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At least 523 records · Page 29Linked to original sources
PubMed2004

Improved survival of surgery for acute type A aortic dissection: impact of noninvasive diagnosis and hemostatic surgical management.

OBJECTIVES: In the past decade, progress in cardiovascular technology has been incorporated into the surgical treatment of acute type A dissection resulting in remarkable improvement. Factors in this progress encompass rapid noninvasive diagnosis, intraoperative introduction of aprotinine, surgical glue, sealed grafts, and refined surgical technique. The objective of this study is to identify which factors contributed to the improvement of the surgical outcome of acute type A dissections. METHODS: Between January 1989 and February 2001, 78 consecutive patients had emergency surgeries for acute type A dissection. The initial 31 patients (group I) received preoperative angiography, when possible. Since 1996, the next 47 patients (group II) have received noninvasive rapid diagnosis with hemostatic surgical management. This included aggressive proximal resection and judicious use of gelatin resorcine formol glue and felt strips. Between the two groups, in-hospital mortality and morbidity, incidence of neurological complications, late survival and cardiovascular events were compared. Risk factors for in-hospital death were investigated with univariate and multivariate analysis. RESULTS: The in-hospital mortality was significantly improved in group II (4.3%) compared with group I (29.0%). Overall mortality was 14.1%. Multivariate analysis revealed preoperative limb ischemia and delayed timing of operation (> 3 hours after arrival) as independent risk factors for in-hospital death. Late survival at 5 years was 61.5+/-7.5%. Between the two groups there was no significant difference in late survival or cardiovascular events. CONCLUSIONS: Immediate surgical intervention, using rapid noninvasive diagnosis with hemostatic management, substantially improves the surgical outcome of acute aortic dissection.

Adult↗
PubMed1982

The injury-spasm (ischemia-induced hemostatic vasoconstrictive) and vascular autoregulatory hypothesis of ischemic disease. Resistance vessel-spasm hypothesis of ischemic disease.

THe injury-spasm concept assumes that severe myocardial ischemia secondary to stenotic coronary artery disease causes spasm of resistance vessels through ischemic tissue injury. In this communication the concept is developed further and is now extended to include other diseases. It is suggested that relative arterial insufficiency, as traditionally understood, is an invalid concept and that disorders usually attributed to it, including congestive heart failure and peripheral vascular disease, should be attributed to injury-spasm. Because a basic reaction to injury is to prevent bleeding, injury-spasm is identified as an exaggerated form of hemostatic vasoconstriction, and spasm is related to distorted vascular autoregulatory activities of resistance vessels. It is asserted that blood platelets probably are not involved int he initiation of ischemic attacks, and instead of a platelet thromboxane/vessel prostacyclin vasomotor balance of epicardial coronary arteries, the vasoconstrictive/vasodilative balance is centered in resistance vessels and is based on autoregulatory processes such as the hemostatic injury-spasm reaction and reactive hyperemia.

Animals↗
PubMed1993

Effects of nadolol on hemodynamic and hemostatic responses to potential mental and physical triggers of myocardial infarction in subjects with mild systemic hypertension.

Although beta-adrenergic blocking agents are known to reduce the risk of myocardial infarction, the mechanism of this protective effect is not well understood. The recent demonstration that beta blockers selectively blunt the increased morning risk of myocardial infarction suggests that these agents block the pathophysiologic consequences of stressors concentrated in the morning. We determined the effect of nadolol on the hemodynamic and hemostatic responses to mental stress and isometric exertion (handgrip), 2 potential triggers of infarction. The study was conducted in 15 subjects with mild systemic hypertension, using a placebo-controlled, double-blind, crossover design. Nadolol reduced systolic pressure and heart rate after mental stress. Poststress systolic pressure was 139 +/- 4 mm Hg during therapy with nadolol versus 161 +/- 4 mm Hg during placebo administration (p < 0.05). Heart rate increased to 61 +/- 2 during nadolol therapy versus 89 +/- 5 beats/min during placebo therapy (p < 0.05). The systolic pressure increase was similar during therapy with nadolol and placebo (29 +/- 2 vs 33 +/- 2 beats/min, p = NS); however, heart rate increase was less during nadolol therapy (4 +/- 1 vs 12 +/- 4 vs beats/min, p < 0.01). The responses to handgrip and their modification during nadolol therapy were similar to those observed after mental stress. Neither platelet aggregability nor fibrinolytic potential was altered by nadolol. Thus, nadolol modified hemodynamic indexes without altering the hemostatic indexes measured. This hemodynamic effect may contribute to the decrease in morning cardiovascular events by beta-adrenergic blockers and their well-documented cardioprotective effect.

