Genetic determinants of Platelet Large-Cell Ratio, Immature Platelet Fraction, and other platelet-related phenotypes

Pujol-Moix, Núria; Vázquez-Santiago, Miquel; Morera, Agnès; Ziyatdinov, Andrey; Remacha, Ángel F.; Nomdedeu, Josep; Fontcuberta, Jordi; Soria, José Manuel Nieto; Souto, Juan Carlos

doi:10.1016/j.thromres.2015.06.016

Cited by 18 publications

(17 citation statements)

References 46 publications

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“…In a previous study including 35 large Spanish families, Pujol-Moix et al have evaluated the quote of genetic and environmental determinants on following parameters: platelet volume, platelet count and platelet function indexes, including IPF. Their results were consistent with an impact of smoking in a covariance model on platelet volume and IPF, 43 while Butkiewicz et al have found a significant higher percentage of reticulated platelet among smoking women compared to nonsmokers. 44 On the other side, Joergensena et al have reported no impact of smoking status on IPF assessment in general population of Denmark.…”

Section: Discussionsupporting

confidence: 63%

Impact of active smoking on the immature platelet fraction and its relationship with the extent of coronary artery disease

Nardin

Verdoia

Negro³

et al. 2020

Eur J Clin Investigation

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Introduction:Smoking represents a major cardiovascular risk factor, due to the induction of oxidative stress and low-grade, continuous, inflammation that contribute to promote atherothrombosis. However, the mechanisms leading to increased platelet aggregability associated with smoking are only partially defined. A potential role has been hypothesized for immature platelets, a younger and potentially more reactive fraction, previously associated with the main determinants of coronary artery disease (CAD). Therefore, the aim of our study was to define the impact of smoking on the immature platelet fraction (IPF) and its relationship with prevalence and extent of coronary artery disease. Methods: We enrolled a cohort of consecutive patients undergoing coronary angiography in a single centre. Significant CAD was defined as at least 1 vessel stenosis >50%, while severe CAD was defined as left main and/or three-vessel disease. IPF was measured at admission by routine blood cell count (Sysmex XE-2100). Results: We included in our study 2553 patients who were divided according to smoking status (active smokers: 512; nonactive smokers: 2041). Smokers were younger, more frequent males, with lower rate of diabetes mellitus, previous PCI and previous CABG (P < .001, respectively) and were in treatment less often with ARB, BB, nitrates, statins, ASA, clopidogrel, CCB and diuretics (P < .001, respectively) as compared to nonactive smokers. Higher percentage of smokers was observed in patients with higher IPF values, and at multivariate analysis, active smoking resulted as an independent predictor of higher IPF (adjusted OR [95% CI] = 1.59[1.03-2.45], P = .035). Among smokers, higher IPF was associated with lower ejection fraction (P = .034), percentage of acute coronary syndrome (P = .002) and platelet count (P < .001) compared to ones with lower IPF. However, the IPF (according to quartiles values) was not associated with the prevalence and extent of CAD (82.5%, 80.4%, 86.1% and 80.9%, from 1st to 4th quartile, respectively, adjusted OR[95% CI] = 0.98[0.79-1.23], P = .89) and severe CAD (31%, 31.1%, 39.1% and 35.2%, from 1st to 4th quartile, respectively, adjusted OR[95% CI] = 1.03[0.86-1.23], P = .76).

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Section: Discussionsupporting

confidence: 63%

Impact of active smoking on the immature platelet fraction and its relationship with the extent of coronary artery disease

Nardin

Verdoia

Negro³

et al. 2020

Eur J Clin Investigation

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“…These BPPs are correlated with the development of adverse events or residual platelet reactivity under antiplatelet therapy in ischemic cardiovascular or cerebrovascular diseases [ 5 – 7 , 9 , 11 , 12 , 14 , 18 – 20 ]. However, several studies have indicated that BPPs are not associated with ischemic events [ 8 , 10 , 16 , 21 ].…”

Section: Discussionmentioning

confidence: 99%

“…These included an elevated mean platelet volume (MPV) [ 11 ], a high platelet–large cell ratio (P-LCR) [ 6 , 7 , 9 , 13 ], an increased platelet distribution width (PDW) [ 9 ], an elevated platelet count (PC) [ 14 ], and high plateletcrit (PCT) [ 15 ]. However, these theories remain controversial [ 10 , 16 ]. Thus, the pre-procedural predictors of the response to platelet inhibitors or CR from the perspective of cost-effectiveness, time-saving, and technical simplicity are in demand.…”

