Reduced platelet aggregability and thromboxane release after rebleeding in patients with subarachnoid hemorrhage

1991 ◽  
Vol 74 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Seppo Juvela ◽  
Marrku Kaste
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Statistical Significance ◽  
Adenosine Diphosphate ◽  
Blood Samples ◽  
Content Type ◽  
Platelet Aggregability ◽  
Before And After ◽  
Fine Print

✓ Serial blood samples were obtained from 80 patients with subarachnoid hemorrhage (SAH) to study adenosine diphosphate-induced platelet aggregation and associated thromboxane B2 release. The goal of the investigation was to detect whether reduced platelet function is involved in rebleeds. Seventeen patients (21%) suffered a rebleed, six of those experiencing their first rebleed within 24 hours after SAH. Therefore, most platelet function studies were performed after rebleeds. Thromboxane release was lower in patients with rebleeds than in the others, both before and after rebleeding, although statistical significance was reached only in samples collected after rebleeds. Patients rebleeding within 24 hours after SAH had lower platelet aggregability (p = 0.037) than patients without a rebleed in the samples taken within 3 days after SAH. The results suggest that reduced platelet aggregability and thromboxane release are involved in rebleeds following primary SAH.

Reduced platelet function in subarachnoid hemorrhage

1986 ◽  
Vol 64 (6) ◽  
pp. 907-910 ◽  
Author(s):  
Sotirios A. Tsementzis ◽  
Jaswinder S. Gill ◽  
Edward R. Hitchcock ◽  
Jennifer A. Hartley ◽  
Surinder K. Gill ◽  
...  
Keyword(s):  
Platelet Count ◽  
Subarachnoid Hemorrhage ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Maximum Rate ◽  
Adenosine Diphosphate ◽  
Platelet Adhesiveness ◽  
Content Type ◽  
Aneurysmal Rupture ◽  
Fine Print

✓ The hypothesis that abnormalities of platelet function may relate to the occurrence or recurrence of subarachnoid hemorrhage (SAH) has been examined. Seventy patients with SAH and 65 control individuals were studied. The adenosine diphosphate (ADP) threshold for secondary platelet aggregation was significantly higher in the SAH group than in the controls. In tests using 4.0 µg/ml ADP, the percent platelet aggregation (at 2 minutes) and the maximum rate of platelet aggregation (over 20 seconds) were significantly lower in the SAH patients. There was no difference in total platelet count between the two groups. Platelet adhesiveness was lower in the SAH patients when compared to controls. Circulating microaggregates did not differ between the two groups. The results indicate that reduced platelet function does relate to SAH and may either contribute to aneurysmal rupture in cases of SAH or be a consequence of it.

Platelet thromboxane release and delayed cerebral ischemia in patients with subarachnoid hemorrhage

1991 ◽  
Vol 74 (3) ◽  
pp. 386-392 ◽  
Author(s):  
Seppo Juvela ◽  
Matti Hillbom ◽  
Markku Kaste
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Delayed Cerebral Ischemia ◽  
Adenosine Diphosphate ◽  
Content Type ◽  
Platelet Aggregability ◽  
Before And After ◽  
Ischemic Complications ◽  
Cerebral Ischemic ◽  
Permanent Neurological Deficit

✓ Adenosine diphosphate-induced platelet aggregation and associated thromboxane B2 release were studied in 52 patients with subarachnoid hemorrhage (SAH) in order to detect a possible association between altered platelet function and development of cerebral ischemic complications after SAH. Compared to the values on admission, the patients showed significantly increased platelet aggregability (p < 0.05) and thromboxane release (p < 0.001) 1 to 2 weeks after SAH. The highest values of thromboxane release were seen in patients who deteriorated due to delayed cerebral ischemia with a permanent neurological deficit. Thromboxane release was significantly higher (p < 0.05) before the onset of severe delayed ischemia in six patients with preoperative ischemia compared to the patients without delayed ischemia. In five others, both ischemic deterioration and elevated thromboxane release occurred after operation. These patients had preoperative values similar to the values in those without ischemic symptoms. The observations suggest that increased platelet aggregability and thromboxane release are associated with delayed cerebral ischemia both before and after surgery.