Adult↗
PubMed1994

Hypercoagulable state under low-intensity warfarin anticoagulation assessed with hemostatic markers in cardiac disorders.

The hemostatic condition under low-intensity anticoagulation in cardiac disorders is not fully elucidated. The aim of this study was to ascertain whether hemostatic molecular markers are a useful assessment for anticoagulation to detect the hypercoagulable state. A hematologic study was performed in 75 outpatients, without thromboembolic episodes, treated with low-intensity anticoagulation (average international normalized ratio [INR] 1.72) because of potential cardiac sources of arterial emboli, and in 40 age-matched control subjects. The average level of thrombin-antithrombin III complex (TAT) was significantly lower in patients than in control subjects (p = 0.005), and the mean value of D-dimer was not statistically different between patients and control subjects. Although TAT correlated moderately with D-dimer (r = 0.45, p = 0.0001), INR did not correlate with TAT or D-dimer. Elevated TAT > 3.0 ng/ml and/or D-dimer S 150 ng/ml were observed in 15 patients (20.0%), whereas the remaining 60 patients (80.0%) had no obvious increase in the level of TAT or D-dimer at overall INR. Antithrombin III activity did not correlate significantly with INR, but protein C activity and free protein S antigen showed a significant negative relation to INR (r = 0.82, r = 0.62, respectively, p = 0.0001). Low-intensity anticoagulation was sufficient to reduce coagulation and subsequent fibrinolytic activation in cardiac disorders, but may not be sufficient in some patients with elevated TAT or D-dimer concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Antithrombin III↗
PubMed1989

Congenital antithrombin III deficiency: insights into the pathogenesis of the hypercoagulable state and its management using markers of hemostatic system activation.

Hereditary antithrombin III (ATIII) deficiency predisposes patients to venous thrombosis. The prothrombin fragment F1+2 radioimmunoassay demonstrates that many asymptomatic patients with this disorder not receiving antithrombotic therapy have elevated plasma factor Xa activity. The hemostatic system hyperactivity as measured by this assay could be specifically corrected by rising plasma ATIII levels of several persons into the normal range. This indicates that the prethrombotic state can be defined as an imbalance between the production and inhibition of factor Xa enzymatic activity. The effects of warfarin on factor Xa enzymatic activity in persons with congenital ATIII deficiency have also been evaluated. At equivalent intensities of oral anticoagulation, the mean plasma F1+2 level in patients with ATIII deficiency was significantly elevated as compared with anticoagulated persons without this inherited thrombotic disorder. It is concluded that the effect of warfarin on hemostatic system activation is modulated by the endogenous heparan sulfate-ATIII mechanism. This suggests that the F1+2 radioimmunoassay can be employed to improve the understanding of the hypercoagulable state associated with antithrombin III deficiency as well as to develop more effective treatment strategies to prevent thromboembolic events in patients with this disorder.

Antithrombin III Deficiency↗
PubMed1990

Interrelations between carbohydrates, lipids, and the hemostatic system in relation to the risk of thrombotic and cardiovascular disease.

Metabolic diseases, such as obesity, impaired glucose tolerance, type I and type II diabetes, hypercholesterolemia, and hypertriglyceridemia, are among the main risk factors for the development of atherothrombosis. Various abnormalities of the hemostatic system (platelet hyperaggregability, hypercoagulability, and hypofibrinolysis) have been described in all these situations. The individual effect of each of these disease on the hemostatic system is difficult to evaluate because these states are often associated in the same patient and the treatment of one can benefit the others. Therefore it may be queried if a common abnormality of these pathologic states might explain their impact on the cardiovascular system. We have been interested by hyperinsulinemia, which is observed in obesity, impaired glucose tolerance, type II diabetes, and hypertriglyceridemia, and we have shown a very strong correlation between plasma insulin, body mass index, triglyceride levels, and one of the main inhibitors of the fibrinolytic system, plasminogen activator inhibitor-1. Partial correlation analysis showed that only the correlation between insulin and plasminogen activator inhibitor-1 was independent. Therefore a high plasma insulin level could be responsible for elevated levels of plasminogen activator inhibitor-1, which by inducing an hypofibrinolysis, could play a role in the deposition of fibrin and the development of atherothrombosis. The description of some interrelations between metabolic diseases and hemostasis is satisfactory but does not exclude specific effects of these diseases on hemostasis, such as glycation of the coagulation and fibrinolytic factors in diabetes or toxic action of lipoprotein on endothelial cells in hyperlipoproteinemia.

