Arterial thrombosis in essential thrombocythemia

Hussain, Shujaat; Schwartz, Joel; Friedman, Sandor A.; Chua, Segundina N.

doi:10.1016/0002-8703(78)90123-0

Cited by 50 publications

(19 citation statements)

References 15 publications

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“…Spontaneous platelet aggregation, proposed as a sign of platelet hyperreac tivity associated with thrombosis (28,35,38), was observed in 4 out of 7 pa tients with recurrent ischaemic attacks but also in 4 out of 9 patients with bleed ing tendency and in 3 asymptomatic cases. In a recent study spontaneous aggre gation was absent in 4 patients with ET and well-documented arterial thrombosis (18). In agreement with other reports (1, 3, 18, 24, 32) the most consistent defect of platelet aggregation observed in our patients was the lack of response to epinephrine whereas abnormalities of ADP-induced aggregation were found less frequently and defective collagen-induced aggregation was rare.…”

Section: Other Platelet Function Studiessupporting

confidence: 93%

Reduced Platelet Factor X-Activating Activity

Cortellazzo¹,

Colucci²,

Barbui³

et al. 1981

Pathophysiol Haemos Thromb

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A recently described platelet coagulant activity, factor X-activating activity (FXAA), was studied in 33 patients with polycythaemia vera and in 5 with essential thrombocythaemia, in order to gain information about possible mechanisms responsible for the haemostatic disorders observed in myeloproliferative diseases. Other parameters of platelet function including bleeding time, spontaneous and ADP-, epinephrine- or collagen-induced platelet aggregation, serotonin content and malondialdehyde (MDA) production in response to thrombin, were investigated simultaneously. Compared to the range obtained from 27 control subjects (60–150%), FXAA was low in all 9 patients with bleeding complications (range: 5–39%), in 1 out of 7 patients with thrombotic manifestations (range: 38–200%) and in 9 out of 22 patients without symptoms (range: 38–500%). Only the bleeding group differed significantly from each of the others. Moreover, of all patients with reduced FXAA, those with bleeding could be clearly distinguished from those without such symptoms on the basis of the degree of the defect. Increased FXAA (above 150%) was found in 2 out of 7 thrombotic patients and in 2 out of 22 asymptomatics. MDA production was significantly lower in the haemorrhagic group and enhanced in the thrombotic one as compared to control subjects or asymptomatic patients. However, a large area of overlap was observed between the four groups. None of the other platelet function parameters studied (bleeding time, platelet aggregation, platelet serotonin content) correlated with the clinical type of haemostatic complication. Our results suggest a significant association between reduced

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Section: Other Platelet Function Studiessupporting

confidence: 93%

Reduced Platelet Factor X-Activating Activity

Cortellazzo¹,

Colucci²,

Barbui³

et al. 1981

Pathophysiol Haemos Thromb

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“…Not infrequently, they may occur as the presenting manifestation of polycythemia vera and if superimposed on an already compromised vascular system could lead to a stroke, myocardial infarction, or peripheral gangrene. 352,355 While the mechanism for platelet-associated microvascular occlusion is unknown, it is associated with increased platelet thromboxane B formation 356 and increased platelet turnover. 357,358 Both can be reversed or prevented by aspirin-induced platelet inactivation or a reduction in platelet count, though not necessarily to normal, suggesting that both platelet activation and platelet number are important.…”

Section: Hemorrhage and Microvascular Thrombosismentioning

confidence: 99%

Polycythemia vera: myths, mechanisms, and management

Spivak

2002

Blood

408

331

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“…Left ventricule end diastolic pressure was 12 mmHg. 3 In the catheter laboratory, tirofiban hydrochlorur (thrombocyte glycoprotein receptor antagonist) infusion was started after bolus injection and ticlopidin 250 mg tablet 2 · 1 was added to treatment. At the same time, 0.014 inch floppy guide wire was moved forward to distal LAD and the direct stent implantation (4.0 · 16 mm NIR primo stent) was done to severe stenosis in LAD with maximum 12 atmospheric pressure for 25 seconds, and there was no residual stenosis ( Figure 6).…”

Section: Case Reportmentioning

confidence: 99%

Acute anterior myocardial infarction in a young man with essential thrombocythemia: A case report

et al. 2011

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Essential thrombocythemia is a rare cause of ischemic cardiovascular events. A 23-year-old young man was admitted with chest pain to the coronary care unit. Electrocardiogram revealed acute anterior myocardial infarction (AMI). He had a platelet count 748,000/mm 3 and detailed hematologic investigation led to the diagnosis of essential thrombocythemia. Coronary angiography revealed two vessel disease, with 95% stenosis in the middle of left anterior descending artery (LAD), thrombotic occlusion of distal LAD and recanalized thrombus in the right coronary artery (RCA). Apical akinesia and anterolateral hypokinesia was present by left ventriculography. In the same session, glycoprotein IIb/IIIa receptor antagonist drug (tirofiban) therapy was started and after 4 · 16 mm NIR primo stent was implanted in the middle of the LAD. With aspirin 300 mg/ day and ticlopidine 500 mg/day therapy, platelet count was found to be around 530,000-550,000/mm 3 . Clinical follow-up of the patient showed no chest pain. Six months after angioplasty, stent in the LAD and distal of LAD was found to be open with control coronary angiography. Recanalized thrombus in RCA showed no difference. Medical follow up is decided. We decided to report this case since essential thrombocythemia is a rare disease that may result in serious life-threatening cardiovascular complication.

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Arterial thrombosis in essential thrombocythemia

Cited by 50 publications

References 15 publications

Reduced Platelet Factor X-Activating Activity

Reduced Platelet Factor X-Activating Activity

Polycythemia vera: myths, mechanisms, and management

Acute anterior myocardial infarction in a young man with essential thrombocythemia: A case report

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