Platelet aggregability measured by screen filtration pressure method in cerebrovascular diseases.

Kobayashi, I; Fujita, Tsuyoshi; Yamazaki, Hiroh

doi:10.1161/01.str.7.4.406

Cited by 20 publications

(5 citation statements)

References 13 publications

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“…Thus even the younger patients with primary haemorrhagic stroke have platelets that are hyporeactive. Previous studies of platelet behaviour in cerebral haemorrhage are scanty; Petrova et al (13) and Kobayashi et al (14) indicated that platelets may be less active after haemorrhagic than occlusive stroke but their patients were less clearly charac terised than ours, in whom we were able to define the nature of the stroke by CT scanning or at necropsy. From our observations we would put forward the following hypothesis; patients with major platelet abnormalities (idiopathic thrombocytopenia, and congenital platelet defects) can develop intracranial haemorrhage in the absence of any other risk factors.…”

Section: Discussioncontrasting

confidence: 65%

ADP-Induced Platelet Release Reaction in Acute Stroke

et al. 1983

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SummaryThe extent of the ADP-induced platelet release reaction has been determined in 107 patients admitted to hospital with acute stroke. In 43 of the patients a precise diagnosis was obtained and in those with proven thromboembolic stroke the mean extent of the release reaction was significantly higher than for those with either primary haemorrhagic stroke or those with subarachnoid haemorrhage. Enhanced platelet reactivity was also found in the patients in whom a precise diagnosis could not be obtained, most of whom probably had cerebral infarction. Comparison of the results obtained for patients with stroke with those obtained for individuals who had not experienced a stroke showed that thromboembolic stroke is associated with platelet hyperactivity while haemorrhagic stroke is associated with platelet hypoactivity. The part that abnormalities of platelet behaviour, whether causal or consequential, might play in occlusive stroke and intra-cranial haemorrhage is discussed and the need for large scale prospective studies is emphasised.

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Section: Discussioncontrasting

confidence: 65%

ADP-Induced Platelet Release Reaction in Acute Stroke

et al. 1983

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“…Increased platelet aggregation, both in TIAs and in major strokes, has been reported by some investigators [10,14], whereas others were able to confirm these findings in patients with TIAs but not in those affected by cerebral infarction [7]. These last findings also agree with the considerable discordances among several clinical trials [1][2][3]5,6,[8][9][10]12,13,16] concerned with the prevention of recurrence TIAS and/or occurrence of ischemic strokes in patients subjected to antiplatelet treatments. Moreover, some reports suggest that no prediction of the risk of subsequent stroke or death is provided by the data from in vitro measurements of platelet aggregation [15].…”

Section: Discussionsupporting

confidence: 65%

A multiparametric index of platelet in vitro aggregation in cerebrovascular disease

Gazzaniga

Ferroni

Minà³

et al. 1987

Ital J Neuro Sci

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148 patients with various forms of cerebrovascular disease (CVD) were studied by means of a multiparametric analysis of in vitro platelet aggregation, based on the following six parameters: ADP and epinephrine primary and secondary aggregation thresholds and percent maximum aggregation induced by optimal concentrations of ADP and epinephrine. These patients were assigned to four study groups, according to clinical diagnosis supported by CT scan, of transient ischemic attack and reversible neurological deficit (TIA-RIND), or completed stroke, in the presence or absence respectively of antiplatelet medical treatment at the time of the study. A statistically significant increase of the in vitro platelet aggregation was found in 44.4% of the untreated TIA-RIND patients and in 33.9% of the untreated stroke patients. However this last group showed a higher percentage of very marked hyperaggregation. Differences between the two treated study groups and controls were not significant. No difference was found in collagen- and ristocetin-induced aggregation between the patient groups and the controls.

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“…Danta 65 Sano et al 271 Kobayashi et al 163 Andersen and Gormsen 5 Couch and Hassanein 60 Louet al 175 Dougherty et al 74 Zahavi 348 TenCateetal. 314 No.…”

Section: Aggregationmentioning

confidence: 99%

Platelet Consumption in Cardiovascular Disease

Ag¹,

Ac²,

Genton³

1982

Semin Thromb Hemost

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Many tests have been devised to investigate the role of platelets in arterial or venous thromboembolism. The mechanisms of platelet reactivity that the tests have measured have been variable and the early studies have been of little value in determining the contribution of platelet consumption in thromboembolic diseases. More recently, tests of in vivo platelet release and of platelet survival and turnover have been introduced and thought to be of great potential in the investigation of thromboembolic disorders. However, the data published thus far using more tests are far from conclusive that platelet activation and consumption occurs in thromboembolic disorders associated with arteriosclerosis. It may be that they are neither sensitive nor specific enough to detect minor changes in platelet activation. There is, however, some consistency that in conditions involving the larger vessels, prosthetic surfaces, or in association with active and recurrent venous thromboembolism, platelet release and platelet consumption measured by platelet survival time may occur. In particular, the abnormal results are consistently found in acute and recurrent venous thromboembolism, cardiac valve replacement with the older prosthetic devices, and arteriosclerosis of the larger arteries with clinical episodes of thromboembolism. However, in coronary artery disease, cerebrovascular disease, and peripheral vascular disease, the data are inconclusive, probably because the tests lack sensitivity. In addition, the value of the tests in the management of patients with thromboembolic disorders appears to be limited.

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Platelet aggregability measured by screen filtration pressure method in cerebrovascular diseases.

Cited by 20 publications

References 13 publications

ADP-Induced Platelet Release Reaction in Acute Stroke

ADP-Induced Platelet Release Reaction in Acute Stroke

A multiparametric index of platelet in vitro aggregation in cerebrovascular disease

Platelet Consumption in Cardiovascular Disease

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