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1.  Mean Platelet Volume and Long-Term Mortality in Patients Undergoing Percutaneous Coronary Intervention 
The American journal of cardiology  2012;111(2):185-189.
Increased platelet activity is associated with adverse cardiovascular events. Mean platelet volume (MPV) correlates with platelet activity but the relationship between MPV and long-term mortalityin patients undergoing percutaneous coronary intervention(PCI) is not well established. Furthermore, the role of change in MPV over time has not been previously evaluated. We evaluatedMPV at baseline, 30 days, 60 days, 90 days, 1 year, 2 years, and 3 years post-procedure in 1,512 patients who underwent PCI. The speed of change in MPV was estimated using slope of linear regression. Mortality was determined by query of social security death index. Over a median of 8.7 years, mortality was 49.3% post-PCI. There was no significant difference in mortality when stratified by MPV quartiles (1stquartile 50.1%, 2nd quartile 47.7%, 3rd quartile 51.3%, 4thquartile 48.3%, p=0.74). In patients with available data to determine a change in MPV over time post-PCI (n=839), mortality was 49.1% and significantly higher in patients with an increase (52.9%) compared to those with a decrease (44.2%) or no change (49.1%) in MPV over time (p<0.0001). In conclusion, there was no association between baseline MPV and long-term mortality in patients undergoing PCI. However, there was increased mortality when MPV increasedover time post-PCI. Monitoring MPV after coronary revascularization may play a role in risk stratification.
doi:10.1016/j.amjcard.2012.09.014
PMCID: PMC3538911  PMID: 23102880
Mean platelet volume; percutaneous coronary intervention; long-term mortality
2.  Hyperreactive platelet phenotypes: Relationship to altered serotonin transporter number, transport kinetics and intrinsic response to adrenergic co-stimulation 
Thrombosis and haemostasis  2012;109(1):85-92.
Summary
The mechanism underlying a hyperreactive platelet phenotype remains unknown. Since serotonin has been shown to influence platelet biology and atherothrombosis, we sought to investigate the association of platelet serotonin transporter number, binding affinity, and uptake kinetics to platelet aggregation. A total of 542 healthy volunteers had light transmittance platelet aggregometry measured in response to varying concentrations of epinephrine, serotonin, epinephrine plus serotonin, ADP and collagen. Transporter-dependent serotonin uptake rate was determined (Vmax), as were serotonin transporter number (Bmax) and binding affinity (Kd) using 3H paroxetine binding in a homologous displacement assay, nonlinear regression and validated algorithms for kinetic modeling. Stimulation with submaximal (2 μM) epinephrine concentration elicited a distinct, bimodal pattern of platelet aggregation in this population. In contrast, subjects exhibited minimal aggregation in response to serotonin alone. Co-stimulation with submaximal epinephrine and serotonin induced platelet aggregation to a level beyond that observed with either agonist alone and maintained a bimodal response distribution. Subjects with heightened (>60%) platelet aggregation to both epinephrine alone and epinephrine plus serotonin exhibited increased platelet serotonin uptake, and transporter number and affinity. In a population of healthy subjects, co-stimulation with submaximal concentrations of epinephrine and serotonin identifies a subset of individuals with a hyperreactive platelet aggregation profile that is associated with changes in platelet serotonin function.
doi:10.1160/TH12-03-0202
PMCID: PMC3582386  PMID: 23223800
Platelets; platelet activity; serotonin; epinephrine; transporter
3.  Anesthesiology Residents-as-Teachers Program: A Pilot Study 
Background
The role of residents as teachers has grown over time. Programs have been established within various specialties to formally develop these skills. Anesthesiology residents are frequently asked to provide supervision for novice learners and have numerous opportunities for teaching skills and clinical decision making. Yet, there are no educational programs described in the literature to train anesthesiology residents to teach novice learners.
Objective
To explore whether a resident-as-teacher program would increase anesthesiology residents' self-reported teaching skills.
Methods
An 8-session interactive Anesthesiology Residents-as-Teachers (ART) Program was developed to emphasize 6 key teaching skills. During a 2-year period, 14 anesthesiology residents attended the ART program. The primary outcome measure was resident self-assessment of their teaching skills across 14 teaching domains, before and 6 months after the ART program. Residents also evaluated the workshops for quality with a 9-item, postworkshop survey. Paired t testing was used for analysis.
