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(Stroke. 1995;26:995-999.)
© 1995 American Heart Association, Inc.

Articles

Platelet Size in Stroke Patients

T. O'Malley, MRCP(UK); P. Langhorne, PhD, MRCP(UK); R.A. Elton, PhD C. Stewart, MD, FRCP(UK)

From the Department of Medicine for the Elderly, Royal Infirmary of Edinburgh and Liberton Hospital (T.O'M., P.L., C.S.), and the Department of Medical Statistics, University of Edinburgh (R.A.E.), Edinburgh, Scotland.

Correspondence to Dr T. O'Malley, Cardiovascular Research Unit, Hugh Robson Bldg, George Sq, Edinburgh EH8 9XF, Scotland.

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Background and Purpose Large platelets are more reactive, produce more prothrombotic factors, and aggregate more easily. Platelet size can be readily estimated using automated analyzers, although accurate estimation depends on precise methodology. The disparate results from previous studies of mean platelet volume in cerebral ischemia may be explained by varying methodology. We have studied these variables using a precise methodology in an unselected group of stroke patients and compared them with data from age- and sex-matched control subjects.

Methods We studied 58 stroke patients consecutively admitted to a geriatric medical unit. Platelet variables were measured in the acute (<48 hours after stroke) and chronic (>6 months) phases of cerebral ischemia and compared with control variables. Control patients, admitted to the same unit, were of similar age and sex and without evidence of acute vascular events.

Results Mean platelet volume was higher in acute stroke (11.3 compared with 10.1 fL in control subjects; P<.001, Student's t test). In addition, platelet count was reduced in stroke patients (255x10⁹/L) compared with control subjects (299x10⁹/L; P<.01). Repeated measurements of mean platelet volume and platelet count in available survivors showed no significant change from the acute phase. Platelet changes did not relate to outcome measured at 6 months.

Conclusions With the use of more precise methodology, these findings show that an increase in mean platelet volume and a reduction in platelet count are features of both the acute and nonacute phases of cerebral ischemia. It is possible that these changes precede the vascular event, and further studies are warranted.

Key Words: cerebral ischemia • platelets • risk factors • thrombosis

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
The platelet plays a major role in the pathogenesis of vascular disease,¹ and mean platelet volume (MPV) is a physiological variable of hemostatic importance.² Large platelets are more reactive, produce more prothrombotic factors,^{3 4} and aggregate more easily.⁵ They also contain more dense granules and release more serotonin and ß-thromboglobulin than do small platelets.^{6 7} Platelets have no nuclei, and their characteristics are determined by their progenitor cell, the bone marrow megakaryocyte. It is generally accepted that platelet volume and density are determined at thrombopoiesis and that, once in the circulation, platelets do not change in size.^{8 9} The mechanisms controlling platelet production are obscure, although it has been suggested that both MPV and platelet count are under independent hormonal control.¹⁰

Increases in platelet volume have been reported in acute myocardial infarction,^{11 12 13 14 15} acute cerebral ischemia,^{16 17} and transient ischemic attack.¹⁸ A recent study has shown that an increase in MPV is an independent risk factor for death and recurrent vascular events after myocardial infarction.¹⁹ This association was of a magnitude similar to that of better-known risk factors such as elevated fibrinogen, blood viscosity, and white cell count. Studies that have measured platelet volume in acute ischemic stroke have shown inconsistent results that may relate to the highly selected patient populations or to the different methods of measuring MPV.^{16 17} Our aim was to study a broad spectrum of stroke patients using a more exact methodology for MPV measurement.

