hypothesis that the efficacy of ischemic
preconditioning under potassium cardioplegia is dependent on protein
kinase C isoform. METHODS: Isolated and crystalloid-perfused rat
hearts underwent 5 cycles of 1 minute of ischemia and 5 minutes of
reperfusion (low-grade ischemic preconditioning) or 3 cycles of 5
minutes of ischemia and 5 minutes of reperfusion (high-grade ischemic
preconditioning) or time-matched continuous perfusion. These hearts
received a further 5 minutes of infusion of normal buffer or
oxygenated potassium cardioplegic solution. The isoform nonselective
protein kinase C inhibitor chelerythrine (5 mumol/L) was administered
throughout the preischemic period. All hearts underwent 35 minutes of
normothermic global ischemia followed by 30 minutes of reperfusion.
Isovolumic left ventricular function and creatine kinase release were
measured as the end points of myocardial protection. Distribution of
protein kinase C alpha, delta, and epsilon in the cytosol and the
membrane fractions were analyzed by Western blotting and quantified
by a densitometric assay. RESULTS: Low-grade ischemic preconditioning
was almost as beneficial as potassium cardioplegia in improving
functional recovery; left ventricular developed pressure 30 minutes
after reperfusion was 70 +/- 15 mm Hg (P <.01) in low-grade
ischemic preconditioning and 77 +/- 14 mm Hg (P <.001) in
potassium cardioplegia compared with values found in unprotected
control hearts (39 +/- 12 mm Hg). Creatine kinase release during
reperfusion was also equally inhibited by low-grade ischemic
preconditioning (18.2 +/- 10.6 IU/g dry weight, P <.05) and
potassium cardioplegia (17.6 +/- 6.7 IU/g, P <.01) compared with
control values. However, low-grade ischemic preconditioning in
combination with potassium cardioplegia conferred no significant
additional myocardial protection; left ventricular developed pressure
was 80 +/- 17 mm Hg, and creatine kinase release was 14.8 +/- 11.0
IU/g. In contrast, high-grade ischemic preconditioning with potassium
cardioplegia conferred better myocardial protection than potassium
cardioplegia alone; left ventricular developed pressure was 121 +/-
16 mm Hg (P <.001), and creatine kinase release was 8.3 +/- 5.8
IU/g (P <.05). Chelerythrine itself had no significant effect on
functional recovery and creatine kinase release in the control
hearts, but it did inhibit the salutary effects not only of low-grade
and high-grade ischemic preconditioning but also those of potassium
cardioplegia. Low-grade ischemic preconditioning and potassium
cardioplegia enhanced translocation of protein kinase C alpha to the
membrane, whereas high-grade ischemic preconditioning also enhanced
translocation of protein kinase C delta and epsilon. Chelerythrine
inhibited translocation of all 3 protein kinase C isoforms.
CONCLUSIONS: These results suggest that myocardial protection by
low-grade ischemic preconditioning and potassium cardioplegia are
mediated through enhanced translocation of protein kinase C alpha to
the membrane. It is therefore suggested that activation of the novel
protein kinase C isoforms is necessary to potentiate myocardial
protection under potassium cardioplegia.
SOURCE: J Thorac Cardiovasc Surg 2001 Jan;121(1):137-148
|
| 10 |
TITLE: Tranexamic Acid Administration after Cardiac Surgery: A Prospective,
Randomized, Double-blind, Placebo-controlled Study.
AUTHORS: Casati V; Bellotti F; Gerli C; Franco A; Oppizzi M
Cossolini M; Calori G; Benussi S; Alfieri O; Torri G
AUTHOR AFFILIATION:
Submitted for publication December 1, 1999.
PUBLICATION TYPES:
JOURNAL ARTICLE
LANGUAGES:
ENG
ABSTRACT:
BACKGROUND: Many different doses and administration schemes have been
proposed for the use of the antifibrinolytic drug tranexamic acid
during cardiac surgery. This study evaluated the effects of the
treatment using tranexamic acid during the intraoperative period only
and compared the results with the effects of the treatment continued
into the postoperative period. METHODS: Patients undergoing elective
cardiac surgery with use of cardiopulmonary bypass (N = 510) were
treated intraoperatively with tranexamic acid and then were
randomized in a double-blind fashion to one of three postoperative
treatment groups: group A: 169 patients, infusion of saline for 12 h;
group B: 171 patients, infusion of tranexamic acid, 1 mg. kg-1. h-1
for 12 h; group C: 170 patients, infusion of tranexamic acid, 2 mg.
kg-1. h-1 for 12 h. Bleeding was considered to be a primary outcome
variable. Hematologic data, allogeneic transfusions, thrombotic
complications, intubation time, and intensive care unit and hospital
stay duration also were evaluated. RESULTS: No differences were found
among groups regarding postoperative bleeding and outcomes; however,
the group treated with 1 mg.kg-1.h-1 tranexamic acid required more
units of packed red blood cells because of a significantly lower
basal value of hematocrit, as shown by multivariate analysis.
CONCLUSIONS: Prolongation of treatment with tranexamic acid after
cardiac surgery is not advantageous with respect to intraoperative
administration alone in reducing bleeding and number of allogeneic
transfusions. Although the prevalence of postoperative complications
was similar among groups, there is an increased risk of procoagulant
response because of antifibrinolytic treatment. Therefore, the use of
tranexamic acid during the postoperative period should be limited to
patients with excessive bleeding as a result of primary fibrinolysis.
SOURCE: Anesthesiology 2001 Jan;94(1):8-14
|
International Page on Extracorporeal Technology
Perfusion Line ©