The Effect of a Platelet Inhibiting Drug (Sulfinpyrazone) in the Therapy of Patients with Transient Ischemic Attacks (Tia’s) and Minor Strokes

1975 ◽  
Author(s):  
J. T. Robertson ◽  
M. Dugdale ◽  
N. Salky ◽  
H. Robinson
Keyword(s):  
Risk Factors ◽  
Platelet Aggregation ◽  
Routine Laboratory ◽  
Transient Ischemic Attacks ◽  
Double Blind ◽  
Survival Studies ◽  
A Minor ◽  
Cerebrovascular Occlusive Disease ◽  
Subsequent Failure

A prospective double blind randomized trial of sulfinpyrazone and placebo is described in patients with TIA’S and minor strokes. The criteria for entry into the Study were patients with at least two transient ischemic attacks within a two-week period or patients with a minor fixed neurological deficit resulting from cerebrovascular occlusive disease. All patients had routine laboratory, special platelet aggregation studies, and cerebral arteriography. Several had initial and subsequent platelet survival studies. To insure equivalence of the two groups, patients were randomly assigned to categories reflecting their risk factors and age. Patients were followed every three months with appropriate laboratory and platelet studies. Interval follow-up occured when side effects or additional symptoms appeared.When patients failed on sulfinpyrazone, they were placed on sulfinpyrazone and Coumadin. Patients who failed on placebo were placed on sulfinpyrazone followed by sulfinpyrazone and Coumadin if subsequent failure occured. Failure was defined as two transient ischemic attacks within a two-week period or an additional stroke syndrome.New patients will be enrolled for three years, and all patients will be followed for five years. All data is incorporated into computer files.Preliminary results relating to the first sixty patients will be presented.

Ventriculoperitoneal shunt failure in pediatric patients: an analysis of a national hospitalization database in Thailand

2021 ◽  
pp. 1-11
Author(s):  
Phumtham Limwattananon ◽  
Amnat Kitkhuandee
Keyword(s):  
Risk Factors ◽  
Pediatric Patients ◽  
Public Hospitals ◽  
Shunt Operation ◽  
Shunt Failure ◽  
Cumulative Hazard ◽  
Multiple Failures ◽  
Ventriculoperitoneal Shunting ◽  
Subsequent Failure

OBJECTIVE Shunt failure is common among patients undergoing ventriculoperitoneal shunting for treatment of hydrocephalus. The present study examined long-term shunt failure and associated risk factors in pediatric patients by using a national hospitalization database of Thailand. METHODS Patients 17 years or younger who had been admitted to 71 public hospitals in 2012–2017 for first-time ventriculoperitoneal shunting for diseases with known etiology and discharged alive were followed through 2019 to ascertain shunt failure. Shunt survivals were calculated using Kaplan-Meier estimates and time to failure was analyzed to identify risk factors for the first failure by using Cox proportional hazards regression. Differences in risks of subsequent failures with respect to place in the order of failures (i.e., first, second, third) were determined using a cumulative hazard function. RESULTS Over a median follow-up of 29.9 months, shunt failure occurred in 33.7% of 2072 patients (median age 8.8 months), with a higher proportion in patients < 1 year than in patients 1–17 years (37.8% vs 28.9%, p < 0.001), and ranged from 26.1% of those having posttraumatic hydrocephalus to 35.9% of those having infectious diseases. The shunt failure rates at 3, 6, and 12 months were 11.5%, 19.0%, and 25.2%, respectively. Patients < 1 year had a higher risk of the first failure than patients 1–17 years (hazard ratio 1.45, 95% CI 1.20–1.76). Among those with shunt failure, 35.8% had multiple failures and 52.9% failed within 180 days after the index shunting. The cumulative hazard of subsequent failure was consistently higher than that of an earlier failure regardless of age and etiology, and the cumulative hazard of the second failure in the patients with 180-day failure was higher than that in the patients in whom shunts failed beyond 180 days. CONCLUSIONS Shunt failure occurred more frequently in younger pediatric patients. Much attention should be placed on the initial shunt operation so as to mitigate the failure risk. Close follow-up was crucial once patients had developed the failure, because the risk of subsequent failure was more likely than an earlier one among those with multiple failures.