	Subjects and Methods

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We studied 58 consecutive admissions to a geriatric medical unit with acute ischemic hemispheric stroke as defined by the World Health Organization (mean age, 79 years; range, 65 to 93 years; 19 men, 39 women) and 50 control patients (mean age, 81 years; range, 67 to 97 years; 15 men, 35 women). Patients were studied within 48 hours of stroke, and available survivors were studied after 6 months (median, 10 months). The clinical characteristics of the patient and control groups are shown in Table 1. The control subjects were less acutely ill and were admitted predominantly for rehabilitation (38%; Table 1). They were consecutive admissions to the same unit from the same demographic area; they had no clinical evidence of active vascular disease, previous cerebral vascular disease, malignancy, or infection and were not taking medications known to affect platelet function. They served as a reference population who were not quite as ill as the patients but nevertheless had undergone the stress of an unplanned hospital admission. They were similar with regard to age, sex, vascular risk factors, number of additional medical problems, and medications. Blood was withdrawn from the antecubital vein into the potassium salt of ethylenediaminetetraacetic acid (K₂EDTA) and was stored at room temperature. Platelet volume was measured in all patients at 24 hours after venesection. MPV and platelet count were measured using a Sysmex 8000 autoanalyzer (TOA Medical Electronics UK Ltd) that uses aperture-impedance technology to size platelets. In addition to this, cells are hydrodynamically focused through a small aperture, and a voltage pulse is generated that is proportional in size to the volume of the cell. Mobile "autodiscriminators" distinguish between machine noise at the lower end and red blood cells at the upper end of each individual platelet volume distribution. MPV is calculated by the following formula: MPV (fL)=Pct (%)x1000÷Plt (x10³/µL), where Plt is the platelet count and is the number of particles between the upper and lower discriminators, Pct is the platelet crit and is calculated electronically from the raw histogram data. Stroke patients were divided into subgroups according to a clinical classification²⁰ of (1) total middle cerebral circulation infarct: patients with new higher cerebral dysfunction, homonymous hemianopsia, and ipsilateral motor and/or sensory deficit of at least two areas of the face, arm, and leg; (2) partial middle cerebral circulation infarct: only two of the three components of the latter or cortical deficit alone; and (3) lacunar infarct: patients presenting with a pure motor stroke, pure sensory stroke, sensorimotor stroke, or ataxic hemiparesis. Outcome was determined at 6 months using a modified Rankin scale (score of 3 to 5, dependent; 0 to 2, independent).

View this table: [in this window] [in a new window]   Table 1. Characteristics of the Study Populations

Results were compared using Student's paired and unpaired t tests. Multiple logistic regression analysis was applied to determine the relative importance of different factors in predicting stroke.

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Table 2 shows hematologic and biochemical variables in acute stroke patients and control subjects. MPV was significantly raised and platelet count significantly reduced in acute stroke patients compared with control subjects. The hemoglobin, hematocrit, and admission random glucose levels of stroke patients were greater than those of control subjects. Table 3 shows platelet variables in the stroke subtypes and their relation to outcome; there was no significant difference in MPV or platelet count between large-vessel or lacunar strokes, nor were there significant differences among dead, dependent, or independent patients when assessed at 6 months. There was no significant difference in MPV in those with previous stroke (11.39±0.87) compared with no previous stroke (11.29±0.85; n=18 versus n=40, respectively) or those taking aspirin at the time of stroke (11.21±0.73) compared with no aspirin (11.38±0.90; n=19 versus n=39, respectively). Of the clinical variables shown in Table 1, only the average systolic blood pressure was shown to be significantly different. Multiple regression analysis showed that MPV was significantly associated with stroke (P<.01) even after adjustment for other factors that differed between the two groups (platelet count, hemoglobin, hematocrit, systolic blood pressure, and glucose).

View this table: [in this window] [in a new window]   Table 2. Hematology and Biochemical Variables in Acute Stroke Patients and Control Subjects

View this table: [in this window] [in a new window]   Table 3. Mean Platelet Volume and Platelet Count in Subtypes of Stroke and Relation to Outcome

There was a significant negative (r=-.37, P<.003; n=58) correlation between platelet count and MPV in stroke patients. There was no such relation in control subjects (r=.07, P=.61; n=50). There was no significant difference in estimated platelet mass (MPVxplatelet count), although MPV was clearly greater in stroke patients, as shown in Fig 1. Follow-up blood samples were possible in 29 of 38 (76.3%) survivors. MPV and platelet count did not change significantly between the acute stroke period and late follow-up (median, 10 months; range, 6 to 16 months). Fig 2 shows changes in MPV (0.6±1.7; mean±95% confidence interval), and Fig 3 shows changes in platelet count (56±101)x10⁹/L.

