Dataset Information

Mean Platelet Volume and Arterial Stiffness - Clinical Relationship and Common Genetic Variability.

ABSTRACT: Vessel wall stiffening is an important clinical parameter, but it is unknown whether platelets, key elements in the pathogenesis of arterial thrombosis, are associated with arterial stiffness. The present studies sought to determine whether mean platelet volume (MPV), a potential marker of platelet activation, is linked to vascular elasticity as assessed by the augmentation index (AIx), in 15,010 individuals from the population-based Gutenberg Health Study. Multivariable analysis showed that MPV in both males (? 0.776; 95thCI [0.250;1.16]; p?=?0.0024) and females (? 0.881[0.328;1.43]; p?=?0.0018) is strongly associated with AIx. Individuals with MPV and AIx above the sex-specific medians had worse survival. Association analysis between MPV-related genetic variants and arterial stiffness identified four genetic variants in males and one in females related with AIx. Cox regression analysis for mortality identified one of these joint genetic variants close to ring finger protein 145 gene (RNF145, rs10076782) linked with increased mortality (hazard ratio 2.02; 95thCI [1.35;3.02]; p?=?0.00061). Thus, these population-based data demonstrate a close relation between platelet volume as a potential marker of platelet activation and arterial stiffness in both sexes. Further research is warranted to further elucidate the mechanisms underlying larger platelets' role in arterial stiffening including the role of shared common genetics.

SUBMITTER: Panova-Noeva M

PROVIDER: S-EPMC5216402 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature

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Mean Platelet Volume and Arterial Stiffness - Clinical Relationship and Common Genetic Variability.

Panova-Noeva Marina M Arnold Natalie N Hermanns M Iris MI Prochaska Jürgen H JH Schulz Andreas A Spronk Henri M HM Binder Harald H Pfeiffer Norbert N Beutel Manfred M Blankenberg Stefan S Zeller Tanja T Lotz Johannes J Münzel Thomas T Lackner Karl J KJ Ten Cate Hugo H Wild Philipp S PS

Scientific reports 20170106

Vessel wall stiffening is an important clinical parameter, but it is unknown whether platelets, key elements in the pathogenesis of arterial thrombosis, are associated with arterial stiffness. The present studies sought to determine whether mean platelet volume (MPV), a potential marker of platelet activation, is linked to vascular elasticity as assessed by the augmentation index (AIx), in 15,010 individuals from the population-based Gutenberg Health Study. Multivariable analysis showed that MPV ...[more]

PMID: 28059166

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Project description:IntroductionSepsis is a public health problem due to its high prevalence and mortality. Mean platelet volume (MPV), a biomarker reported in routine blood counts, has been investigated and shows promise for determining fatal outcomes in septic patients.ObjectiveEvaluate whether the mean platelet volume (MPV) and mean platelet volume-to-platelet count (MPV/P) ratio are predictors of clinical severity and mortality in patients with sepsis.MethodsA prospective population cohort of 163 patients aged 18-97 years was recruited at the Intensive Care Unit of Pablo Arturo Hospital, Quito, Ecuador from 2017-2019 and followed up for 28 days. Patients were diagnosed with sepsis based on SEPSIS-3 septic shock criteria; in which the MPV and the MPV/P ratio were measured on days 1, 2, and 3. Sequential organ failure assessment (SOFA) score and presence of septic shock assessed clinical severity. Mortality on day 28 was considered the fatal outcome.ResultsThe average age of the patients was 61,15 years (SD 20,94) and female sex was predominant. MPV cutoff points at days 1, 2 and 3 were >9,45fL, >8,95fL and >8, 85fL; and (MPV/P) ratio >8, 18, >4, 12 y >3, 95, respectively. MPV at days 2 (9,85fL) and 3 (8,55fL) and (MPV/P) ratio at days 1 (4,42), 2 (4,21), and 3 (8,55), were predictors of clinical severity assessed by septic shock, which reached significance in the ROC curves. MPV and (MPV/P) ratio were also predictors of clinical severity determined by SOFA at days 1, 2, and 3, where higher values were observed in non-survivors reaching significance in all categories. MPV and MPV/P ratio at days 1, 2 and 3 were independent predictor factors of mortality using Cox proportional hazards model (HR 2,31; 95% CI 1,36-3,94), (HR 2,11; 95% CI 1,17-3,82), (HR 2,13; 95% CI 1,07-4,21) and (HR 2,38; 95% CI 1,38-4,12), (HR 2,15; 95% CI 1,14-4,06), (HR 4,43; 95% CI, 1,72-11,37) respectively.ConclusionsMPV and the MPV/P ratio are predictors of clinical severity and mortality in sepsis. The MPV and its coefficient are indicators of the biological behavior of platelets in sepsis. They should be considered as a cost-effective and rapidly available tool that guides the treatment.