Traumatic subarachnoid hemorrhage on the computerized tomography scan obtained at admission: a multicenter assessment of the accuracy of diagnosis and the potential impact on patient outcome

2003 ◽  
Vol 98 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Cristina Mattioli ◽  
Luigi Beretta ◽  
Simonetta Gerevini ◽  
Fabrizio Veglia ◽  
Giuseppe Citerio ◽  
...  
Keyword(s):  
Patient Outcome ◽  
Subarachnoid Hemorrhage ◽  
Computerized Tomography ◽  
Statistical Significance ◽  
Unfavorable Outcome ◽  
Content Type ◽  
Ct Findings ◽  
Traumatic Subarachnoid Hemorrhage ◽  
Injured Patients ◽  
Fine Print

Object. The goal of this study was fourfold: 1) to determine the incidence of traumatic subarachnoid hemorrhage (tSAH) in patients with traumatic brain injury (TBI); 2) to verify agreement in the diagnosis of tSAH in a multicenter study; 3) to assess the incidence of tSAH on the outcome of the patient; and 4) to establish whether tSAH itself leads to an unfavorable outcome or whether it is a sign of major brain trauma associated with severe posttraumatic lesions. Methods. Computerized tomography (CT) scans obtained in 169 head-injured patients on admission to 12 Italian intensive care units during a 3-month period were examined. The scans were collected for neuroradiological review and were used for the analysis together with data from a multicenter database (Neurolink). A review committee found a high incidence of tSAH (61%) in patients with TBI and a moderate agreement among centers (K = 0.57). Significant associations were observed between the presence and grading of tSAH and patient outcomes, and between the presence of tSAH and the severity of the CT findings. Logistic regression analysis showed that the presence of tSAH and its grading alone do not assume statistical significance in the prediction of unfavorable outcome. Conclusions. Traumatic SAH frequently occurs in patients with TBI, but it is difficult to detect and grade. Traumatic SAH is associated with more severe CT findings and a worse patient outcome.

Aspirin and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

1995 ◽  
Vol 82 (6) ◽  
pp. 945-952 ◽  
Author(s):  
Seppo Juvela
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Platelet Function ◽  
Delayed Cerebral Ischemia ◽  
Aneurysm Rupture ◽  
Content Type ◽  
Reduced Risk ◽  
Fine Print

✓ This follow-up study was designed to evaluate whether the use of aspirin either before or after aneurysm rupture affects the occurrence of delayed cerebral ischemia. Aspirin inhibits platelet function and thromboxane production and has been shown to reduce the risk of various cardiovascular and cerebrovascular ischemic diseases. Following admission, the patients in this study were interviewed regarding their use of aspirin and other medicines prior to and after hemorrhage, and their urine was screened qualitatively for salicylates. Patient outcome and the occurrence of hypodense lesions consistent with cerebral infarction on follow-up computerized tomography (CT) were studied prospectively up to 1 year after hemorrhage. Of 291 patients, 31 (11%) died because of the initial hemorrhage and 18 (6%) died due to rebleeding within 4 days after hemorrhage. Of the remaining 242 patients, 90 (37%) had delayed cerebral ischemia, which caused a permanent neurological deficit or death in 54 patients (22%). Of 195 patients undergoing follow-up CT, 85 (44%) had cerebral infarction that was not seen on the CT scan obtained on admission. Those who had salicylates in the urine on admission had a relative risk of 0.40 (95% confidence interval (CI), 0.15 to 1.10) of delayed ischemia with fixed deficit and a risk of 0.40 (95% CI, 0.18 to 0.93) of cerebral infarction compared with patients who did not have salicylates in their urine. This reduced risk of ischemic complications with aspirin use was restricted to those patients who used aspirin before hemorrhage, when the risk of ischemia was 0.21 (95% CI, 0.03 to 1.63) and the risk of infarct was 0.18 (95% CI, 0.04 to 0.84) compared with those who had not used aspirin. The reduced risk of cerebral infarction remained significant after adjustment for several potential confounding factors (adjusted risk 0.19; 95% CI, 0.04 to 0.89). These observations suggest that platelet function at the time of subarachnoid hemorrhage may be associated with delayed cerebral ischemia after aneurysm rupture.

