Background and Purpose-Identifying paroxysmal atrial fibrillation/flutter is an essential part of the etiological workup of patients with ischemic stroke. However, there is controversy in the literature regarding the use of noninvasive cardiac rhythm monitoring with previous reviews reporting a low detection rate with routine monitoring. We performed a systematic review to determine the frequency of occult atrial fibrillation/flutter detected by noninvasive methods of continuous cardiac monitoring after acute ischemic stroke or transient ischemic attack. Methods-Studies were identified from comprehensive searches of PubMed, EMBASE, Science Citation Index, and bibliographies of relevant articles. Only English language articles were included. Randomized controlled trials and prospective cohort studies of consecutive patients with acute ischemic stroke that fulfilled predefined criteria were eligible. Two authors conducted searches and abstracted data from eligible studies independently. Results-Sixty studies were deemed potentially eligible. After application of eligibility criteria, 5 studies (736 participants) were included in the analysis. All studies evaluated Holter monitoring; 2 also evaluated event loop recording. In studies that evaluated Holter monitoring (588 participants), new atrial fibrillation/flutter was detected in 4.6% (95% CI: 0% to 12.7%) of consecutive patients with ischemic stroke. Duration of monitoring ranged from 24 to 72 hours. Two studies (140 participants) evaluated event loop recorders after Holter monitoring. New atrial fibrillation/flutter was detected in 5.7% and 7.7% of consecutive patients in these 2 studies. Conclusions-Screening consecutive patients with ischemic stroke with routine Holter monitoring will identify new atrial fibrillation/flutter in approximately one in 20 patients. Although based on limited data, extended duration of monitoring may improve the detection rate. Further research is required before definitive recommendations can be made. (Stroke.

A systematic literature review was conducted using PubMed, Embase and the Cochrane Library to determine the effect of acute, chronic and passive smoking on arterial stiffness and to determine whether these effects are reversible after smoking cessation. A total of 39 relevant studies were identified and included. Acute smoking was found to cause an acute increase in arterial stiffness. Similarly, passive smoking increased arterial stiffness acutely and chronically. The majority of studies identified chronic smoking as a risk factor for increasing arterial stiffness. However, some studies found no statistical difference in arterial stiffness between nonsmokers and long-term smokers, although chronic smoking seems to sensitize the arterial response to acute smoking. In addition, whether arterial stiffness is reversed after smoking cessation and the timeline in which this may occur could not be determined from the identified literature. The effect of smoking discontinuation on arterial stiffness remains to be established by prospective smoking cessation trials.

RationaleProgressive fibrosing interstitial lung disease (PF-ILD) is characterised by progressive physiologic, symptomatic, and/or radiographic worsening. The real-world prevalence and characteristics of PF-ILD remain uncertain.MethodsPatients were enrolled from the Canadian Registry for Pulmonary Fibrosis between 2015–2020. PF-ILD was defined as a relative forced vital capacity (FVC) decline ≥10%, death, lung transplantation, or any 2 of: relative FVC decline ≥5 and <10%, worsening respiratory symptoms, or worsening fibrosis on computed tomography of the chest, all within 24 months of diagnosis. Time-to-event analysis compared progression between key diagnostic subgroups. Characteristics associated with progression were determined by multivariable regression.ResultsOf 2746 patients with fibrotic ILD (mean age 65±12 years, 51% female), 1376 (50%) met PF-ILD criteria in the first 24 months of follow-up. PF-ILD occurred in 427 (59%) patients with idiopathic pulmonary fibrosis (IPF), 125 (58%) with fibrotic hypersensitivity pneumonitis (HP), 281 (51%) with unclassifiable ILD (U-ILD), and 402 (45%) with connective tissue disease-associated ILD (CTD-ILD). Compared to IPF, time to progression was similar in patients with HP (hazard ratio [HR] 0.96, 95% confidence interval, CI 0.79–1.17), but was delayed in patients with U-ILD (HR 0.82, 95% CI 0.71–0.96) and CTD-ILD (HR 0.65, 95% CI 0.56–0.74). Background treatment varied across diagnostic subtypes with 66% of IPF patients receiving antifibrotic therapy, while immunomodulatory therapy was utilised in 49%, 61%, and 37% of patients with CHP, CTD-ILD, and U-ILD respectively. Increasing age, male sex, gastroesophageal reflux disease, and lower baseline pulmonary function were independently associated with progression.InterpretationProgression is common in patients with fibrotic ILD, and is similarly prevalent in HP and IPF. Routinely collected variables help identify patients at risk for progression and may guide therapeutic strategies.

BackgroundIdiopathic pulmonary fibrosis (IPF) is a respiratory disorder with a poor prognosis. Our objective is to assess the comparative effectiveness of 22 approved or studied IPF drug treatments.MethodsWe searched MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials and clinicaltrials.gov from inception to 2 April 2021. We included randomised controlled trials (RCTs) for adult patients with IPF receiving one or more of 22 drug treatments. Pairs of reviewers independently identified randomised trials that compared one or more of the target medical treatments in patients with IPF. We assessed the certainty of evidence using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach for network meta-analysis. We calculated pooled relative risk (RR) ratios and presented direct or network estimates with 95% credibility intervals (95% CI), within the GRADE framework.ResultsWe identified 48 (10 326 patients) eligible studies for analysis. Nintedanib [RR 0.69 (0.44 to 1.1), pirfenidone [RR 0.63 (0.37 to 1.09); direct estimate), and sildenafil [RR (0.44 (0.16 to 1.09)] probably reduce mortality (all moderate certainty). Nintedanib (2.92% (1.51 to 4.14)), nintedanib+sildenafil (157 mL (–88.35 to 411.12)), pirfenidone (2.47% (–0.1 to 5)), pamrevlumab (4.3% (0.5 to 8.1)) and pentraxin (2.74% (1 to 4.83)) probably reduce decline of overall forced vital capacity (all moderate certainty). Only sildenafil probably reduces acute exacerbation and hospitalisations (moderate certainty). Corticosteroids+azathioprine+N-acetylcysteine increased risk of serious adverse events versus placebo (high certainty).Conclusion and relevanceFuture guidelines should consider sildenafil for IPF and further research needs to be done on promising IPF treatments such as pamrevlumab and pentraxin as phase 3 trials are completed.