Length of carotid stenosis predicts peri-procedural stroke or death and restenosis in patients randomized to endovascular treatment or endarterectomy.

BACKGROUND: The anatomy of carotid stenosis may influence the outcome of endovascular treatment or carotid endarterectomy. Whether anatomy favors one treatment over the other in terms of safety or efficacy has not been investigated in randomized trials. METHODS: In 414 patients with mostly symptomatic carotid stenosis randomized to endovascular treatment (angioplasty or stenting; n = 213) or carotid endarterectomy (n = 211) in the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS), the degree and length of stenosis and plaque surface irregularity were assessed on baseline intraarterial angiography. Outcome measures were stroke or death occurring between randomization and 30 days after treatment, and ipsilateral stroke and restenosis ≥50% during follow-up. RESULTS: Carotid stenosis longer than 0.65 times the common carotid artery diameter was associated with increased risk of peri-procedural stroke or death after both endovascular treatment [odds ratio 2.79 (1.17-6.65), P = 0.02] and carotid endarterectomy [2.43 (1.03-5.73), P = 0.04], and with increased long-term risk of restenosis in endovascular treatment [hazard ratio 1.68 (1.12-2.53), P = 0.01]. The excess in restenosis after endovascular treatment compared with carotid endarterectomy was significantly greater in patients with long stenosis than with short stenosis at baseline (interaction P = 0.003). Results remained significant after multivariate adjustment. No associations were found for degree of stenosis and plaque surface. CONCLUSIONS: Increasing stenosis length is an independent risk factor for peri-procedural stroke or death in endovascular treatment and carotid endarterectomy, without favoring one treatment over the other. However, the excess restenosis rate after endovascular treatment compared with carotid endarterectomy increases with longer stenosis at baseline. Stenosis length merits further investigation in carotid revascularisation trials

Dental and microbiological risk factors for hospital-acquired pneumonia in non-ventilated older patients

We obtained a time series of tongue/throat swabs from 90 patients with lower limb fracture, aged 65-101 in a general hospital in the North East of England between April 2009-July 2010. We used novel real-time multiplex PCR assays to detect S. aureus, MRSA, E. coli, P. aeruginosa, S. pneumoniae, H. influenza and Acinetobacter spp. We collected data on dental/denture plaque (modified Quigley-Hein index) and outcomes of clinician-diagnosed HAP.The crude incidence of HAP was 10% (n = 90), with mortality of 80% at 90 days post discharge. 50% of cases occurred within the first 25 days. HAP was not associated with being dentate, tooth number, or heavy dental/denture plaque. HAP was associated with prior oral carriage with E. coli/S. aureus/P.aeruginosa/MRSA (p = 0.002, OR 9.48 95% CI 2.28-38.78). The incidence of HAP in those with carriage was 35% (4% without), with relative risk 6.44 (95% CI 2.04-20.34, p = 0.002). HAP was associated with increased length of stay (Fishers exact test, p=0.01), with mean 30 excess days (range -11.5-115). Target organisms were first detected within 72 hours of admission in 90% participants, but HAP was significantly associated with S. aureus/MRSA/P. aeruginosa/E. coli being detected at days 5 (OR 4.39, 95%CI1.73-11.16) or 14 (OR 6.69, 95%CI 2.40-18.60).Patients with lower limb fracture who were colonised orally with E. coli/ S. aureus/MRSA/P. aeruginosa after 5 days in hospital were at significantly greater risk of HAP (p = 0.002)

Causal mechanisms proposed for the Alcohol Harm Paradox - a systematic review

Background and Aims The Alcohol Harm Paradox (AHP) posits that disadvantaged groups suffer from higher rates of alcohol-related harm compared with advantaged groups, despite reporting similar or lower levels of consumption on average. The causes of this relationship remain unclear. This study aimed to identify explanations proposed for the AHP. Secondary aims were to review the existing evidence for those explanations and investigate whether authors linked explanations to one another. Methods Systematic review. We searched MEDLINE (1946-January 2021), EMBASE (1974 – January 2021) and PsycINFO (1967 – January 2021), supplemented via manual searching of grey literature. Included papers either explored the causes of the AHP or investigated the relationship between alcohol consumption, alcohol-related harm, and socioeconomic position. Papers were set in Organisation for Economic Co-operation and Development high income countries. Explanations extracted for analysis could be evidenced in the empirical results or suggested by researchers in their narrative. Inductive thematic analysis was applied to group explanations. Results Seventy-nine papers met the inclusion criteria and initial coding revealed these papers contained 41 distinct explanations for the AHP. Following inductive thematic analysis, these explanations were grouped into 16 themes within six broad domains: Individual, Lifestyle, Contextual, Disadvantage, Upstream and Artefactual. Explanations related to risk behaviours, which fit within the Lifestyle domain, were the most frequently proposed (n=51) and analysed (n=21). Conclusions While there are many potential explanations for the Alcohol Harm Paradox, most research focuses on risk behaviours while other explanations lack empirical testing

Colinearity between covaiates which were significantly associated with HAP.

<p>Abbreviations: HABAM = Hierarchical Assessment of Balance and Mobility, ABX = antibiotics, orgs. = organisms. Variables which were co-linear (correlation estimate >0.20) are highlighted in boldface. The higher the number, the stronger the correlation. Negative correlation estimates mean the variable on the ‘y’ axis was associated with a lower score of the variable in the ‘x’ axis (e.g. higher Charlson index was associated with a lower or worse HABAM/mobility score). Where covariates are binomial (e.g. Admitted from hospital/institution, a negative correlation estimate refers to that event NOT having happened (e.g. higher HABAM/mobility score was associated with not having been admitted from hospital/institution, or in other words, having been admitted from home.). Covariates in the ‘y’ axis have been abbreviated to make viewing the table easier.</p><p>Colinearity between covaiates which were significantly associated with HAP.</p

Association between HAP and presence of opportunistic organisms by day sampled.

<p>Association between HAP and presence of opportunistic organisms by day sampled.</p

Baseline characteristics of study cohort, shown by patients with or without HAP (Fisher’s exact test).

<p>HAP = hospital acquired pneumonia, HABAM = Hierarchical Assessment of Balance and Mobility, PQS = Plaque quartile score, COPD = Combined obstructive pulmonary disease, d.p. = decimal places</p><p>*statistically significant p<0.01</p><p>^aincludes benzodiazepines, selective serotonin reuptake inhibitors, tricyclic antidepressants, opiates, gabapentin or anti-epileptic drugs.</p><p>¹Where mean and median were similar, only the mean is shown. Where there was large disparity between these values, mean, median and range are given.</p><p>Baseline characteristics of study cohort, shown by patients with or without HAP (Fisher’s exact test).</p