View larger version (11K): [in this window] [in a new window]   Figure 1. Graph shows mean platelet volume (MPV) and platelet mass in stroke patients and control subjects. indicates stroke patients; , control subjects.

View larger version (21K): [in this window] [in a new window]   Figure 2. The change in mean platelet volume in individual stroke patients between the acute and poststroke phases. Error bars indicate mean±SD; , patients for whom follow-up data were not available.

View larger version (23K): [in this window] [in a new window]   Figure 3. The change in platelet count in individual stroke patients between the acute and chronic phase. Error bars indicate mean±SD; , patients for whom follow-up data were not available.

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Previous studies have documented various platelet abnormalities in cerebrovascular disease, eg, circulating platelet aggregates,²¹ platelet aggregation,²² and increased release of platelet-specific -granule proteins,²³ thereby indicating platelet activation. Others have shown that platelet aggregation is not increased in the acute phase but occurs several days after the event.²⁴ This lack of activation in the acute phase has been attributed to platelet consumption during the event. However, the lack of agreement between these studies may relate to specimen handling and different methodology. Earlier studies of platelet size relied on microscopic evaluation of platelet diameters until accurate measurement became available with the development of aperture-impedance cell counting systems.

Two principal technologies are used to size platelets: aperture impedance of Coulter and Sysmex and flow cytometry laser optics used by Technicon. In the Coulter series, cells are held in fluid suspension and flowed through a small aperture, thereby creating a change in voltage proportional to particle size. A raw histogram is generated, and a log-normal curve is fitted to the data. Platelet count is derived from this together with the MPV, which is calculated by numerical integration. Similarly, the Sysmex measures parameters with cells in fluid suspension, although in addition the cells are hydrodynamically focused, ensuring that cells travel in a straight line through the aperture. This prevents cells flowing through at the edge of the aperture and causing spurious changes in the electrical field. It also differs from Coulter in that the upper and lower discriminators are both mobile. The distribution curve obtained is thus the actual data and not a fitted curve. MPV is calculated from the curve by a formula (see "Subjects and Methods"). In contrast, Technicon instruments use laser-optic technology to measure the size and granularity of cells in suspension. A beam of light is passed through cells, and the amount of forward scatter is proportional to size of particles, whereas side scatter equates to density or granularity. A platelet histogram is derived from the data, and MPV is calculated as the mode. Differences of up to 40% have been found when Coulter and Technicon results have been compared.²⁵ Further differences were noted with regard to anticoagulants used: over a 39-hour period, MPV increased in EDTA by 17% when measured in the Coulter compared with a 22% decrease when the same sample was analyzed by Technicon.²⁵ On exposure to EDTA, the most commonly used anticoagulant, there is an immediate change in shape of platelets from discoid to spherical.²⁵ Furthermore, EDTA is thought to increase intracellular cyclic AMP and change plasma membrane permeability.^{26 27} This explains the progressive platelet swelling and concomitant reduction in density with time seen with the anticoagulant and explains the differences in MPV values observed between aperture-impedance and light-scattering methods. The effects of EDTA on MPV using the Sysmex autoanalyzer, as we used in this study, have been documented. Similar to Coulter systems, we found time- dependent changes using EDTA, which were maximal in the first 7 hours and stabilized after 24 hours.²⁸ Thus, to standardize methodology in a study, it is imperative to state the anticoagulant used, time from venipuncture, cell-sizing technology, and temperature for storage of bloods.^{29 30 31}

Our results do not agree with the earlier studies that have suggested that platelet changes occur as a result of acute stroke.^{16 17} Moreover, these studies may have failed to recognize time-dependent changes in MPV that occur with both EDTA and citrate anticoagulants.³¹ D'Erasmo et al¹⁶ measured MPV within 2 hours of venesection, when changes in platelet volume are likely to be greatest and therefore most unpredictable. A second study found a decrease in platelet count, MPV, and platelet crit (percentage volume of platelets, MPVxplatelet count) in patients with lacunar infarction.¹⁷ These authors postulated a selective loss of large active platelets to explain the decreased MPV. This study did not specify the time after venipuncture at which samples were analyzed or the temperature at which they were stored. We have used a methodology with a fixed time of analysis after venipuncture, and we maintained samples at room temperature. D'Erasmo et al¹⁶ have further suggested that the reduction in platelet count may be an early predictor of poor outcome, although the results in our less selective population do not agree with this. We found no relationship with outcome but acknowledge that our numbers are too small to provide accurate data on mortality.

