Zhe Li

Aims: Cardiac implantable electronic device (CIED) infection carries a substantial burden of morbidity, mortality, and cost. The Prevention of Arrhythmia Device Infection Trial (PADIT) risk score improves identification of high-risk patients and may guide targeted strategies to reduce infection. Recent work has categorized CIED infection into localized pocket vs. systemic infection, with early reports suggesting different risk factors for each. However, no current risk score has been validated for infection subtypes. ObjectivesIndependently validate the PADIT infection risk score.Compare risk factors for infection subtypes.Assess PADIT performance in predicting subtype-specific infection. Methods and results: A prospective registry was initiated at the University of Ottawa Heart Institute in 2007 to capture all CIED procedures and prospectively identify infections in collaboration with the infection prevention team. PADIT risk score components were documented for each procedure. All suspected infections were adjudicated independently by two physicians (with a third if required), blinded to PADIT score and baseline variables, and subclassified as pocket or systemic infection. Logistic regression models were generated to validate PADIT performance for each subtype, with evaluation using Akaike and Bayesian information criteria (AIC/BIC), C-statistics, and calibration slope. Between 2007 and 2020, 14,225 procedures were performed (mean age 72 ± 14 years, 35% female, 70% new implants, 18% generator changes, 11% upgrades). A total of 103 infections (0.73%) were adjudicated, of which 71 (69%) were pocket and 32 (31%) systemic. The PADIT score showed good predictive performance with a C-statistic of 0.687 (95% CI 0.655–0.743), similar to the derivation cohort (0.702, 95% CI 0.661–0.741). Notably, the number of prior procedures was strongly associated with pocket infection but not systemic infection. PADIT discrimination was consistent across subtypes: pocket infection C-statistic 0.691 (95% CI 0.649–0.761) and systemic infection 0.746 (95% CI 0.707–0.848). Calibration slopes demonstrated good agreement between predicted and observed events, with the best fit for systemic infection. Conclusion: The PADIT score was independently validated with discrimination and calibration similar to the original derivation cohort. Importantly, prior procedures predicted pocket but not systemic infection. Overall, PADIT performed well in predicting both subtypes, with the strongest model fit observed for systemic infection.

Background: Despite associations between atrial fibrillation (AF) and cognitive decline independent of stroke, pathways underlying this relationship remain unclear. Inflammatory markers, such as CRP (C‐reactive protein), are associated with blood–brain barrier (BBB) permeability, potentially leading to neuroinflammation and neurodegeneration. We estimated associations of CRP with cognitive impairment and death in aging adults with AF. Methods: Adults aged ≥45 years with prevalent AF and no cognitive impairment were identified from the REGARDS (Reasons for Geographic and Racial Differences in Stroke) cohort (N=30 239). Plasma CRP was measured at baseline and cognitive status measured annually using the Six‐Item Screener. Competing risks Cox proportional hazards regression was used to estimate cause‐specific hazard for cognitive impairment (Six‐Item Screener score ≤3). Cognitive trajectories were identified using latent class growth models and adjusted binomial logistic regression used to estimate associations between CRP and cognitive trajectories, with interactions by sex. Results: Among 2109 participants, 285 developed cognitive impairment and 786 died over a median 9‐year follow‐up. A doubling of baseline CRP levels was associated with increased death (hazard ratio [HR], 1.13 [95% CI, 1.08–1.19]) but not incident cognitive impairment (HR, 0.98 [95% CI, 0.91–1.04]). Latent class analyses identified 2 unique cognitive trajectories: 91% had a stable trajectory, while 9% showed progressive decline. Sex‐specific models showed a 9% increased odds of progressive cognitive decline in men (odds ratio, 1.09 [95% CI, 1.01–1.17]) but not women (odds ratio, 1.04 [95% CI, 0.97–1.12]). Conclusions: Higher CRP was associated with cognitive impairment in aging men with AF, highlighting inflammation‐mediated blood–brain barrier dysfunction as a potential pathway linking AF to cognitive decline.

Background and aims Randomised controlled trials comparing transcatheter aortic valve replacement (TAVR) and surgical aortic valve replacement (SAVR) were performed in highly selected populations and data regarding long-term secondary complications beyond mortality are scarce. This study used data from Ontario, Canada to compare mid-term and long-term clinical outcomes in a representative real-world cohort of patients who underwent TAVR and SAVR from 2007 to 2016. Methods A novel overlap weighting propensity score method was used to match patients undergoing TAVR or SAVR. Primary outcomes were all-cause, cardiovascular and non-cardiovascular mortality either in-hospital or at 1, 3 and 5 years postdischarge. Secondary outcomes included adverse outcomes and readmission. Long-term primary and secondary outcomes were compared using a weighted competing risks subdistribution proportional hazards model. Results The study included 9355 SAVR and 2641 TAVR patients. All-cause mortality at 1 year (HR 1.21; 95% CI 1.02 to 1.43), 3 years (HR 1.45; 95% CI 1.28 to 1.64) and 5 years (HR 1.48; 95% CI 1.33 to 1.65) was significantly higher among patients underwent TAVR compared with SAVR, with both cardiovascular mortality at 3 and 5 years and non-cardiovascular mortality at 1, 3 and 5 years significantly higher for TAVR. Hazards of myocardial infarction and readmission for angina at 1, 3 and 5 years were significantly greater for TAVR. Conclusions In this overlap weighted cohort, both cardiac and non-cardiac mortality rates were increased in TAVR patients. Residual or unmeasured confounding may have contributed to these findings. More studies are needed to identify factors predictive of long-term outcomes in real-world cohorts.

Objectives Our objectives were to review the literature to identify frailty instruments in use for transcatheter aortic valve implantation (TAVI) recipients and synthesise prognostic data from these studies, in order to inform clinical management of frail patients undergoing TAVI. Methods We systematically reviewed the literature published in 2006 or later. We included studies of patients with aortic stenosis, diagnosed as frail, who underwent a TAVI procedure that reported mortality or clinical outcomes. We categorised the frailty instruments and reported on the prevalence of frailty in each study. We summarised the frequency of clinical outcomes and pooled outcomes from multiple studies. We explored heterogeneity and performed subgroup analysis, where possible. We also used Grading of Recommendations, Assessment, Development and Evaluation (GRADE) to assess the overall certainty of the estimates. Results Of 49 included studies, 21 used single-dimension measures to assess frailty, 3 used administrative data-based measures, and 25 used multidimensional measures. Prevalence of frailty ranged from 5.67% to 90.07%. Albumin was the most commonly used single-dimension frailty measure and the Fried or modified Fried phenotype were the most commonly used multidimensional measures. Meta-analyses of studies that used either the Fried or modified Fried phenotype showed a 30-day mortality of 7.86% (95% CI 5.20% to 11.70%) and a 1-year mortality of 26.91% (95% CI 21.50% to 33.11%). The GRADE system suggests very low certainty of the respective estimates. Conclusions Frailty instruments varied across studies, leading to a wide range of frailty prevalence estimates for TAVI recipients and substantial heterogeneity. The results provide clinicians, patients and healthcare administrators, with potentially useful information on the prognosis of frail patients undergoing TAVI. This review highlights the need for standardisation of frailty measurement to promote consistency. PROSPERO registration number CRD42018090597.