Section: Introductionmentioning

confidence: 99%

Baseline platelet parameters for predicting early platelet response and clinical outcomes in patients with non-cardioembolic ischemic stroke treated with clopidogrel

Xie

Wei

et al. 2017

Oncotarget

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PurposeThe present study investigated whether routine baseline platelet parameters(BPPs) detected before clopidogrel therapy in acute non-cardioembolic ischemic stroke(NCIS) could predict early platelet response and future clinical outcomes.ResultsThe CYP2C19 polymorphisms constituted independent risk factors for LCR. The number of female patients, the incidence of diabetes mellitus (DM), the level of low-density lipoprotein(LDL) cholesterol, and the neutrophil-to-lymphocyte ratio(NLR) were significantly high in the clinical clopidogrel resistance (CCR) group. However, none of the BPPs had a significant association with laboratory clopidogrel resistance (LCR) or discriminated with the cut-off values regarding LCR or CCR. The patients were divided into two groups according to the average mean platelet volume(MPV) or platelet count(PC). We found that the HbA1c level, the number of female patients, and the CCR were higher in the groups with elevated MPV (≥ 10.6fL) and PC (≥ 235 × 109/L); the LCR, the NIHSS score at discharge, and elevated MPV and PC were risk predictors for CCR.Materials and MethodsThis study included 196 patients with acute NCIS who underwent routine blood tests upon admission, were treated with clopidogrel, and were followed up for 6 months. Early platelet response was assessed and the CYP2C19 genetic variants were screened for. All participants were categorized into either laboratory clopidogrel resistance(LCR) or clinical clopidogrel resistance (CCR) groups.ConclusionsElevated baseline MPV and PC before clopidogrel therapy, as well as CYP2C19 gene variants, should be included in a risk algorithm for NCIS. Furthermore, other nongenetic clinical risk factors should be assessed for optimal prediction of the risk for thrombotic events because of individual variability in platelet response to clopidogrel.

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“…There are around 3000 publications relative to genetic determinants of PLT count both in pathological conditions and general population studies. Many of these studies have been performed based on the evidence that PLT count variability is strongly affected by genetic components [18][19][20] and is highly heritable [19,21,22]. Several genes have been identified to concomitantly influence PLT count, MPV and platelet activation/ function, a matter extensively reviewed by Eicher et al [23].…”

Section: Genetic Determinants and Non-genetic Variables Associated Wimentioning

confidence: 99%

Learning by counting blood platelets in population studies: survey and perspective a long way after Bizzozero

Izzi

Bonaccio

Gaetano

et al. 2018

Journal of Thrombosis and Haemostasis

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Platelet count represents a useful tool in clinical practice to discriminate individuals at higher risk of bleeding. Less obvious is the role of platelet count variability within the normal range of distribution in shaping the individual's disease risk profile. Epidemiological studies have shown that platelet count in the adult general population is associated with a number of health outcomes related to hemostasis and thrombosis. However, recent studies are suggesting a possible role of this platelet index also as an independent risk factor. In this review of adult population studies, we will first focus on known genetic and non-genetic determinants of platelet number variability. Next, we will evaluate platelet count as a marker and/or a predictor of disease risk and its interaction with other risk factors. We will then discuss the role of platelet count variability within the normal distribution range as a contribution to disease and mortality risk. The possibility of considering platelet count as a simple, inexpensive indicator of increased risk of disease and death in general populations could open new opportunities to investigate novel platelet pathophysiological roles as well as therapeutic opportunities. Future studies should also consider platelet count, not only platelet function, as a modulator of disease and mortality risk.

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Genetic determinants of Platelet Large-Cell Ratio, Immature Platelet Fraction, and other platelet-related phenotypes

Cited by 18 publications

References 46 publications

Impact of active smoking on the immature platelet fraction and its relationship with the extent of coronary artery disease

Impact of active smoking on the immature platelet fraction and its relationship with the extent of coronary artery disease

Baseline platelet parameters for predicting early platelet response and clinical outcomes in patients with non-cardioembolic ischemic stroke treated with clopidogrel

Learning by counting blood platelets in population studies: survey and perspective a long way after Bizzozero

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