Circulating platelet count shows a wide range, which was previously interpreted as indicating that platelet production might not be tightly regulated. In 1974, it was first observed that platelet count and MPV were inversely related.³² Further studies confirmed this and showed little variability in both variables over time, suggesting that platelet production is regulated to maintain a constant platelet mass (the product of platelet count and MPV).^{3 33 34} A rise in MPV and a reduction in platelet count have been described previously in acute myocardial infarction, persisting for up to 6 weeks after infarct.^{11 12} These abnormalities have been related to changes at the bone marrow level.¹¹ Our findings indicate that similar changes may occur in acute cerebral infarction, which persist for at least 6 months after infarct. Our results also suggest that stroke patients show a significant change in the relationship that exists between MPV and platelet count,³⁵ even though the total platelet mass did not change. We found no difference in platelet mass, unlike a previous study that showed a reduction,¹⁷ but we did see a clear increase in MPV compared with the reference population (Fig 1). We have shown changes in this axis in stroke patients and have further demonstrated by multiple logistic regression analysis that MPV is the most important significant variable of the factors associated with stroke. It has been suggested that MPV and platelet count are under independent hormonal control,¹⁰ although control of platelet production remains obscure. Some have suggested a role for interleukin-6, interleukin-3, thrombopoietin, and colony-stimulating factors.^{36 37 38 39} It is, however, generally accepted that platelet volume and count are determined at thrombopoiesis,^{8 9} and as in ischemic heart disease, these findings may implicate primary changes occurring at the bone marrow (megakaryocyte) level. Moreover, an increase in megakaryocyte size and ploidy (DNA content) coincides with an increase in MPV.⁴⁰ This direct association suggests the possibility that activation of megakaryocytes, as heralded by an increase in MPV, is a feature of ischemic stroke.

There is indirect evidence that the changes in MPV and platelet count are likely to have preceded the vascular event and are unlikely to be due to platelet consumption at the infarct site. Because the average life span of the platelet is about 8 days, the elevated MPV seen within the first 48 hours after stroke probably represents platelets released before infarction. Furthermore, it is unlikely that platelet consumption due to localized thrombosis would affect peripheral venous estimations of platelet variables. The observation that there was no difference in MPV between large cortical strokes and smaller lacunar infarctions also lends support to this view. In addition, the fact that the observed increase in MPV and reduction in platelet count have remained unchanged in poststroke survivors is further evidence that changes are likely to precede the acute event. We suggest that large platelets may promote the thrombotic event in a susceptible individual. We suggest that the increase in MPV may have contributed to the development of the stroke rather than simply being a consequence of the acute event itself.

In conclusion, this study has shown an elevation of MPV and reduction of platelet count in acute stroke that persist long after the acute event. Within this relationship and confounding for other significant variables in univariate analysis, an increase in MPV is independently associated with stroke. The observations here suggest a role for larger platelets in the genesis of cerebral thrombosis and are likely to represent changes occurring at thrombopoiesis. Further research is required into the role of platelet volume in stroke pathology, outcome, and, most importantly, in individuals at risk for stroke.

	Acknowledgments

 
We thank Dr Christopher Ludlam and Dr Alistair Parker for putting the facilities of the Department of Haematology, Royal Infirmary, Edinburgh, at our disposal. We thank the paramedical staff at Liberton Hospital for their generous help. We also thank Audrey Trotter for typing the manuscript.

Received August 13, 1994; revision received December 20, 1994; accepted February 20, 1995.