Complementary Effects of Multivitamin and Omega-3 Fatty Acid Supplementation on Indices of Cardiovascular Health in Individuals with Elevated Homocysteine

2012 ◽  
Vol 82 (1) ◽  
pp. 41-52 ◽  
Author(s):  
P. Earnest ◽  
S. Kupper ◽  
M. Thompson ◽  
Guo ◽  
S. Church
Keyword(s):  
Risk Factors ◽  
Cardiovascular Health ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
C Reactive Protein ◽  
Fatty Acid Supplementation ◽  
Omega 3 Fatty Acid ◽  
Reactive Protein ◽  
Daily Ingestion

Homocysteine (HCY), C-reactive protein (hsCRP), and triglycerides (TG) are risk factors for cardiovascular disease (CVD). While multivitamins (MVit) may reduce HCY and hsCRP, omega-3 fatty acids (N3) reduce TG; yet, they are seldom studied simultaneously. We randomly assigned 100 participants with baseline HCY (> 8.0 umol/L) to the daily ingestion of: (1) placebo, (2) MVit (VitC: 200 mg; VitE: 400 IU; VitB6: 25 mg; Folic Acid: 400 ug; VitB12: 400 ug) + placebo, (3) N3 (2 g N3, 760 mg EPA, 440 mg DHA)+placebo, or (4) MVit + N3 for 12 weeks. At follow-up, we observed significant reductions in HCY (umol/L) for the MVit (- 1.43, 95 %CI, - 2.39, - 0.47) and MVit + N3 groups (- 1.01, 95 %CI, - 1.98, - 0.04) groups, both being significant (p < 0.05) vs. placebo (- 0.57, 95 %CI, - 1.49, 0.35) and N3 (1.11, 95 % CI, 0.07, 2.17). hsCRP (nmol/L) was significantly reduced in the MVit (- 6.00, 95 %CI, - 1.04, - 0.15) and MVit + N3 (- 0.98, 95 %CI, - 1.51, - 0.46) groups, but not vs. placebo (- 0.15, 95 %CI, - 0.74, 0.43) or N3 (- 0.53, 95 %CI, - 1.18, 0.12). Lastly, we observed significant reductions in TG for the N3 (- 0.41, 95 %CI, - 0.69, - 0.13) and MVit + N3 (- 0.71, 95 %CI, - 0.93, - 0.46) groups, both significant vs. placebo (- 0.10, 95 %CI, - 0.36, 0.17) and MVit groups (0.15, 95 %CI, - 12, 0.42). The co-ingestion of MVit + N3 provides synergistic affects on HCY, hsCRP, and plasma TG.

Psychological Resilience Provides No Independent Protection From Suicidal Risk

Crisis ◽  
2016 ◽  
Vol 37 (2) ◽  
pp. 130-139 ◽  
Author(s):  
Danica W. Y. Liu ◽  
A. Kate Fairweather-Schmidt ◽  
Richard Burns ◽  
Rachel M. Roberts ◽  
Kaarin J. Anstey
Keyword(s):  
Risk Factors ◽  
Well Being ◽  
Current Status ◽  
Psychological Resilience ◽  
Cross Sectional ◽  
Life Project ◽  
Resilience Factors ◽  
First Time

Abstract. Background: Little is known about the role of resilience in the likelihood of suicidal ideation (SI) over time. Aims: We examined the association between resilience and SI in a young-adult cohort over 4 years. Our objectives were to determine whether resilience was associated with SI at follow-up or, conversely, whether SI was associated with lowered resilience at follow-up. Method: Participants were selected from the Personality and Total Health (PATH) Through Life Project from Canberra and Queanbeyan, Australia, aged 28–32 years at the first time point and 32–36 at the second. Multinomial, linear, and binary regression analyses explored the association between resilience and SI over two time points. Models were adjusted for suicidality risk factors. Results: While unadjusted analyses identified associations between resilience and SI, these effects were fully explained by the inclusion of other suicidality risk factors. Conclusion: Despite strong cross-sectional associations, resilience and SI appear to be unrelated in a longitudinal context, once risk/resilience factors are controlled for. As independent indicators of psychological well-being, suicidality and resilience are essential if current status is to be captured. However, the addition of other factors (e.g., support, mastery) makes this association tenuous. Consequently, resilience per se may not be protective of SI.