Carbohydrate Metabolism, Inborn Errors↗
PubMed1982

Maintenance of ligature tension by a single operator with simultaneous removal of a hemostatic clamp.

Two new techniques that enable a single operator to maintain ligature tension while removing a hemostatic clamp are described. With the first technique a needle holder is used to grasp one tail of the ligature and maintain tension while the hemostatic clamp is removed with the opposite hand. The second technique loops one end of the ligature over the flexed index finger while fixing both tails with the remaining fingers. By extending the finger, tension is maintained.

Constriction↗
PubMed1992

Hemostatic abnormalities in total artificial heart patients as detected by specific blood markers.

We retrospectively evaluated the hemostatic system of 13 patients during implantation (2 to 35 days) of the Jarvik 7-70 total artificial heart (TAH). Although all patients were clinically manageable while on the TAH, 5 had excessive generalized bleeding. After the heart transplant procedure, 2 patients had neurological events and 1 patient, thrombosis of the leg. While the patients were supported by the TAH, the routine coagulation assays (prothrombin time, activated partial thromboplastin time, fibrinogen, factor assays, and platelet count) showed slight abnormalities but no correlation to hemorrhagic or thrombotic events. In contrast, plasma and cellular activation markers, which are highly sensitive and specific for hypercoagulability, fibrinolysis, or platelet activation, revealed activation in all patients. Most striking was the marked activation of the fibrinolytic system (p less than 0.05 to 0.001). Correlations of individual patient data compared with the average TAH group response could be made between excessive enhancement of fibrinolysis (increased D-dimer and tissue plasminogen activator and decreased plasminogen activator inhibitor) and bleeding. A hypercoagulable state (increased fibrinogen and thrombin-antithrombin complex and decreased antithrombin III and protein C), decreased fibrinolysis (decreased tissue plasminogen activator and D-dimer), activated platelets (increased thromboxane B2), or combinations of these were associated with thrombosis. The hemostatic activation returned to normal 1 day after removal of the TAH. These data suggest that the patient with a TAH requires more sophisticated laboratory monitoring and individualized treatment for excessive fibrinolysis, hypercoagulable state, or platelet activation to avoid thrombotic and hemorrhagic complications.

6-Ketoprostaglandin F1 alpha↗
PubMed1993

Hemostatic and metabolic effects of lowering the ethinyl-estradiol dose from 30 mcg to 20 mcg in oral contraceptives containing desogestrel.

The metabolic and hemostatic effects of two oral contraceptives containing 150 mcg desogestrel and 20 mcg ethinyl-estradiol (EE) (MERCILON) or 30 mcg EE (MARVELON) were compared in order to examine the effect of reducing the EE dose in contraceptive pills. Forty-nine women participated in this randomized study during 6 cycles. In both groups, there was a significant increase in triglycerides, HDL-cholesterol and apoprotein A1; the same increase was observed for SBP and CBG. Slight and transient variations of fasting blood glucose levels were seen in the 30 mcg EE group and in the two groups for fasting insulin levels. The increase in renin substrate was significantly higher with the 30 mcg EE than with the 20 mcg EE pill. In both groups, plasminogen increased significantly, but antithrombin III, total and free protein S and fibrinogen decreased significantly only in women taking the 30 mcg EE pill, whereas there was no significant change in the 20 mcg EE group. Reducing the dose of EE in oral contraceptives from 30 mcg to 20 mcg minimizes their impact on renin substrate and hemostatic parameters.

Apolipoprotein A-I↗
PubMed1993

Hemostatic variables in patients with intrauterine fetal death.

OBJECTIVE: To assess the occurrence of hemostatic disturbances in patients with intrauterine fetal death (IFD). METHOD: The occurrence of abnormal results of hemostatic variables and of bleeding complications was noted from the medical records of 41 patients with IFD, 6 of whom had a multiple pregnancy. RESULT: Apart from the increased platelet count, results of blood coagulation tests in all except one patient with IFD did not differ from normal values. This patient, who had a twin pregnancy with one dead fetus, had an increase in fibrin degradation products and fibrin monomers 4 weeks after IFD and fibrinogenopenia and thrombocytopenia 2 weeks later. CONCLUSION: The deterioration of systemic hemostasis in women with IFD is rare and only occurs after 4 weeks of dead fetus retention; the main signs of this deterioration are fibrinogenopenia and thrombocytopenia.