Effects of the Ca++-permeable nonselective cation channel blocker LOE 908 on subarachnoid hemorrhage—induced vasospasm in the basilar artery in rabbits

2003 ◽  
Vol 98 (3) ◽  
pp. 561-564 ◽  
Author(s):  
Yoshifumi Kawanabe ◽  
Tomoh Masaki ◽  
Nobuo Hashimoto
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Intravenous Administration ◽  
Basilar Artery ◽  
Channel Blocker ◽  
Autologous Blood ◽  
Content Type ◽  
Dependent Part ◽  
Before And After ◽  
Fine Print

Object. The Ca++ influx into vascular smooth-muscle cells (VSMCs) plays a fundamental role in the development and chronic effects of vasospasm after subarachnoid hemorrhage (SAH). The Ca++-permeable nonselective cation channels (NSCCs) are activated by several endothelium-derived constricting factors such as endothelin 1 (ET-1) and thromboxane A2. Moreover, the receptor-operated Ca++ channel blocker LOE 908 inhibits ET-1—induced extracellular Ca++ influx via NSCCs in the VSMCs of the basilar artery (BA) and the NSCC-dependent part of ET-1—induced vasoconstriction of BA rings. The purpose of the present study was to evaluate the in vivo role of LOE 908 on SAH-induced vasospasm. Methods. Forty-two Japanese white rabbits were assigned to seven groups. Treatment groups consisted of the following: 1) control rabbits without SAH that received a cisternal injection of saline; 2) rabbits with SAH that were subjected to the intravenous administration of saline; 3 through 6) rabbits with SAH that underwent the intravenous administration of 0.01, 0.1, 1, or 10 mg/kg LOE 908, respectively; and 7) rabbits without SAH that underwent the intravenous administration of 10 mg/kg LOE 908. Autologous blood was injected into the cisterna magna. The caliber of the BA was measured on angiographic studies before and after the cisternal injection of autologous blood. The intravenous injection of LOE 908 inhibited the magnitude of an SAH-induced vasosapsm. In addition, the concentration of LOE 908 required to relax vasospasm (1 mg/kg) correlated with that required to block Ca++ influx into VSMCs. Conclusions. The Ca++ channel blocker LOE 908 may inhibit the magnitude of an SAH-induced vasospasm by blocking the influx of Ca++ through NSCCs in rabbit BAs. Blocking the NSCCs may represent a new treatment for cerebral vasospasm after SAH.

Influence of premorbid factors on survival following subarachnoid hemorrhage

2001 ◽  
Vol 95 (4) ◽  
pp. 555-559 ◽  
Author(s):  
Louis H. Pobereskin
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cigarette Smoking ◽  
Protective Effect ◽  
Statistical Significance ◽  
Patient Characteristics ◽  
Population Based ◽  
Prior History ◽  
Content Type ◽  
Risk Of Death ◽  
Fine Print

Object. The goal of this study was to explore the relationships between premorbid patient characteristics, especially cigarette smoking, and the risk of death following subarachnoid hemorrhage (SAH). Methods. A population-based study design was used with multiple overlapping methods of case identification. A strict definition of SAH was used. Relationships between patients' age and sex as well as their cigarette smoking and hypertension statuses were explored by calculating relative risks (RRs). Confounding effects were examined using logistic regression analysis. The author identified 800 cases in which the patient had experienced his or her first SAH. Seventy-seven percent of cases were verified by review of computerized tomography scans, 22% by autopsy, and 1% by lumbar puncture. A prior history of hypertension had no effect on the risk of mortality. There was a higher case mortality rate in female patients than in male patients, but this did not reach statistical significance. The RR of death at 30 days post-SAH for patients older than 60 years compared with those who were younger was 2.95 (95% confidence interval [CI] 2.18–3.97). The RR of death at all time intervals was lower for smokers than for nonsmokers (smokers/nonsmokers RR 0.47 [95% CI 0.32–0.69] at 7 days). The protective effect of smoking diminished on Day 3 post-SAH and increased again on Day 7. Conclusions. Advanced age is an important determinant of survival following SAH. Smoking appears to have a protective effect. The author presents evidence indicating that increased vasospasm in smokers may reduce the severity of the initial hemorrhage.