Results
Resident self-assessment led to a mean increase in teaching skills of 1.04 in a 5-point Likert scale (P < .001). Residents reported the greatest improvement in writing/using teaching objectives (+1.29, P < .001), teaching at the bedside (+1.57, P  =  .002), and leading case discussions (+1.64, P  =  .001). Residents rated the workshops 4.2 out of 5 (3.9–4.7).
Conclusions
Residents rated their teaching skills as significantly improved in 13 of 14 teaching domains after participation in the ART program. The educational program required few resources and was rated highly by residents.
doi:10.4300/JGME-D-11-00300.1
PMCID: PMC3546586  PMID: 24294434
4.  The Relationship Between Diabetes, Metabolic Syndrome, and Platelet Activity as Measured by Mean Platelet Volume 
Diabetes Care  2012;35(5):1074-1078.
OBJECTIVE
The association between platelet activity, diabetes, and glucometabolic control is uncertain. We aim to investigate mean platelet volume (MPV), a marker of platelet size and platelet activity, with the prevalence of diabetes, metabolic syndrome, and degree of glycemic control.
RESEARCH DESIGN AND METHODS
This is a retrospective analysis of 13,021 participants in the National Health and Nutrition Examination Survey from 1999 to 2004. Prevalence of diabetes was defined as nonfasting glucose >200 mg/dL, fasting glucose ≥126 mg/dL, or treatment with hypoglycemic agents. Presence of metabolic syndrome was determined by the National Cholesterol Education Program Adult Treatment Panel III definition. Odds ratios and 95% CIs were estimated by logistic regression.
RESULTS
MPV was significantly higher in subjects with diabetes (8.20 vs. 8.06 femtoliter [fL], P < 0.01) but not in subjects with metabolic syndrome (8.09 vs. 8.07 fL, P = 0.24). For the metabolic syndrome components, MPV was significantly higher in abdominal obesity (P = 0.03) and low HDL (P = 0.04), and not different in high blood pressure (P = 0.07), abnormal glucose metabolism (P = 0.71), or hypertriglyceridemia (P = 0.46). There was a significant correlation between MPV and glucose (P < 0.0001) and between MPV and hemoglobin A1c (P < 0.0001) in subjects with diabetes. These correlations were no longer significant in those without diabetes. The adjusted odds of diabetes rose with increasing MPV levels and were most pronounced in subjects with MPV levels exceeding the 90th percentile (≥9.31 fL). The association between MPV and diabetes was most apparent in those with the poorest glucose control.
CONCLUSIONS
Mean platelet volume is strongly and independently associated with the presence and severity of diabetes.
doi:10.2337/dc11-1724
PMCID: PMC3329806  PMID: 22410814
5.  Lipid and Lipoprotein Biomarkers and the Risk of Ischemic Stroke in Postmenopausal Women 
Background
Few studies simultaneously investigated lipids and lipoprotein biomarkers as predictors of ischemic stroke. The value of these biomarkers as independent predictors of ischemic stroke remains controversial.
Methods
We conducted a prospective nested case-control study among postmenopausal women from the Women’s Health Initiative Observational Study to assess the relationship between fasting lipids (total cholesterol, LDL-C, HDL-C, and triglycerides), lipoproteins (LDL, HDL and VLDL particle number and size, IDL particle number, and lipoprotein [a]) and risk of ischemic stroke. Among women free of stroke at baseline, 774 ischemic stroke patients were matched according to age and race to controls using a 1:1 ratio.
Results
In bivariate analysis, baseline triglycerides (P<0.001), IDL particles (P<0.01), LDL particles (P<0.01), VLDL triglyceride (P<0.001), VLDL particles (P<0.01), VLDL size (P<0.001), LDL size (P=0.03), and total/HDL cholesterol ratio (P<0.01) were significantly higher among women with incident ischemic stroke, while levels of HDL-C (P<0.01) and HDL size (P<0.01) were lower. No significant baseline difference for total cholesterol (P=0.15), LDL-C (P=0.47), and lipoprotein (a) (P=0.11) was observed. In multivariable analysis, triglycerides, (OR for the highest vs lowest quartile, 1.56; 95% CI, 1.13-2.17, P for trend =0.02), VLDL size (OR 1.59, 95% CI, 1.10-2.28, P for trend =0.03) and IDL particle number (OR 1.46, 95% CI, 1.04-2.04, P for trend =0.02) were significantly associated with ischemic stroke.
