Hyperaggregability of Platelets in Thromboembolic Disorders

Yamazaki, Hiroh; Takahashi, Takéo; Sano, Tadahiro

doi:10.1055/s-0038-1651449

Cited by 63 publications

(15 citation statements)

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“…Tests of platelet activation were not performed. Transient platelet hyperaggregability occurs [34]. Acute hemorrhage may cause reactive thrombocytosis, but this was not the cause in any of our patients.…”

Section: Discussionmentioning

confidence: 56%

Cerebral and retinal vascular complications of inflammatory bowel disease

Schneiderman

Sharpe

Sutton

1979

Annals of Neurology

120

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Recurrent retinal branch artery occlusions, carotid thromboembolism, cerebral venous thrombosis, transient brainstem ischemia, and massive brainstem and cerebral infarction complicated the course of inflammatory bowel disease in 5 patients. Three patients had ulcerative colitis and 2 had regional enteritis. The usual risk factors for stroke were absent. Neuropathological examination in 1 patient showed in situ thrombosis of small cerebral and brainstem arteries and veins. Coagulation studies showed thrombocytosis, short partial thromboplastin times, and elevation of fibrinogen and Factor VIII levels. Platelet counts and coagulation factors returned toward normal after control of intestinal inflammation in each of the 4 surviving patients. Inflammatory bowel disease can be accompanied by a hypercoagulable state that predisposes to stroke.

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Section: Discussionmentioning

confidence: 56%

Cerebral and retinal vascular complications of inflammatory bowel disease

Schneiderman

Sharpe

Sutton

1979

Annals of Neurology

120

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“…It has been reported that circulating platelet aggregates occur more frequently in patients with transmural myocardial infarction than in patients with subendocardial infarction; 108 ' 274 this is somewhat unexpected because the former condition is more frequently associated with coronary artery thrombosis, and it has been suggested that subendocardial infarction might be asso- 227 Goldenfarbetal. 103 Sano et al 270 Steele et al 304 Salky and Dugdale 267 Frishman et al 97 Yamazaki et al 346 Gormsen et al 104 Zahavi 348 Knudsen et al 162 No 342 Gjesdal 102 Guyton and Willerson 108 Rohrer et al 257 Lowe et al 176 Schwartz et al 274 Amodeo et al 4 Salem et al 264 No ciated with occlusion of the distal coronary vasculature with platelets or platelet-fibrin microthrombi.…”

Section: Referencementioning

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 aggregation curves induced by ADP, adrenaline and collagen were recorded by a platelet aggregation meter (Model DP 247E, Sienco Co., Morrison, Colo., USA). The precise method applied and parameters measured in the aggregation curves have been described in detail previously (Yamazaki et al 1975). A line was tangentially drawn at the steepest part of tracing which occured immediately after the addition of reagents.…”

Section: Methodsmentioning

confidence: 99%

“…The ratio of bp, bs, and b5 to the deflection of platelet free plasma was taken and expressed in percentages. The rate of appearance of bs in the aggregation curves induced by ADP or adrenaline was also counted (Yamazaki et al 1975). Lag time was also measured in collageninduced aggregation curve.…”

Section: Methodsmentioning

confidence: 99%

Changes in Platelet Aggregability after Ovariectomy

et al. 1979

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SummaryChanges in platelets in 48 patients with uterine myoma before and after hysterectomy with and without ovariectomy were examined. Bilateral ovariectomy in 25 cases (ovariec-tomized group) and unilateral or non-ovariectomy in 23 cases (control group) were performed at the hysterectomy. Platelet count and an appearance rate of secondary aggregation decreased at one day after and increased at one week after the operation, similarly in both the ovariectomized and the control group. The appearance rate of secondary aggregation was reflected in an intensity of aggregation at 5 min after the addition of reagent to PRP. At one month after the operation, the appearance rate of secondary aggregation induced by 3 μM ADP showed a statistically significant decrease in comparison with the preoperation value (P <0.05) and the enhancement of 5-min aggregation was still observed in the control group, while ceased in the ovariectomized group. The difference between the two groups was significant (P < 0.05). There was almost no change in the speed and intensity of primary and secondary aggregation during the observation period. No significant differences in collagen-induced aggregation were noted between the two groups. The results suggest that ovarian hormones, mainly estrogen, facilitate platelet activation which is mediated by the so-called secondary aggregation.

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Hyperaggregability of Platelets in Thromboembolic Disorders

Cited by 63 publications

References 0 publications

Cerebral and retinal vascular complications of inflammatory bowel disease

Cerebral and retinal vascular complications of inflammatory bowel disease

Platelet Consumption in Cardiovascular Disease

Changes in Platelet Aggregability after Ovariectomy

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