Serial changes of hemostasis in aneurysmal subarachnoid hemorrhage with special reference to delayed ischemic neurological deficits

1997 ◽  
Vol 86 (4) ◽  
pp. 594-602 ◽  
Author(s):  
Yukihiko Fujii ◽  
Shigekazu Takeuchi ◽  
Osamu Sasaki ◽  
Takashi Minakawa ◽  
Tetsuo Koike ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Multivariate Analyses ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Neurological Deficits ◽  
Ct Scans ◽  
Blood Samples ◽  
Content Type ◽  
Significant Difference ◽  
D Dimer ◽  
Fine Print

✓ This study was undertaken to elucidate comprehensively the serial changes occurring in hemostatic systems after aneurysmal subarachnoid hemorrhage (SAH) and thereby to ascertain whether the examination of the integrity of these systems is helpful in predicting delayed ischemic neurological deficits (DINDs). The authors examined 117 patients admitted to the hospital within 24 hours after onset of SAH. Blood samples were collected from each patient on Days 0 (at admission), 3, 6, 14, and 30. A number of hemostatic parameters were examined in these samples, and the relationships between their changes and DINDs were assessed. Eighteen (15.4%) of the patients exhibited DINDs, and their frequency increased as the severity of subarachnoid clotting increased. Also, the frequency of DINDs was significantly higher in the patients with hydrocephalus on initial computerized tomography (CT) scans than in those without hydrocephalus. Regarding the hemostatic parameters at admission, there was no significant difference between the patients with and without DINDs. On Day 3, however, the fibrinogen and D-dimer levels were higher in the patients with than in those without DINDs. The fibrinogen and thrombin—antithrombin complex levels on Day 6 and the D-dimer level on Day 14 in the patients with DINDs were higher than the corresponding levels in those without DINDs. Multivariate analyses revealed that the following variables (in order of importance) were independent predictors of DINDs: the levels of D-dimer on Day 3, fibrinogen on Day 6, and the presence of hydrocephalus on admission. These data indicate that the levels of hemostatic parameters in concert with the CT findings may enable us to predict the appearance of DINDs.

Influence of aspirin on outcome following aneurysmal subarachnoid hemorrhage

2004 ◽  
Vol 101 (6) ◽  
pp. 921-925 ◽  
Author(s):  
L. Gerard Toussaint ◽  
Jonathan A. Friedman ◽  
Eelco F. M. Wijdicks ◽  
David G. Piepgras ◽  
Mark A. Pichelmann ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Statistical Significance ◽  
Anticoagulation Therapy ◽  
Neurological Deficits ◽  
Permanent Disability ◽  
Content Type ◽  
Regular Aspirin ◽  
Rebleeding Rate ◽  
Fine Print

Object. Previous studies have indicated an increased incidence of death in patients with subarachnoid hemorrhage (SAH) who are currently receiving anticoagulation therapy. The significance of previous aspirin use in patients with SAH is unknown. The authors analyzed the effects of prior aspirin use on clinical course and outcomes following aneurysmal SAH. Methods. The medical records of 305 patients with angiogram-confirmed aneurysmal SAH who consecutively presented to our institution between 1990 and 1997 within 7 days of ictus were analyzed. Twenty-nine (9.5%) of these patients had a history of regular aspirin use before onset of the SAH. The Glasgow Outcome Scale (GOS) was used to measure patient outcome at the longest available follow up. Aspirin users were older on average than nonusers (59 years of age compared with 53 years; p = 0.018). The mean admission Hunt and Hess grades of patients with and without aspirin use were similar (2 compared with 2.3; p = 0.51). Two trends, which did not reach statistical significance, were observed. 1) The rebleeding rate in aspirin users was 14.3%, compared with a 4.7% rebleeding rate in nonusers (p = 0.06). 2) Permanent disability from vasospasm was less common among aspirin users (23% compared with 50%; p = 0.069). Outcomes did not differ between aspirin users and nonusers (mean GOS Score 3.83 compared with GOS Score 3.86, respectively; p = 0.82). Conclusions. Despite trends indicating increased rebleeding rates and a lower incidence of permanent disability due to delayed ischemic neurological deficits, there was no significant effect of previous aspirin use on overall outcome following aneurysmal SAH. Based on these preliminary data, the presence of an intracranial aneurysm is not a strict contraindication to aspirin use.