Conclusion
Among a panel of lipid and lipoprotein biomarkers, baseline triglycerides, VLDL size and IDL particle number were significantly associated with incident ischemic stroke in postmenopausal women.
doi:10.1161/STROKEAHA.111.641324
PMCID: PMC3547588  PMID: 22308251
Lipids; Lipoproteins; Ischemic Stroke; Women; Triglycerides
6.  Aspirin in primary prevention: can we individualize care? 
doi:10.3978/j.issn.2223-3652.2012.04.07
PMCID: PMC3839141  PMID: 24282710
7.  A Prospective Randomized Controlled Trial of the Effects of Vitamin D Supplementation on Cardiovascular Disease Risk 
PLoS ONE  2012;7(5):e36617.
Vitamin D (VitD) supplementation has been advocated for cardiovascular risk reduction; however, supporting data are sparse. The objective of this study was to determine whether VitD supplementation reduces cardiovascular risk. Subjects in this prospective, randomized, double-blind, placebo-controlled trial of post-menopausal women with serum 25-hydroxyvitamin D concentrations >10 and <60 ng/mL were randomized to Vitamin D3 2500 IU or placebo, daily for 4 months. Primary endpoints were changes in brachial artery flow-mediated vasodilation (FMD), carotid-femoral pulse wave velocity (PWV), and aortic augmentation index (AIx). The 114 subjects were mean (standard deviation) 63.9 (3.0) years old with a 25-hydroxyvitamin D level of 31.3 (10.6) ng/mL. Low VitD (<30 ng/mL) was present in 47% and was associated with higher body-mass index, systolic blood pressure, glucose, CRP, and lower FMD (all p<0.05). After 4 months, 25-hydroxyvitamin D levels increased by 15.7 (9.3) ng/mL on vitamin D3 vs. −0.2 (6.1) ng/mL on placebo (p<0.001). There were no significant differences between groups in changes in FMD (0.3 [3.4] vs. 0.3 [2.6] %, p = 0.77), PWV (0.00 [1.06] vs. 0.05 [0.92] m/s, p = 0.65), AIx (2.7 [6.3] vs. 0.9 [5.6] %, p = 0.10), or CRP (0.3 [1.9] vs. 0.3 [4.2] mg/L, p = 0.97). Multivariable models showed no significant interactions between treatment group and low VitD status (<30 ng/mL) for changes in FMD (p = 0.65), PWV (p = 0.93), AIx (p = 0.97), or CRP (p = 0.26).In conclusion, VitD supplementation did not improve endothelial function, arterial stiffness, or inflammation. These observations do not support use of VitD supplementation to reduce cardiovascular disease risk.
Trial Registration
ClinicalTrials.gov NCT00690417
Trial Registration
ClinicalTrials.gov NCT01049048
doi:10.1371/journal.pone.0036617
PMCID: PMC3346736  PMID: 22586483
8.  Growth in Height in Childhood and Risk of Coronary Heart Disease in Adult Men and Women 
PLoS ONE  2012;7(1):e30476.
Background
Adult height is inversely associated with the risk of coronary heart disease (CHD), but it is still unknown which phase of the human growth period is critical for the formation of this association. We investigated the association between growth in height from 7 to 13 years of age and the risk of CHD in adulthood.
Methods and Findings
The heights of almost all children born 1930 through 1976 who attended school in the Copenhagen municipality (232,063 children) were measured annually from 7 to 13 years of age. Birth weight data were available since 1936. Fatal and non-fatal CHD events were ascertained by register linkage until 2008 (25,214 cases). Hazard ratios (HR) with 95% confidence intervals (CI) were estimated by Cox proportional hazards regression for height z-scores (standard deviation units) and change in height z-scores. Height z-scores were inversely related to the risk of CHD. The association was strongest at 7 years of age (HR = 0.91, CI 0.90–0.92 in boys and 0.88, CI 0.86–0.90 in girls) and steadily weakened thereafter, yet it still remained at 13 years of age (HR = 0.95, CI 0.94–0.97 and 0.91, CI 0.89–0.93, boys and girls respectively). The associations were not modified by birth weight. Independent of the age-specific risk, rapid growth was associated with an increased CHD risk, most pronounced between 9 and 11 years in girls (HR = 1.22, CI 1.14–1.31) and between 11 and 13 years in boys (HR = 1.28, CI 1.22–1.33) per unit increase in z-score. Adjustment for body mass index somewhat strengthened the associations of CHD risk with height and weakened the association with growth.
Conclusions/Significance
Risk of CHD in adulthood is inversely related to height at ages 7 through 13 years, but strongest in the youngest, and, independently hereof, the risk increased by growth velocity.
doi:10.1371/journal.pone.0030476
PMCID: PMC3265486  PMID: 22291964

Results 1-8 (8)