Project description:BackgroundIncreased or decreased blood pressure variability may affect the perfusion of tissues and organs, leading to acute kidney injury and death. This study was conducted to explore the relationship between mean arterial pressure variability and short- and long-term mortality in critically ill patients.MethodsWe used patient data from the MIMIC-III database for cohort study. According to the recorded mean arterial pressure during the first 24 h in the intensive care unit, we calculated each patient's two variability parameters -coefficient of variation and average real variability. The primary outcome was in-hospital mortality and the secondary outcomes were 28-day mortality and 1-year mortality. We conducted smooth spline models to examine the possible nonlinear associations between blood pressure variability and mortality. According to the smoothing curve, we further developed a two-piecewise linear regression model to find out the threshold effect. Multivariable logistic regression or Cox proportional hazards model was used to evaluate the relationship. Kaplan-Meier survival analysis for 28-day and 1-year mortality was performed. Subgroup analysis explored the factors modifying the relationship between them.ResultsA total of 12,867 patients were enrolled in the study, 1,320 in-hospital death, 1,399 28-day death, and 2,734 1-year death occurred. The smooth spline showed death risk was the lowest when average real variability was around 7.2 mmHg. After adjusting for covariates, logistic or Cox regression showed the highest MAP variability level was strongly associated with increased mortality in the hospital (odds ratio: 1.44; 95% CI, 1.21∼1.72), at 28 days (hazard ratio: 1.28; 95% CI, 1.1∼1.5), and at 1 year (hazard ratio: 1.27; 95% CI, 1.14∼1.42) compared with the second level of average real variability group. The survival curve plot showed patients with higher average real variability had a higher risk of 28-day and 1-year mortality. This relationship remained remarkable in patients with low or high Sequential Organ Failure Assessment scores in the sensitivity analysis. The two-piecewise linear regression model showed that lower ARV was a risk factor for 28-day (HR 0.72, 95% CI, 0.57∼0.91) and 1-year mortality (HR 0.81, 95% CI, 0.68∼0.96) when ARV was less than 7.2 mmHg, higher ARV was a risk factor for 28-day mortality (HR 1.1, 95% CI, 1.04∼1.17) and 1-year mortality (HR 1.07, 95% CI, 1.02∼1.12) when ARV was greater than 7.2 mmHg.ConclusionBlood pressure variability predicts mortality in critically ill patients. Individuals with higher or lower mean arterial pressure average real variability during the first day in ICU may have an increased risk of death.

Project description:Inflammation causes vascular dysfunction and perpetuates proatherosclerotic processes. We hypothesized that a broad panel of inflammatory biomarkers and single nucleotide polymorphisms in inflammatory genes is associated with vascular stiffness. We assessed 12 circulating inflammatory biomarkers (C-reactive protein, fibrinogen, interleukin-6, intercellular adhesion molecule-1, lipoprotein-associated phospholipase-A2 [mass and activity], monocyte chemoattractant protein-1, myeloperoxidase, CD40 ligand, osteoprotegerin, P-selectin, and tumor necrosis factor receptor-II) in relation to tonometry variables (central pulse pressure, mean arterial pressure, forward pressure wave, reflected pressure wave, carotid-femoral pulse wave velocity, and augmentation index) measured in 2409 Framingham Heart Study participants (mean age: 60 years; 55% women; 13% ethnic/racial minorities). Single nucleotide polymorphisms (n=2195) in 240 inflammatory candidate genes were related to tonometry measures in 1036 white individuals. In multivariable analyses, biomarkers explained <1% of any tonometry measure variance. Applying backward elimination, markers related to tonometry (P<0.01) were as follows: tumor necrosis factor receptor-II (inversely) with mean arterial pressure; C-reactive protein (positively) and lipoprotein-associated phospholipase-A2 (inversely) with reflected pressure wave; and interleukin-6 and osteoprotegerin (positively) with carotid-femoral pulse wave velocity. In genetic association analyses, lowest P values (false discovery rate <0.50) were observed for rs10509561 (FAS), P=6.6x10(-5) for central pulse pressure and rs11559271 (ITGB2), P=1.1x10(-4) for mean arterial pressure. These data demonstrate that, in a community-based sample, circulating inflammatory markers tumor necrosis factor receptor-II (mean arterial pressure), C-reactive protein, lipoprotein-associated phospholipase-A2 activity (reflected pressure wave), interleukin-6, and osteoprotegerin (carotid-femoral pulse wave velocity) were significantly but modestly associated with measures of arterial stiffness and wave reflection. Additional studies are needed to determine whether variation in inflammatory marker genes is associated with tonometry measures.

Dataset Information

Mean Platelet Volume and Arterial Stiffness - Clinical Relationship and Common Genetic Variability.

Publications

Mean Platelet Volume and Arterial Stiffness - Clinical Relationship and Common Genetic Variability.

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