Blood Coagulation Tests↗
PubMed1990

Comparison of the lipoprotein and hemostatic changes after a triphasic and a monophasic low dose oral contraceptive in premenopausal middle-aged women.

Metabolic and hemostatic effects of 2 low dose oral contraceptives (OCs), a triphasic (ethinylestradiol + (-)-norgestrel) and a monophasic (ethinylestradiol + desogestrel) preparation, were compared in a cross-over trial in fertile women over 35 years of age. Both combinations moderately affected plasma lipids, with 17-24% increases of total triglyceridemia. Triglycerides accumulate in low density lipoproteins, thus suggesting the possible formation of an atherogenic lipoprotein particle. Only the monophasic preparation increased high density lipoprotein (HDL)-cholesterol levels significantly, with a rise in HDL3 mass and cholesterol. OC treatment led to slight changes in HDL2 and HDL3 structure, with a rise of the cholesteryl ester and triglyceride contents, indicative of a stimulated cholesterol esterification and reverse transport. Changes in the hemostatic indexes (fibrinogen, antithrombin III and protein C) were negligible. The new low dose OCs, even when prescribed to relatively older women, affect to a relatively small extent lipid/lipoprotein metabolism, with the exception of changes in the low density lipoprotein composition.

Adult↗
PubMed1975

Disorders of hemostatic function in patients with systemic lupus erythematosus.

A wide spectrum of hemostatic abnormalities is found in patients with SLE. Thrombocytopenia and qualitative platelet disorder (impaired aggregation to collagen) are probably both due to antiplatelet antibodies, which can be found in most patients with the disease. About 10% of patients with SLE have a circulating anticoagulant. These circulating anticoagulants are broadly heterogeneous. Although most reported cases act at the level of the prothrombin converting complex, 15 of the 74 cases here reviewed had other points of action. The anticoagulants are probably all antibodies; they differ (with rare exceptions) from other naturally occurring circulating anticoagulants in having an immediate rather than a progressive effect, and in acting, not against pre-existing procoagulants, but against unstable complexes. An anticoagulant of the type found in SLE is only rarely observed in the absence of SLE; its presence in a patient is thus of some diagnostic importance. Hypoprothrombinemia is a common second lesion in patients with circulating anticoagulants. Its pathogenesis is obscure. Two patients with acquired von Willebrand's disease have been observed. All the hemostatic abnormalities found in SLE probably have immunologic bases; all respond to glucocorticoid treatment.

Anticoagulants↗
PubMed1988

Relationship between serum lipoproteins and hemostatic parameters in men with prostatic cancer.

Serum lipoprotein concentrations were related to hemostatic parameters in a group of 31 men before and during three different hormone treatment regimens for prostate cancer in an attempt to analyse to what extent the changes in these two systems correlate. In a correlation matrix the number of significant relationships at the 5% and 1% level corresponded to what could be expected by chance. The study thus failed to demonstrate any consistent relationship between any lipoprotein lipid concentration and the hemostatic parameters in men treated for prostate cancer. Most significant relationships were found for HDL-TG versus plasminogen, but the clinical significance of this observation is not clear.

Estradiol Congeners↗
PubMed1996

Morphological and hemostatic changes in rats with abdominal arterial prosthesis.

We evaluated the changes over time in hemostatic factors during ongoing arterial thrombosis in rats, as induced by a loop-shaped aortic prosthesis. Moreover, we investigated this condition by inspecting in parallel local thrombus growth, systemic vascular prostacyclin and t-PA production. One minute after loop insertion, activated platelets spread on the internal surface of the prosthesis and 24 hrs later numerous platelet aggregates supported by a fibrin network could be observed. However, no evidence for platelet activation could be concomitantly found in peripheral blood. A sustained increased in PGI2 formation was detected together with a progressive increase in plasma fibrinolytic activity during thrombus growth. The levels of fibrinogen as well as antithrombin III (ATIII) and heparin cofactor II (HCII) activities were steadily increased in loop-bearing animals. In conclusion, the dynamic phases of thrombus formation, in an aortic prosthesis, produce changes in vascular function and in hemostatic factors at the level of systemic blood.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Postoperative radiographic appearance of intracranial hemostatic gelatin sponge.