Acute microvascular platelet aggregation after subarachnoid hemorrhage

2005 ◽  
Vol 102 (6) ◽  
pp. 1094-1100 ◽  
Author(s):  
Fatima A. Sehba ◽  
Gulam Mostafa ◽  
Victor Friedrich ◽  
Joshua B. Bederson
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Platelet Aggregation ◽  
Subsequent Increase ◽  
Platelet Surface ◽  
Content Type ◽  
Acute Cerebral Ischemia ◽  
Vessel Structure ◽  
Surface Receptor ◽  
Platelet Aggregates ◽  
Fine Print

Object. The mechanisms underlying acute cerebral ischemia after subarachnoid hemorrhage (SAH) are not well established. Platelets aggregate within major cerebral vessels hours after SAH, but this has not been studied in the microvasculature. Platelet aggregates within the microvasculature could mechanically obstruct the lumen and initiate events that injure vessel structure. In the present study the authors examined the hypothesis that platelets aggregate within the cerebral microvasculature acutely after SAH. Methods. Subarachnoid hemorrhage was induced in the rat by using the endovascular perforation model. The animals were killed between 10 minutes and 48 hours after SAH. Immunostaining for the platelet surface receptor glycoprotein (GP)IIb/IIIa, which mediates platelet aggregation, was used to detect platelet aggregation. Sham-operated animals were used as controls. The GPIIb/IIIa immunoreactive platelet aggregates were abundant in the microvasculature of the basal and frontal cortex, striatum, and hippocampus 10 minutes after SAH. These aggregates decreased in number from 1 to 6 hours post-SAH and then increased to a peak at 24 hours. No immunoreactive aggregates were observed 48 hours after SAH. Conclusions. The data indicate that widespread platelet aggregation occurs very rapidly in response to SAH followed by a decrease within 6 hours and a subsequent increase 24 hours after SAH. Microvascular platelet aggregates may contribute to decreased cerebral blood flow and ischemic injury after SAH via a number of mechanisms.

Ticlopidine Facilitates the Deaggregation of Human Platelets Aggregated by Thrombin

1994 ◽  
Vol 71 (01) ◽  
pp. 091-094 ◽  
Author(s):  
M Cattaneo ◽  
B Akkawat ◽  
R L Kinlough-Rathbone ◽  
M A Packham ◽  
C Cimminiello ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Platelet Aggregation ◽  
Prostaglandin E1 ◽  
Human Platelet ◽  
Adenosine Diphosphate ◽  
Human Platelets ◽  
Before And After ◽  
Normal Human ◽  
Platelet Aggregates ◽  
Induced Aggregation

SummaryNormal human platelets aggregated by thrombin undergo the release reaction and are not readily deaggregated by the combination of inhibitors hirudin, prostaglandin E1 (PGE1) and chymotrypsin. Released adenosine diphosphate (ADP) plays an important role in the stabilization of thrombin-induced human platelet aggregates. Since ticlopidine inhibits the platelet responses to ADP, we studied thrombin-induced aggregation and deaggregation of 14C-serotonin-labeled platelets from 12 patients with cardiovascular disease before and 7 days after the oral administration of ticlopidine, 250 mg b.i.d. Before and after ticlopidine, platelets stimulated with 1 U/ml thrombin aggregated, released about 80–90% 14C-serotinin and did not deaggregate spontaneously within 5 min from stimulation. Before ticlopidine, hirudin (5× the activity of thrombin) and PGE1 (10 μmol/1) plus chymotrypsin (10 U/ml) or plasmin (0.06 U/ml), added at the peak of platelet aggregation, caused slight or no platelet deaggregation. After ticlopidine, the extent of platelet deaggregation caused by the same inhibitors was significantly greater than before ticlopidine. The addition of ADP (10 μmol/1) to platelet suspensions 5 s after thrombin did not prevent the deaggregation of ticlopidine-treated platelets. Thus, ticlopidine facilitates the deaggregation of thrombin-induced human platelet aggregates, most probably because it inhibits the effects of ADP on platelets.

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