Ex Vivo Inhibition of Platelet Aggregation in Patients with Severe Limb Arteriopathy Treated with BAY U3405, a Specific IX A2 Receptor Antagonist

1994 ◽  
Vol 72 (05) ◽  
pp. 659-662 ◽  
Author(s):  
S Bellucci ◽  
W Kedra ◽  
H Groussin ◽  
N Jaillet ◽  
P Molho-Sabatier ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Ex Vivo ◽  
Randomized Study ◽  
In Vivo Studies ◽  
Walking Distance ◽  
Peripheral Blood Flow ◽  
Walking Ability ◽  
Double Blind ◽  
Platelet Factor

SummaryA double-blind, placebo-controlled randomized study with BAY U3405, a specific thromboxane A2 (TX A2) receptor blocker, was performed in patients suffering from severe stade II limb arteriopathy. BAY U3405 or placebo was administered in 16 patients at 20 mg four times a day (from day 1 to day 3). Hemostatic studies were done before therapy, and on day 2 and day 3 under therapy. On day 3, BAY U3405 was shown to induce a highly statistically significant decrease of the velocity and the intensity of the aggregations mediated by arachidonic acid (56 ± 37% for the velocity, 58 ± 26% for the intensity) or by U46619 endoperoxide analogue (36 ± 35% for the velocity, 37 ± 27% for the intensity). Similar results were already observed on day 2. By contrast, such a decrease was not noticed with ADP mediated platelet aggregation. Furthermore, plasma levels of betathrombo-globulin and platelet factor 4 remained unchanged. Peripheral hemodynamic parameters were also studied. The peripheral blood flow was measured using a Doppler ultrasound; the pain free walking distance and the total walking ability distance were determined under standardized conditions on a treadmill. These last two parameters show a trend to improvement which nevertheless was not statistically significant. All together these results encourage further in vivo studies using BAY U3405 or related compounds on a long-term administration.

The d-Enantiomer Form of Indobufen Totally Accounts for the Anti-Cyclooxygenase and Antiplatelet Activity Ex Vivo and for the Increase in Bleeding Time by Indobufen in Man

1992 ◽  
Vol 67 (02) ◽  
pp. 258-263 ◽  
Author(s):  
Raffaele De Caterina ◽  
Rosa Sicari ◽  
An Yan ◽  
Walter Bernini ◽  
Daniela Giannessi ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Plasma Levels ◽  
Bleeding Time ◽  
Ex Vivo ◽  
Random Sequence ◽  
Antiplatelet Agent ◽  
Antiplatelet Drug ◽  
Double Blind

SummaryIndobufen is an antiplatelet drug able to inhibit thromboxane production and cyclooxygenase-dependent platelet aggregation by a reversible inhibition of cyclooxygenase. Indobufen exists in two enantiomeric forms, of which only d-indobufen is active in vitro in inhibiting cyclooxygenase. In order to verify that also inhibition of platelet function is totally accounted for by d-indobufen, ten patients with proven coronary artery disease (8 male, 2 female, age, mean ± S.D., 58.7 ± 7.5 years) were given, in random sequence, both 100 mg d-indobufen and 200 mg dl-indobufen as single administrations in a double-blind crossover design study with a washout period between treatments of 72 h. In all patients thromboxane (TX) B2 generation after spontaneous clotting (at 0, 1, 2, 4, 6, 8, 12, 24 h), drug plasma levels (at the same times), platelet aggregation in response to ADP, adrenaline, arachidonic acid, collagen, PAF, and bleeding time (at 0, 2, 12 h) were evaluated after each treatment. Both treatments determined peak inhibition of TXB2 production at 2 h from administration, with no statistical difference between the two treatments (97 ±3% for both treatments). At 12 h inhibition was 87 ± 6% for d-indobufen and 88 ± 6% for dl-indobufen (p = NS). Inhibition of TXB2 production correlated significantly with plasma levels of the drugs. Maximum inhibitory effect on aggregation was seen in response to collagen 1.5 pg/ml (63 ± 44% for d-indobufen and 81 ± 22% for dl-indobufen) and arachidonic acid 0.5-2 mM (78 ± 34% for d-indobufen and 88 ± 24% for dl-indobufen) at 2 h after each administration. An effect of both treatments on platelet aggregation after 12 h was present only for adrenaline 2 μM (55 ± 41% for d-indobufen and 37 ± 54% for dl-indobufen), collagen 1.5 pg/ml (69 ± 30% for d-indobufen and 51 ± 61% for dl-indobufen), arachidonic acid 0.5-2 mM (56 ± 48% for d-indobufen and 35 ± 49% for dl-indobufen). The extent of inhibition of TX production and the extent of residual platelet aggregation were never significantly different between treatments. Bleeding time prolongation was similar in the two treatment groups without showing a pronounced and long lasting effect (from 7.0 ± 2.0 min to 10.0 ± 3.0 min at 2 h and 8.0 ± 2.0 min at 12 h for d-indobufen; from 6.0 ±1.0 min to 8.5 ± 2.0 min at 2 h and 8.0 ± 1.0 min at 12 h for dl-indobufen). These results demonstrate that the biological activity of dl-indobufen as an antiplatelet agent in vivo is totally accounted for by d-indobufen.