Hemostatic gelatin sponges were placed in hemispheric defects created in four dogs which were then periodically scanned by computed tomography to determine the postoperative appearance of the sponges. The hemostatic sponges appeared as low attenuation regions for 7-10 days. The attenuation value of these Gelfoam cavities was intermediate between fat and air. Subsequently, clinical cases were selected in which the location of gelatin sponges were known to demonstrate the appearance of the material in patients. In addition to enhancing the accuracy of computed tomographic interpretation, we have found that the gelatin sponge can be useful as a transient computed tomography marker for localization of surgical activity.

Adolescent↗
PubMed1996

'Hemostatic pause' in pediatric tonsillectomy?

A randomized prospective study was performed on 101 children undergoing dissection tonsillectomy in two different sequences. In the 'pause' sequence, a period of inactivity lasting 1.5 min ('hemostatic pause') with the Boyle-Davis gag relaxed and the fossae packed with gauze swabs was implemented after the tonsils were excised. Hemorrhage was controlled exclusively by ligatures. The duration of tonsillectomy and the number of ligatures used were accurately recorded. The procedure was identical in the 'no pause' group but the pause period was omitted. No reactionary haemorrhage occurred. There was no significant difference in the operating time between the two groups, but the mean number of ligatures required was significantly reduced in the 'pause' sequence. We conclude that 'hemostatic pause' in tonsillectomy reduces the amount of ligatures needed for satisfactory hemostasis.

Child↗
PubMed1995

Hemostatic risk factors of coronary artery disease in the Chinese.

In order to find out the hemostatic risk factors of coronary artery disease in the Chinese, antithrombin III concentration, factor VII and fibrinogen assays, plasminogen activator inhibitor-1 antigen and platelet count were determined in 51 healthy controls (mean age 63.5 years, S.D. 10.3), 55 diabetics (mean age 66.0 years, S.D. 4.8) and 56 patients with arteriographically proved coronary artery disease (mean age 63.8 years, S.D. 8.7). Of the coronary artery disease group, 19 had single vessel disease, 21 had double vessel disease and 16 had triple vessel disease. Sixteen of this group also had a past history of myocardial infarction. There was no significant difference of the hemostasis parameters between diabetics and controls. Fibrinogen and factor VII, but not plasminogen activator inhibitor, were significantly higher in coronary artery disease patients than in controls (P = 0.0001, both) and in diabetics (P = 0.0001, both). No significant difference in the parameters was found in the coronary artery disease group, whether the patients had single vessel disease, double vessel disease, or triple vessel disease, or were with or without past myocardial infarction. In the myocardial infarction group, fibrinogen and factor VII were significantly higher than in the controls (P < 0.00005 and 0.0001, respectively) and in the diabetics (P = 0.0002 and 0.0004, respectively). We suggest that increased levels of fibrinogen and factor VII, but not plasminogen activator inhibitor, would be the hemostatic risk factors of coronary artery disease in the Chinese.

Adult↗
PubMed1987

[Structural principles of hemostatic processes].

The formation of the hemostatic plug on areas of skin injury is characterized as a sequence of structure-forming processes ending in the formation of an impenetrable barrier. The morphology of this barrier is further elucidated by means of scanning- and transmission electron microscopy. Especially the fibrin coating of the injury shows a completely different formation than is deducible from the solely hemostaseologically orientated view of the formation of the hemostatic plug. These structure-forming processes are: activation of the intrinsic clotting system by means of explosion-like destruction of thrombocytes with an immediate formation of a fibrin clot within seconds after the injury. Later during the process the fibrin clot is then condensed and as a function of thrombocyte dependent retraction receives its final fibrin stabilisation and modellation towards an occluding plug. The very narrow net formation of fibrin fibers is interpreted as dependent on the destruction of thrombocyte pseudopodia using their round shape as a rail for fibrin fiber formation. Disturbances of clot formation of postmortal clots compared to vital clots are interpreted as functional thrombocytic distortions, especially of the thrombocytic energy metabolism. Extracorporal clotting of blood drops after extreme ischemia resemble fibrin structures and fibrin structure formation distortions of postmortal origin.

Animals↗