The arterial complications of polycythaemia vera

Barabas, A. P.; Offen, Daniel; Meinhard, E

doi:10.1002/bjs.1800600305

Cited by 75 publications

(42 citation statements)

References 9 publications

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“…Published data indicate that thrombosis was the presenting feature in 12% to 49% of patients, 133,149,156,194,239,244,252,253 occurred in up to 40% during the course of the illness, 194 and was the cause of death in 20% to 40%. 145,149,156,239,244,254 Furthermore, in 2 studies, 14% to 15% of patients had a history of a thrombotic event at least 2 years before diagnosis.…”

Section: Phlebotomy and Polycythemia Vera: Women Are Not Small Men Thmentioning

confidence: 99%

“…145,149,156,239,244,254 Furthermore, in 2 studies, 14% to 15% of patients had a history of a thrombotic event at least 2 years before diagnosis. 244,248 In general, the central nervous system was the most frequent site of thrombosis, 156,244,253,255 arterial thrombosis was more common than venous 156,244,[253][254][255] and the latter was characteristically cerebral or intraabdominal and more frequent in women, 151,194,241 possibly in keeping with their higher incidence of splenomegaly at presentation. 239 Indeed, polycythemia vera was the most common cause of hepatic vein thrombosis in the Western hemisphere.…”

Section: Phlebotomy and Polycythemia Vera: Women Are Not Small Men Thmentioning

confidence: 99%

“…345,346 In this regard, it is worth noting that the frequency of coronary artery thrombosis in the PVSG-01 trial 243 was more in keeping with the latter than the frequency found by others for polycythemia vera patients in the absence of atherosclerotic disease. 253 Indeed, when one considers the vaso-occlusive havoc initiated by heparin-induced thrombocytopenia or thrombotic thrombocytopenic purpura, it becomes immediately obvious that platelet number alone is not a critical determinant of hypercoagulability.…”

Section: Fact Versus Fictionmentioning

confidence: 99%

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Polycythemia vera: myths, mechanisms, and management

Spivak

2002

Blood

405

331

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Section: Phlebotomy and Polycythemia Vera: Women Are Not Small Men Thmentioning

confidence: 99%

Section: Phlebotomy and Polycythemia Vera: Women Are Not Small Men Thmentioning

confidence: 99%

Section: Fact Versus Fictionmentioning

confidence: 99%

See 1 more Smart Citation

Polycythemia vera: myths, mechanisms, and management

Spivak

2002

Blood

405

331

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“…In earlier studies 79 -80 of this theory, patients who had experienced TIAs or who had carotid artery stenosis or occlusion were investigated. In a report 81 of 35 patients who had their blood pressure reduced with hexamethonium and tilting in an attempt to reproduce their TIAs, in only one patient did evidence of focal ischemia appear. The response of these patients was the usual one caused by diffuse cerebral ischemia-syncope or near-syncope.…”

Section: Hemodynamic Cause Of Strokementioning

confidence: 99%

The fallacy of the lacune hypothesis.

Millikan

Futrell

1990

Stroke

153

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We review the definition, pathogenesis, natural history, and prognosis and describe the first experimental model of lacunes. Defined pathologically or radiologically, lacunes are small cerebral infarcts which become cystic and are caused by occlusion of small arteries. The clinical definition of lacune is confused. The word "lacune" means a small stroke. While the immediate mortality rate from a small stroke is low, many patients are unable to return to work and the long-term prognosis is guarded. Photochemical damage to the carotid artery of rats produces microemboli to the brain, resulting in cavitary lesions resembling lacunes in humans. The "lacune hypothesis" is a fallacy because small cerebral infarcts are not caused solely by a combination of hypertension and small vessel disease, and the various "lacunar syndromes" are simply small strokes which should be investigated as such. (Stroke 1990;21:1251-1257) T he "lacune hypothesis" states that lacunes are caused by a combination of hypertension and characteristic vascular lesions involving single perforating brain arteries.

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“…It is widely accepted that the clinical course of polycythaemia vera (PV) is characterized by thrombotic complications which represent the main cause of morbidity and mortality [1,2]. It is also agreed that a high incidence of vascular complications is seen in PV patients with increased packed cell volume (PCV) [3].…”

Section: Introductionmentioning

confidence: 99%

The measurement of venous haematocrit in patients with polycythaemia vera

Andréasson

Wahlström²,

Jacobsson

et al. 1999

Journal of Internal Medicine

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Abstract. Andre Âasson B, Wahlstro Èm E, Jacobsson S, Bjo Èrkholm M, Samuelsson J, Birgega Êrd G, Wadenvik H, Kutti J (Medical Clinic, Ka Èrnsjukhuset, Sko Èvde; Sahlgrenska University Hospital, Go Èteborg; Karolinska Hospital, Stockholm; Huddinge University Hospital, Huddinge; and Akademiska Hospital, Uppsala, Sweden). The measurement of venous haematocrit in patients with polycythaemia vera. J Intern Med 1999; 246: 293±297.Objective. In clinical practice, patients with polycythaemia vera (PV) are monitored by measurement of venous packed cell volume (PCV). However, whereas treatment recommendations are still based upon studies in which the results were obtained with the centrifuged microhaematocrit, currently in most instances automated blood cell counters are used to calculate PCV. In a group of patients with polycythaemia we therefore compared the results obtained by the microhaematocrit method with PCV calculated by haematology analysers. Design. The study was carried out on a prospective basis. Duplicate venous blood samples were collected. The centrifuged microhaemotocrit was obtained by using an IEC Micro-MB Centrifuge. Depending on different routine methods used in the participating hospitals, the blood cell counter PCV was calculated using Coulter STKS, Bayer Technicon H2 or H3. Setting. Patients were included from four Swedish university hospitals: Akademiska (Uppsala), Huddinge and Karolinska (Stockholm) and Sahlgrenska (Go Èteborg). Subjects. Seventy-four patients with PV and 10 patients with secondary polycythaemia were included and a total of 150 duplicate blood samples were analysed from these subjects. Results. In the 150 measurements the mean blood cell counter calculated PCV was 0.448 6 0.037; the mean for centrifuged microhaematocrit was 0.467 6 0.037 and the difference between means was highly significant (P = 6.8 3 10 225 ). The means for centrifuged haematocrit and calculated PCV differed significantly in the groups of PV patients treated with phlebotomy only, hydroxyurea or radiophosphorous (P , 0.0001, respectively). In PV patients treated with a-interferon and in patients with secondary polycythaemia the difference in means did not reach statistical significance (P = 0.07 and P = 0.13, respectively). The groups of patients with MCV ,80 fL and $80 fL both presented significant differences between means for calculated PCV and centrifuged haematocrit. Conclusions. If PV patients are monitored with blood cell counter calculated PCV it appears that the therapeutic goal should be to maintain the calculated PCV below 0.43, provided the local differences in calculated PCV and centrifuged haematocrit are of the same magnitude as in this study.

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The arterial complications of polycythaemia vera

Cited by 75 publications

References 9 publications

Polycythemia vera: myths, mechanisms, and management

Polycythemia vera: myths, mechanisms, and management

The fallacy of the lacune hypothesis.

The measurement of venous haematocrit in patients with polycythaemia vera

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