The Effect of Warfarin Sodium on the Duration of Platelet Aggregation

1967 ◽  
Vol 18 (03/04) ◽  
pp. 766-778 ◽  
Author(s):  
H. J Knieriem ◽  
A. B Chandler
Keyword(s):  
Platelet Count ◽  
Placebo Group ◽  
Platelet Aggregation ◽  
Prothrombin Time ◽  
Platelet Rich Plasma ◽  
Healthy Adults ◽  
Double Blind Study ◽  
Double Blind ◽  
Warfarin Sodium

SummaryThe effect of the administration of warfarin sodium (Coumadin®) on the duration of platelet aggregation in vitro was studied. Coumadin was given for 4 consecutive days to 10 healthy adults who were followed over a period of 9 days. The duration of adenosine diphosphate-induced platelet aggregation in platelet-rich plasma, the prothrombin time, and the platelet count of platelet-rich plasma were measured. Four other healthy adults received placebos and participated in a double-blind study with those receiving Coumadin.Although administration of Coumadin caused a prolongation of the prothrombin time to 2 or 21/2 times the normal value, a decrease in the duration of platelet aggregation was not observed. In most individuals who received Coumadin an increase in the duration of platelet aggregation occurred. The effect of Coumadin on platelet aggregation was not consistently related to the prothrombin time or to the platelet count. In the placebo group there was a distinct relation between the duration of platelet aggregation and the platelet count in platelet-rich plasma.The mean increase in the duration of platelet aggregation when compared to the control value before medication with Coumadin was 37.7%. In the placebo group there was a mean increase of 8.4%. The difference between the two groups is significant (p <0.001). Increased duration of platelet aggregation also occurred in two individuals who received Coumadin over a period of 10 and 16 days respectively.

Effects of Ticlopidine of Platelet Function in Men with Stable Angina Pectoris

1985 ◽  
Vol 54 (04) ◽  
pp. 808-812 ◽  
Author(s):  
Ulf Berglund ◽  
Henning von Schenck ◽  
Lars Wallentin
Keyword(s):  
Platelet Aggregation ◽  
Angina Pectoris ◽  
Platelet Function ◽  
Plasma Levels ◽  
Platelet Reactivity ◽  
Inhibitory Effect ◽  
Controlled Study ◽  
Double Blind ◽  
Platelet Factor

SummaryThe effects of ticlopidine (T) (500 mg daily) on platelet function were investigated in a double-blind placebo-controlled study in 38 middle-aged men with stable incapacitating angina pectoris. The in vitro platelet reactivity to aggregating agents, the platelet sensitivity to prostacyclin and the plasma levels of platelet specific proteins and fibrinogen were determined before and after 4 and 8 weeks of treatment. T exerted a potent inhibitory effect on ADP- and collagen-induced platelet aggregation. The effect of T was proportional to the pretreatment reactivity to ADP and collagen. The inhibitory effect of T on the epinephrine response was less pronounced. The plasma levels of beta-thromboglobulin, platelet factor 4 and fibrinogen were not influenced by T. The platelet inhibition of prostacyclin was potentiated by T, and it was demonstrated that T and prostacyclin had synergistic inhibitory effects on platelet aggregation.

Inhibition of Spontaneous Platelet Aggregation by Sulfinpyrazone

1979 ◽  
Vol 42 (02) ◽  
pp. 621-625 ◽  
Author(s):  
G G Nenci ◽  
G Agnelli ◽  
M Berrettini ◽  
P Parise ◽  
E Ballatori
Keyword(s):  
Platelet Aggregation ◽  
Crossover Study ◽  
Double Blind ◽  
Platelet Aggregability ◽  
Initiation Of Therapy ◽  
Spontaneous Platelet Aggregation ◽  
Blind Crossover Study ◽  
Double Blind Crossover Study

SummaryIn a randomized double-blind crossover study in 16 patients with enhanced in vitro spontaneous platelet aggregation, sulfinpyrazone proved to be effective in normalizing platelet aggregability within 4 days after initiation of therapy.

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