Background: Recent reports have suggested an association of atherosclerosis with risk of venous thrombosis. Objective: To confirm whether subclinical atherosclerosis is a risk factor for venous ...thrombosis (VT) among men and women age 65 and older. Methods: Participants of the Cardiovascular Health Study (n = 4108) without baseline clinical cardiovascular disease, anticoagulant use or previous VT were followed for a median of 11.7 years after non‐invasive assessment of subclinical atherosclerosis using carotid ultrasound (intima‐media thickness and presence of plaques), ankle‐brachial blood pressure index and electrocardiogram. Each event was classified as idiopathic or secondary. We used Cox proportional hazards regression to estimate the relative risk of overall and idiopathic VT for individuals with and without baseline subclinical atherosclerosis. Results: There were 133 first time VT events. No subclinical atherosclerosis measures were associated with increased risk of overall or idiopathic VT. The adjusted relative risks of overall and idiopathic VT for presence of any type of subclinical disease were 0.60 (95% confidence interval 0.39–0.91) and 0.32 (0.18–0.59), respectively. Most of this association was explained by an inverse association of high‐risk carotid plaques (prevalent in 54% of those at risk) with VT. Conclusion: Non‐invasively measured subclinical atherosclerosis was not associated with increased risk of overall or idiopathic VT in this observational study. Carotid plaques and arterial events during follow up were inversely associated, a finding that requires further study.
Essentials
There is little prospective information on genetic risk scores to predict venous thromboembolism (VT).
Community based cohort followed a median of 22.6 years for VT occurrence.
A 5‐SNP ...risk score identified whites at risk of VT, but not African Americans.
The utility of genetic risk scores for VT is yet to be established.
Summary
Background
Case‐control studies have created genetic risk scores of single nucleotide polymorphisms (SNPs) associated with venous thromboembolism (VTE) and documented their ability to predict VTE, but prospective data are lacking.
Objective
To test the ability of a genetic risk score to predict VTE incidence in a prospective study, particularly in African Americans.
Methods
We computed a previously proposed genetic risk score, based on five established VTE SNPs in the F5, F2, ABO, FGG, and F11 genes, in 9520 whites and 3049 African Americans initially free of VTE. We followed them a median of 22.6 years for VTE occurrence (n = 380 events in whites and n = 187 in African Americans).
Results
In whites, the five‐SNP weighted genetic risk score ranged from 0 to 5.8, and VTE risk increased 1.41‐fold (95% confidence interval CI 1.27‐fold to 1.56‐fold) per allele increment. In African Americans, the weighted genetic risk score ranged from 0 to 4.6 and the hazard ratio per risk allele was 1.14 (95% CI 0.94–1.38), with adjustment for 10 principal components of ancestry. The area under the receiver operating characteristic curve for 20‐year prediction of VTE from the weighted genetic risk score was 0.59 (95% CI 0.56–0.63) in whites and 0.56 (95% CI 0.51–0.61) in African Americans. Adding non‐genetic factors increased the area under the curve to 0.67 in whites and to 0.66 in African Americans.
Conclusions
Higher values for a five‐SNP genetic risk score helped identify white adults at risk of VTE. The genetic risk score did not identify future VTE occurrence in African Americans.
Repetitive rounds of differential subtraction screening, followed by nucleotide sequence determination and northern-blot analysis, identified 84 salt-regulated (160 mM NaCl for 4 h) genes in ...Arabidopsis wild-type (Col-0 gl1) seedlings. Probes corresponding to these 84 genes and ACP1, RD22BP1, MYB2, STZ, and PAL were included in an analysis of salt responsive gene expression profiles in gl1 and the salt-hypersensitive mutant sos3. Six of 89 genes were expressed differentially in wild-type and sos3 seedlings; steady-state mRNA abundance of five genes (AD06C08/unknown, AD05E05/vegetative storage protein 2 VSP2, AD05B11/S-adenosyl-L-Met:salicylic acid carboxyl methyltransferase SAMT, AD03D05/cold regulated 6.6/inducible2 COR6.6/KIN2, and salt tolerance zinc finger STZ) was induced and the abundance of one gene (AD05C10/circadian rhythm-RNA binding1 CCR1) was reduced in wild-type plants after salt treatment. The expression of CCR1, SAMT, COR6.6/KIN2, and STZ was higher in sos3 than in wild type, and VSP2 and AD06C08/unknown was lower in the mutant. Salt-induced expression of VSP2 in sos1 was similar to wild type, and AD06C08/unknown, CCR1, SAMT, COR6.6/KIN2, and STZ were similar to sos3. VSP2 is regulated presumably by SOS2/3 independent of SOS1, whereas the expression of the others is SOS1 dependent. AD06C08/unknown and VSP2 are postulated to be effectors of salt tolerance whereas CCR1, SAMT, COR6.6/KIN2, and STZ are determinants that must be negatively regulated during salt adaptation. The pivotal function of the SOS signal pathway to mediate ion homeostasis and salt tolerance implicates AD06C08/unknown, VSP2, SAMT, 6.6/KIN2, STZ, and CCR1 as determinates that are involved in salt adaptation.
