A systematic review of the measurement properties of the Pennsylvania Shoulder Score.

BACKGROUND: Pennsylvania Shoulder Score (PSS) is a patient-reported outcome measure (PROM) that is gaining use when examining shoulder-specific outcomes. To date, a systematic review of the PSS measurement properties has not been published. PURPOSE: To systematically locate, appraise, and synthesize the evidence concerning the measurement properties of the PSS. STUDY DESIGN: Systematic literature review. METHODS: A pair of raters conducted a literature search using pre-defined keywords from 5 databases (PubMed, CINAHL, SPORTdiscus, PsychINFO, Scopus) during the week of October 23, 2022. Critical appraisal of study design for psychometric articles was used to assess methodological quality and risk of bias. Measurement property data were synthesized with pooled estimates for the indices of test-retest reliability (ICC), standard error of measurement (SEM), minimal detectable change (MDC), Cronbach α (CA), effect size (ES), and standardized response means (SRM) calculated from applicable studies. RESULTS: A total of 13 articles met the inclusion criteria for this review. Methodological quality was agreed upon between the 2 raters with a weighted kappa of 0.77, and 9/13 of the articles were rated above 70%. Test-retest reliability of the PSS total score ranged between 0.90 and 0.94, and construct validity was high when compared to other shoulder-specific PROMs (0.75 < r > 0.96). Responsiveness of the PSS was large across all studies with few PSS subscales dropping to moderate. Pooled MDC90 of the total PSS was 12.13 points, and the pooled ES of the total PSS was 0.85. CONCLUSIONS: The scope of this review demonstrates positive measurement properties of the PSS as a reliable, valid, and responsive measurement of shoulder-specific PROM. However, there are few studies examining the measurement properties of the PSS and more research is needed to assess cross-cultural appropriateness and factor analysis of the questions contained in the PSS.

Comprehensive evaluation of electrophysiological and 3D structural features of human atrial myocardium with insights on atrial fibrillation maintenance mechanisms.

Atrial fibrillation (AF) occurrence and maintenance is associated with progressive remodeling of electrophysiological (repolarization and conduction) and 3D structural (fibrosis, fiber orientations, and wall thickness) features of the human atria. Significant diversity in AF etiology leads to heterogeneous arrhythmogenic electrophysiological and structural substrates within the 3D structure of the human atria. Since current clinical methods have yet to fully resolve the patient-specific arrhythmogenic substrates, mechanism-based AF treatments remain underdeveloped. Here, we review current knowledge from in-vivo, ex-vivo, and in-vitro human heart studies, and discuss how these studies may provide new insights on the synergy of atrial electrophysiological and 3D structural features in AF maintenance. In-vitro studies on surgically acquired human atrial samples provide a great opportunity to study a wide spectrum of AF pathology, including functional changes in single-cell action potentials, ion channels, and gene/protein expression. However, limited size of the samples prevents evaluation of heterogeneous AF substrates and reentrant mechanisms. In contrast, coronary-perfused ex-vivo human hearts can be studied with state-of-the-art functional and structural technologies, such as high-resolution near-infrared optical mapping and contrast-enhanced MRI. These imaging modalities can resolve atrial arrhythmogenic substrates and their role in reentrant mechanisms maintaining AF and validate clinical approaches. Nonetheless, longitudinal studies are not feasible in explanted human hearts. As no approach is perfect, we suggest that combining the strengths of direct human atrial studies with high fidelity approaches available in the laboratory and in realistic patient-specific computer models would elucidate deeper knowledge of AF mechanisms. We propose that a comprehensive translational pipeline from ex-vivo human heart studies to longitudinal clinically relevant AF animal studies and finally to clinical trials is necessary to identify patient-specific arrhythmogenic substrates and develop novel AF treatments.

Unmasking Arrhythmogenic Hubs of Reentry Driving Persistent Atrial Fibrillation for Patient-Specific Treatment.

Background Atrial fibrillation (AF) driver mechanisms are obscured to clinical multielectrode mapping approaches that provide partial, surface-only visualization of unstable 3-dimensional atrial conduction. We hypothesized that transient modulation of refractoriness by pharmacologic challenge during multielectrode mapping improves visualization of hidden paths of reentrant AF drivers for targeted ablation. Methods and Results Pharmacologic challenge with adenosine was tested in ex vivo human hearts with a history of AF and cardiac diseases by multielectrode and high-resolution subsurface near-infrared optical mapping, integrated with 3-dimensional structural imaging and heart-specific computational simulations. Adenosine challenge was also studied on acutely terminated AF drivers in 10 patients with persistent AF. Ex vivo, adenosine stabilized reentrant driver paths within arrhythmogenic fibrotic hubs and improved visualization of reentrant paths, previously seen as focal or unstable breakthrough activation pattern, for targeted AF ablation. Computational simulations suggested that shortening of atrial refractoriness by adenosine may (1) improve driver stability by annihilating spatially unstable functional blocks and tightening reentrant circuits around fibrotic substrates, thus unmasking the common reentrant path; and (2) destabilize already stable reentrant drivers along fibrotic substrates by accelerating competing fibrillatory wavelets or secondary drivers. In patients with persistent AF, adenosine challenge unmasked hidden common reentry paths (9/15 AF drivers, 41±26% to 68±25% visualization), but worsened visualization of previously visible reentry paths (6/15, 74±14% to 34±12%). AF driver ablation led to acute termination of AF. Conclusions Our ex vivo to in vivo human translational study suggests that transiently altering atrial refractoriness can stabilize reentrant paths and unmask arrhythmogenic hubs to guide targeted AF driver ablation treatment.