The Biology of Platelet Volume Heterogeneity

Thompson, Craig B.; Monroy, Rod; Skelly, R R; Quinn, Patrick G.; Jakubowski, Joseph A.

doi:10.1007/978-1-4471-1763-6_2

Cited by 9 publications

(10 citation statements)

References 21 publications

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“…We observed a significant inverse relationship between platelet count and MPV. The relationship between platelet count and MPV is incompletely understood; several studies (including ours) reported an inverse correlation between MPV and platelet count, while one study found that platelet count and platelet volume both increase during stimulated thrombopoiesis, suggesting that platelet count and volume may be regulated by independent mechanisms [31,32]. Consistent with other studies, the present analysis found no significant association between platelet count and PAD (data not shown).…”

Section: Discussionsupporting

confidence: 86%

Mean platelet volume and prevalence of peripheral artery disease, the National Health and Nutrition Examination Survey, 1999–2004

et al. 2010

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Objectives We sought to determine whether mean platelet volume (MPV) is associated with the prevalence of peripheral artery disease (PAD). Background Platelets play a pivotal role in the pathogenesis of atherosclerosis and PAD. MPV, a measure of platelet size available in every blood count, is increasingly recognized as an important marker of platelet activity. Methods We analyzed data from 6354 participants aged 40 years and older from the 1999 to 2004 National Health and Nutrition Examination Survey (NHANES), a nationally representative sample of the US population. PAD was defined as an ankle brachial index ≤0.90 in either leg. Odds ratios and 95% confidence intervals were estimated by logistic regression. Results The prevalence of PAD in the cohort was 5.7%. MPV was significantly associated with PAD prevalence (tertile 1 – 4.4%, tertile 2 – 6.1%, tertile 3 – 7.0%, P for trend = 0.003). After adjustment for age, sex, and race, the odds ratio of PAD comparing the highest tertile to the lowest tertile was 1.57 (95% confidence interval 1.15–2.13). After further adjustment for smoking status, hypertension, hypercholesterolemia, diabetes, glomerular filtration rate, body mass index, and platelet count the corresponding odds ratio was 1.58 (95% confidence interval 1.14–2.19). The addition of triglycerides, hemoglobin A1c, and C-reactive protein did not affect the results. The significant association between MPV and PAD was unchanged when MPV was used as a continuous variable. Conclusions Mean platelet volume is independently associated with PAD. These findings support the hypothesis that platelet size is an independent predictor of increased risk for PAD.

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Section: Discussionsupporting

confidence: 86%

Mean platelet volume and prevalence of peripheral artery disease, the National Health and Nutrition Examination Survey, 1999–2004

et al. 2010

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“…Several studies have reported that increases in platelet volume are often associated with decreases in platelet count [14,24,39], perhaps as a result of small platelets being consumed in order to maintain a constant platelet functional mass [61]. Conversely, one study found that platelet count and platelet volume both increase during stimulated thrombopoiesis [62], indicating that platelet count and volume may be regulated by independent mechanisms [63]. The relationship between MPV and platelet count is not completely understood.…”

Section: Discussionmentioning

confidence: 99%

Mean platelet volume as a predictor of cardiovascular risk: a systematic review and meta‐analysis

Chu

Becker

Berger

et al. 2010

Journal of Thrombosis and Haemostasis

903

781

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Summary Aim To determine whether an association exists between mean platelet volume (MPV) and acute myocardial infarction (AMI) and other cardiovascular events. Platelet activity is a major culprit in atherothrombotic events. MPV, which is widely available in clinical practice, is a potentially useful biomarker of platelet activity in the setting of cardiovascular disease. Methods and Results We performed a systematic review and meta-analysis investigating the association between MPV and AMI, all-cause mortality following myocardial infarction, and restenosis following coronary angioplasty. Results were pooled using random-effects modeling. Pooled results from 16 cross-sectional studies involving 2809 patients investigating the association of MPV and AMI indicated that MPV was significantly higher in those with AMI than those without AMI [mean difference 0.92 fL, 95% confidence interval (CI) 0.67–1.16, P < 0.001). In subgroup analyses, significant differences in MPV existed between subjects with AMI, subjects with stable coronary disease (P < 0.001), and stable controls (P < 0.001), but not vs. those with unstable angina (P = 0.24). Pooled results from three cohort studies involving 3184 patients evaluating the risk of death following AMI demonstrated that an elevated MPV increased the odds of death as compared with a normal MPV (11.5% vs. 7.1%, odds ratio 1.65, 95% CI 1.12–2.52, P = 0.012). Pooled results from five cohort studies involving 430 patients who underwent coronary angioplasty revealed that MPV was significantly higher in patients who developed restenosis than in those who did not develop restenosis (mean difference 0.98 fL, 95% CI 0.74–1.21, P < 0.001). Conclusions Elevated MPV is associated with AMI, mortality following myocardial infarction, and restenosis following coronary angioplasty. These data suggest that MPV is a potentially useful prognostic biomarker in patients with cardiovascular disease. Whether the relationship is causal, and whether MPV should influence practice or guide therapy, remains unknown.