	References

Top Abstract Introduction Subjects and Methods Results Discussion References

 

1. Ross R. The pathogenesis of atherosclerosis: an update. N Engl J Med. 1986;314:488-500. [Medline] [Order article via Infotrieve]
2. Martin JF, Trowbridge A, eds. Platelet Heterogeneity: Biology and Pathology. London, UK: Springer-Verlag; 1990.
3. Jakubowski JA, Thomson CB, Vaillancourt R, Valeri CR, Deykin D. Arachidonic acid metabolism by platelets of differing size. Br J Haematol. 1983;53:503-511. [Medline] [Order article via Infotrieve]
4. Martin JF, Trowbridge EA, Salmon G, Plumb J. The biological significance of platelet volume: its relationship to bleeding time, platelet thromboxane B₂ production and megakaryocyte nuclear DNA concentration. Thromb Res. 1983;32:443-460. [Medline] [Order article via Infotrieve]
5. Haver VM, Gear ARL. Functional fractionation of platelets. J Lab Clin Med. 1981;97:187-204.[Medline] [Order article via Infotrieve]
6. Thompson CB, Eaton KA, Princiotta SM, Kushkin CA, Valeri CR. Size dependent platelet subpopulations: relationship of platelet volume to ultrastructure, enzymatic activity and function. Br J Haematol. 1982;50:509-519. [Medline] [Order article via Infotrieve]
7. Thompson CB, Jakubowski JA, Quinn PG, Deykin D, Valeri CR. Platelet size as a determinant of platelet function. J Lab Clin Med. 1983;101:205-213. [Medline] [Order article via Infotrieve]
8. Thomson CB, Love DG, Quinn PG, Valeri CR. Platelet size does not correlate with platelet age. Blood. 1983;62:487-494. [Abstract/Free Full Text]
9. Martin JF, Pennington DG. The relationship between the age and density of circulating 51-Cr labelled platelets in the sub-human primate. Thromb Res. 1983;30:157-164. [Medline] [Order article via Infotrieve]
10. Martin JF. The relationship between megakaryocyte ploidy and platelet volume. Blood Cells. 1989;15:108-117. [Medline] [Order article via Infotrieve]
11. Martin JF, Plumb J, Kilby RS, Kishk YT. Changes in platelet volume and density in myocardial infarction. Br Med J. 1983;287:456-459.
12. Cameron HA, Philips R, Ibbotson RM, Carson PHM. Platelet size in myocardial infarction. Br Med J. 1983;287:449-451.
13. Trowbridge EA, Slater DN, Kishk YT, Woodcock BW, Martin JF. Platelet production in myocardial infarction and sudden cardiac death. Thromb Haemost. 1984;52:167-171. [Medline] [Order article via Infotrieve]
14. Kishk YT, Trowbridge EA, Martin JF. Platelet volume subpopulation in acute myocardial infarction: an investigation of their heterogeneity for smoking and infarct size and site. Clin Sci. 1985;68:419-425.
15. Erne P, Wardle J, Sanders K, Lewis SM, Maseri A. Mean platelet volume and size distribution and their sensitivity to agonists in patients with coronary artery disease and congestive heart failure. Thromb Haemost. 1988;59:259-263. [Medline] [Order article via Infotrieve]
16. D'Erasmo E, Alberti G, Celi FS, Romagnolie E, Veici E, Mazzuoli GF. Platelet count, mean platelet volume and their relation to prognosis in cerebral infarction. J Intern Med. 1990;227:11-14. [Medline] [Order article via Infotrieve]
17. Toghi H, Suzuki H, Tamura K, Kimura B. Platelet volume, aggregation and adenosine triphosphate release in cerebral thrombosis. Stroke. 1991;22:17-21. [Abstract/Free Full Text]
18. D'Erasmo E, Acca M, Pisani D, Spagna G, Volpe M. Acute platelet changes in transient ischaemic attacks and in stroke. In: Program and abstracts of the international stroke meeting; May 1993; Geneva, Switzerland. Abstract.