: aspiration of total hip arthroplasty (THA) is commonly performed to assist in the diagnosis of prosthetic joint infection (PJI). This study aimed to determine whether fluoroscopic- or ultrasound- ...guided hip aspiration differs in the ability to acquire synovial fluid and in the accuracy of diagnosing infection.
all THA aspirations performed between 2014 and 2021 at our institution were retrospectively identified. Aspirations were classified as successful or dry. If successful, the volume of fluid obtained was recorded. The sensitivity and specificity of hip aspiration in identifying PJI were calculated with four methods: (1) culture results excluding saline lavage, (2) culture results including saline lavage, (3) 2018 Musculoskeletal Infection Society (MSIS) International Consensus Meeting (ICM) criteria, and (4) 2021 European Bone and Joint Infection Society (EBJIS) criteria. Analyses were performed using Student's
test or Wilcoxon rank sum for continuous variables and chi-squared or Fisher's exact test for categorical variables.
290 aspirations were included (155 fluoroscopic-guided and 135 ultrasound-guided). Success of aspiration (
mL) was more common in the ultrasound cohort (69 %) than fluoroscopy (53 %) (
). When successful, more volume was obtained in the ultrasound cohort (mean 13.1 mL vs. 10.0 mL;
). Ultrasound-guided aspiration was more sensitive than fluoroscopy in diagnosing PJI using culture results excluding saline lavage (85 % vs. 73 %;
), culture results including saline lavage (85 % vs. 69 %;
), 2018 MSIS-ICM criteria (77 % vs. 52 %;
), and 2021 EBJIS criteria (87 % vs. 65 %;
). Ultrasound-guided aspiration was more specific than fluoroscopy in diagnosing PJI using 2021 EBJIS criteria (100 % vs. 96 %;
).
ultrasound-guided aspiration is more frequently successful and yields more fluid than fluoroscopic-guided aspiration of THA. Ultrasound-guided aspiration is more sensitive in diagnosing PJI than fluoroscopy using culture data, 2018 MSIS-ICM criteria, and 2021 EBJIS criteria.
Essentials
Observational data suggest taller people have a higher risk of venous thromboembolism (VTE).
We used Mendelian randomization techniques to further explore this association in three ...studies.
Risk of VTE increased by 30–40% for each 10 cm increment in height.
Height was more strongly associated with deep vein thrombosis than with pulmonary embolism.
Summary
Background
Taller height is associated with a greater risk of venous thromboembolism (VTE).
Objectives
To use instrumental variable (IV) techniques (Mendelian randomization) to further explore this relationship.
Methods
Participants of European ancestry were included from two cohort studies (Atherosclerosis Risk in Communities ARIC study and Cardiovascular Health Study CHS) and one case–control study (Mayo Clinic VTE Study Mayo). We created two weighted genetic risk scores (GRSs) for height; the full GRS included 668 single‐nucleotide polymorphisms (SNPs) from a previously published meta‐analysis, and the restricted GRS included a subset of 362 SNPs not associated with weight independently of height. Standard logistic regression and IV models were used to estimate odds ratios (ORs) for VTE per 10‐cm increment in height. ORs were pooled across the three studies by the use of inverse variance‐weighted random effects meta‐analysis.
Results
Among 9143 ARIC and 3180 CHS participants free of VTE at baseline, there were 367 and 109 incident VTE events. There were 1143 VTE cases and 1292 controls included from Mayo. The pooled ORs from non‐IV models and models using the full and restricted GRSs as IVs were 1.27 (95% confidence interval CI 1.11–1.46), 1.34 (95% CI 1.04–1.73) and 1.45 (95% CI 1.04–2.01) per 10‐cm greater height, respectively.
Conclusions
Taller height is associated with an increased risk of VTE in adults of European ancestry. Possible explanations for this association, including taller people having a greater venous surface area, a higher number of venous valves, or greater hydrostatic pressure, need to be explored further.