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“…39 Taken together these findings suggest that platelet number and size are at least partly under independent control during platelet production. 40 They can theoretically occur independently, but they occur together chronologically on most occasions. 41 Platelets produced under conditions of stimulated platelet production, called "stress" platelets by Penington et al 38 show an increase in the MPV compared with normal circulating platelets.…”

Section: The Physiology Of Platelet Size Heterogeneity and Its Biologmentioning

confidence: 99%

A Role for Changes in Platelet Production in the Cause of Acute Coronary Syndromes

Loo

Martin

1999

ATVB

124

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Abstract-Platelets are heterogeneous with respect to their size, density, and reactivity. Large platelets are more active hemostatically, and platelet volume has been found to be increased both in patients with unstable angina and with myocardial infarction. Furthermore, platelet volume is a predictor of a further ischemic event and death when measured after myocardial infarction. Platelets which are anucleate cells with no DNA are derived from their precursor, the megakaryocyte. Therefore, it is suggested that changes in platelet size are determined at thrombopoiesis in the megakaryocyte and that those changes might precede acute cardiac events. Understanding of the signaling system that controls platelet production may also further elucidate the cascade of events leading to acute vascular occlusion in some patients. (Arterioscler Thromb Vasc Biol. 1999;19:672-679.)Key Words: platelets Ⅲ myocardial infarction Ⅲ unstable angina Ⅲ coronary heart disease Ⅲ thrombosis T he biological events that occur in the coronary artery that immediately precede acute coronary syndromes are still not clear. However, platelets are involved, and changes in platelets may be a causal factor in producing a thrombus in the coronary artery.Aspirin is the most widely used antiplatelet drug. As platelets have no nucleus and are therefore unable to synthesize protein de novo, an aspirin-induced functional defect lasts for the whole life span of the platelets (8 to 10 days). 1 The results of large trials 2-4 of the beneficial effect of aspirin treatment in patients with unstable angina are consistent with the hypothesis that platelet activity is causally related to acute coronary syndromes. Both the medium-(12 weeks) 2 and long-term (2 years) 3 risk of cardiac death and myocardial infarction (MI) in patients with unstable angina is reduced. More recently, the significant benefit of antiplatelet therapy with aspirin in protection against acute cardiovascular syndromes and death was further supported in an overview of 145 randomized trials by the Antiplatelet Trialists' Collaboration. 5 Given the known effects of aspirin as an inhibitor of platelet function, these trials are strong evidence that platelets may contribute to the pathophysiology of the acute complications of coronary artery disease. Aspirin is an inhibitor of only one of several specific pathways leading to platelet activation and aggregation. 1 Inhibition of the glycoprotein (GP) IIb/IIIa receptor blocks the binding of fibrinogen, which is the final common pathway of platelet aggregation. 6 Integrelin, which is a GP IIb/IIIa receptor inhibitor, was evaluated in 227 patients with unstable angina and reduced significantly the number and duration of Holter-recorded ischemia compared with aspirin therapy. 7 These recent data are further strong support for the pivotal role of platelets in patients with unstable angina.Circulating platelets are heterogeneous in size, density, and reactivity. 8,9 Changes in these variables may be causal in acute coronary syndromes. 10 Initial plaque ...

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The Biology of Platelet Volume Heterogeneity

Cited by 9 publications

References 21 publications

Mean platelet volume and prevalence of peripheral artery disease, the National Health and Nutrition Examination Survey, 1999–2004

Mean platelet volume and prevalence of peripheral artery disease, the National Health and Nutrition Examination Survey, 1999–2004

Mean platelet volume as a predictor of cardiovascular risk: a systematic review and meta‐analysis

A Role for Changes in Platelet Production in the Cause of Acute Coronary Syndromes

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