19. Martin JF, Bark PM, Burr ML. Influence of platelet size on outcome after myocardial infarction. Lancet. 1991;338:1409-1411. [Medline] [Order article via Infotrieve]
20. Bamford J, Sandercock P, Dennis M, Burn J, Warlow C. Classification and natural history of clinically identifiable subtypes of cerebral infarction. Lancet. 1991;337:1521-1526. [Medline] [Order article via Infotrieve]
21. Andersen LA, Gormsen J. Platelet aggregation and fibrinolytic activity in transient cerebral ischaemia. Acta Neurol Scand. 1977;55:76-82.
22. Dougherty JH Jr, Levy DE, Weksler BB. Platelet activation in acute cerebral ischaemia. Lancet. 1977;1:821-824. [Medline] [Order article via Infotrieve]
23. Shah AB, Beamer N, Coull BM. Enhanced in vivo platelet activation in subtypes of ischaemic stroke. Stroke. 1985;16:643-647. [Abstract/Free Full Text]
24. O'Brien JR. The role of platelets in the thrombotic diathesis. Blood Vessels. 1980;11:1-15.
25. Trowbridge EA, Reardon DN, Hutchinson D, Pickering D. The light scattering and aperture impedance technologies. Clin Phys Physiol Meas. 1985;6:221-238. [Medline] [Order article via Infotrieve]
26. Suvorov AV, Markosyar RA. Some mechanisms of the effect of EDTA on platelet aggregation. Bull Exp Biol Med. 1981;91:651-653.
27. Lusher EF. Thrombosis: Mechanism and Control. Stuttgart, Germany; 1975:251-260.
28. O'Malley T, Ludlam CA, Fox KAA, Elton RA. Measurement of platelet volume using a variety of anticoagulants. Br J Haematol. 1994;86(suppl 1):55. Abstract.
29. Jackson SR, Carter JM. Platelet volumes: laboratory measurement and clinical application. Blood Rev. 1993;7:104-113. [Medline] [Order article via Infotrieve]
30. Thompson CB, Diaz T, Quinn PG, Lapins M, Kurtz SR, Valeric R, Thomson CB. The role of anticoagulation in the measurement of platelet volumes. Am J Clin Pathol. 1983;80:327-332. [Medline] [Order article via Infotrieve]
31. Bath PW. The routine measurement of platelet size using sodium citrate alone as the anticoagulant. Thromb Haemost. 1993;70:687-690. [Medline] [Order article via Infotrieve]
32. O'Brien JR, Jamieson S. A relationship between platelet volume and platelet number. Thromb Diath Haemorrh. 1974;31:363-364. [Medline] [Order article via Infotrieve]
33. Frojmovic MM, Milton JG. Human platelet size, shape, and related functions in health and disease. Physiol Rev. 1982;62:185-261. [Free Full Text]
34. Thompson CB, Jakubowski JA. The pathophysiology and clinical relevance of platelet heterogeneity. Blood. 1988;72:1-8. [Abstract/Free Full Text]
35. Giles C. The platelet count and mean platelet volume. Br J Haematol. 1981;48:31-37. [Medline] [Order article via Infotrieve]
36. Ishibashi T, Kimura H, Shikama H, Uchida T. Interleukin-6 is a potent thrombopoietic factor in vivo in mice. Blood. 1989;74:1241-1244. [Abstract/Free Full Text]
37. Asano S, Okasso A, Ozawa K. In vivo effects of recombinant human IL-6 in primates: stimulated production of platelets. Blood. 1990;75:1602-1605. [Abstract/Free Full Text]
38. Williams N, Gill K, Yasmeen D, McNiece I. Murine megakaryocyte colony stimulating factor: its relationship to interleukin-3. Leuk Res. 1985;9:1487-1489. [Medline] [Order article via Infotrieve]
39. Hoffman R. Regulation of megakaryocytopoiesis. Blood. 1989;74:1196-1212. [Free Full Text]
40. Bessman JD. The relationship of megakaryocyte ploidy to platelet volume. Am J Hematol. 1984;16:161-170.[Medline] [Order article via Infotrieve]

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by O'Malley, T. Articles by Stewart, C. Search for Related Content PubMed PubMed Citation Articles by O'Malley, T. Articles by Stewart, C.