Thrombus formation is the proximate cause of myocardial infarction, but atherosclerosis, the chief underlying cause, is a chronic disease that progresses over decades of life.
1
Laboratory and ...pathological data support the idea that inflammation has a role in both the initiation and the progression of atherosclerosis, and antiinflammatory agents may have a role in the prevention of cardiovascular disease.
2
–
5
However, there are few data to indicate whether inflammation increases the risk of first myocardial infarction, stroke, and venous thrombosis or whether antiinflammatory therapy decreases that risk.
C-reactive protein is an acute-phase reactant that is a marker for underlying systemic . . .
This first of a 2-part series of articles recounts the key points presented in a collaborative symposium sponsored jointly by the Arthritis Foundation and the American Orthopaedic Foot & Ankle ...Society with the intent to survey the state of scientific knowledge related to incidence, diagnosis, pathologic mechanisms, and injection treatment options for osteoarthritis (OA) of the foot and ankle. A meeting was held virtually on December 3, 2021. A group of experts were invited to present brief synopses of the current state of knowledge and research in this area. Part 1 overviews areas of epidemiology and pathophysiology, current approaches in imaging, diagnostic and therapeutic injections, and genetics. Opportunities for future research are discussed. The OA scientific community, including funding agencies, academia, industry, and regulatory agencies, must recognize the needs of patients that suffer from arthritis of foot and ankle. The foot and ankle contain a myriad of interrelated joints and tissues that together provide a critical functionality. When this functionality is compromised by OA, significant disability results, yet the foot and ankle are generally understudied by the research community.
Level of Evidence: Level V - Review Article/Expert Opinion.
Background: Thrombin is an enzyme that is essential for the acceleration of the coagulation cascade and the conversion of fibrinogen to clottable fibrin. Objectives: We evaluated the relationship of ...basal peak thrombin generation with the risk of future venous thromboembolism (VTE), and determined whether associations were independent of other coagulation markers. Methods: The Longitudinal Investigation of Thromboembolism Etiology (LITE) study investigated VTE in two prospective population‐based cohorts: the Atherosclerosis Risk in Communities (ARIC) study and the Cardiovascular Health Study (CHS). Peak thrombin generation was measured on stored plasma in a nested case–control sample (434 cases and 1004 controls). Logistic regression was used to estimate the relationship of peak thrombin generation with VTE, adjusted for age, sex, race, center, and body mass index. Mediation was evaluated by additionally adjusting for factor VIII and D‐dimer. Results: Relative to the first quartile of peak thrombin generation, the odds ratio (OR) of VTE for those above the median was 1.74 95% confidence interval (CI) 1.28–2.37. The association was modestly attenuated by adjustment for FVIII and D‐dimer (OR 1.47, 95% CI 1.05–2.05). Associations appeared to be stronger for idiopathic than for secondary VTE. Elevated peak thrombin generation more than added to the VTE risk associated with FV Leiden or low activated partial thromboplastin time. Conclusions: In this prospective study of two independent cohorts, elevated basal peak thrombin generation was associated with subsequent risk of VTE, independently of established VTE risk factors.
Summary
Background
We sought to define the risk factors present at admission for venous thromboembolism (VTE) in medical inpatients and develop a risk model for clinical use.
Methods
Between January ...2002 and June 2009, 299 cases of hospital‐acquired VTE were frequency matched to 601 controls. Records were ed using a standard form for characteristics of the thrombosis, medical conditions and other risk factors. Weighted logistic regression and survey methods were used to develop a risk model for hospital‐acquired VTE that was validated by bootstrapping.
Results
VTE complicated 4.6 per 1000 admissions. Two risk assessment models were developed, one using laboratory data available at admission (Model 1) and the other excluding laboratory data (Model 2). Model 1 consisted of the following risk factors (points): history of congestive heart failure (5), history of inflammatory disease (4), fracture in the past 3 months (3), history of VTE (2), history of cancer in the past 12 months (1), tachycardia (2), respiratory dysfunction (1), white cell count ≥ 11 × 109/L (1), and platelet count ≥ 350 × 109/L (1). Model 2 was similar, except respiratory dysfunction had 2 points and white cell and platelet counts were removed. The c‐statistic for Model 1 was 0.73 (95% CI 0.70, 0.77) and for Model 2 0.71 (95% CI 0.68, 0.75).
Conclusions
We present a VTE risk assessment model for use in medical inpatients. The score is simple and relies on information known at the time of admission and typically collected in all medical inpatients. External validation is needed.
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