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Level of evidence grading has become widely used in orthopaedics. see more This study reviewed clinical research articles published in leading orthopaedic journals to describe the association between level of evidence and number of future citations, which is one measure of an article’s impact in the field.

The first 100 clinical research articles published in 2014 by each of the Journal of Bone and Joint Surgery, Clinical Orthopaedics and Related Research, and the American Journal of Sports Medicine were reviewed for level of evidence and article characteristics. Web of Science was used to identify the number of citations of each article over the following 5 years. Univariable analyses and multivariable linear regression were used to describe the associations.

Three hundred articles were evaluated. Univariable analysis revealed no association between level of evidence and number of citations, with a median number of citations for level 1 articles of 23 (interquartile range [IQR], 14-49), level 2 articles 24 (IQR, 13-47), level 3 articles 22 (IQR, 13-40), and level 4 or 5 articles 20 (IQR, 10-36). Univariable analyses showed weak associations between other article characteristics and citations. Even after adjusting for other variables, the standardized regression coefficient for level 1 versus level 4 or 5 was only 0.14 and the overall model had a poor fit with an R2 of 0.18.

Among clinical research articles published in leading orthopaedic journals, no notable association was found between level of evidence and future citations.

Readers of the orthopaedic literature should understand that no association was found between level of evidence and future citations. Additional work is needed to better understand the effect level of evidence has on clinicians and researchers.

Readers of the orthopaedic literature should understand that no association was found between level of evidence and future citations. Additional work is needed to better understand the effect level of evidence has on clinicians and researchers.

Coronary atherosclerosis is a systemic chronic inflammatory disease with variable occurrence and progression. Some laboratory parameters, such as the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and C-reactive protein (CRP) level, are used to evaluate the degree of inflammation and the severity of coronary artery disease (CAD). The neutrophil*platelet/lymphocyte is a novel systemic immune-inflammation index (SII), and its relationship with the development and severity of CAD is unclear.

To investigate the association between the SII and the severity of CAD.

Three-hundred and ninety-five patients who underwent coronary angiography were enrolled; among whom, 285 patients were included in the CAD group and 110 patients were included in the non-CAD group according to the WHO guidelines. Patients with CAD were further divided according to the Gensini score into the severe coronary stenosis group and the mild coronary stenosis group. The SII was calculated using the following formula neutrophil*platelet/lymphocyte.

When the cutoff value of the SII was set at 439.44, the predictive power of CAD was the highest, with a sensitivity and specificity of 64.6 and 68.2%, respectively. When the cutoff value of the SII was set at 652.83, the predictive power of severe coronary stenosis was the highest, with a sensitivity and specificity of 71.0 and 86.0%, respectively. The area under the curve of the SII in predicting severe coronary stenosis was greater than that of the NLR, PLR and CRP level.

The SII is an independent risk factor for the occurrence and severity of CAD.

The SII is an independent risk factor for the occurrence and severity of CAD.

High coronary artery calcium score (CAC) is a significant risk factor for cardiovascular morbidity and mortality. We investigated the long-term outcome of subjects with elevated CAC.

We studied 1005 participants of The St. Francis Heart Study who were asymptomatic and apparently healthy and had CAC scores at 80th percentile or higher for age and gender. They were randomized to receive atorvastatin 20 mg daily or placebo for up to 5 years. We used an as-treated study design accounting for cross-overs at the end of the original trial. All-cause mortality risk was assessed using adjusted hazard ratios.

Mean age was 59 ± 6 years and 26% (N = 263) were female. After 17 ± 3 years follow-up 176 subjects died. High CAC at baseline was associated with increased mortality risk with adjusted hazard ratio for logarithmic transformed CAC at 1.33 and 95% confidence interval 1.06-1.68. The mortality risk associated with CAC was similar between the group with high-sensitivity CRP ≥2 and <2 mg/dL. Those with a family history of premature coronary artery disease exhibited a higher mortality risk in association with high CAC with an adjusted hazard ratio 1.51 (1.09, 2.09).

Elevated CAC is an independent risk for long-term all-cause mortality. The screening of CAC score in addition to identifying conventional risk factors can differentiate asymptomatic individuals with and without increased long-term mortality risk.

Elevated CAC is an independent risk for long-term all-cause mortality. The screening of CAC score in addition to identifying conventional risk factors can differentiate asymptomatic individuals with and without increased long-term mortality risk.

There is a persistent controversy regarding the benefit and timing of angiography in patients with stable coronary artery disease (CAD). With this meta-analysis of randomized controlled trials (RCTs) the advantages of initial invasive strategy and medical therapy compared with only medical therapy.

We conducted a literature search of the following databases Pubmed/MEDLINE, Cochrane Library and Embase. Data was collected from all the RCTs that compared early invasive approach with medical therapy alone in treating stable CAD which was conducted by two independent authors. Primary outcomes were all-cause mortality and myocardial infarction (MI), while the secondary outcomes included major adverse cardiovascular events (MACE), cardiovascular mortality, cardiovascular hospitalization, hospitalization due to unstable angina and revascularization events. The Mantel-Haenszel random-effects model was used to estimate risk ratios (RRs) and 95% confidence intervals (CIs).

We included 15 RCTs (13 916 patients, mean age 63.