Pulsed field ablation (PFA) has emerged as a transformative technology for cardiac ablation due to its efficiency and favorable safety profile. However, intravascular hemolysis has been increasingly recognized adverse effect across preclinical and clinical studies, infrequently progressing to acute kidney injury (AKI). The mechanisms, determinants, and clinical relevance of PFA-related hemolysis remain incompletely understood. Herein, we review the pathophysiology of PFA-related hemolysis and measures to mitigate its occurrence, discuss the biomarker-related changes and perform a comprehensive review of preclinical hemolysis models. Continued development of physiological benchtop models including numerical models to better understand PFA-related hemolysis and translation to bedside is needed. Furthermore, transparent cross-platform evaluation of hemolysis will be critical in the light of rapidly evolving PFA technologies.

Atrial standstill (AS) is the complete absence of atrial electrical and mechanical activity caused by diffuse atrial myocardial disease, distinct from sinus node dysfunction. First documented in 1897 and often misdiagnosed as atrial fibrillation, it arises from SCN5A loss-of-function, NPPA, or EMD/LMNA mutations, muscular dystrophies, and infiltrative or idiopathic fibrotic processes. Diagnosis requires absent P waves, absent atrial electrograms, and failure of atrial capture at maximal pacing output, with late gadolinium enhancement MRI and electroanatomic mapping demonstrating diffuse fibrosis. Thromboembolism complicates 30-54% of cases. Management comprises permanent pacing, anticoagulation, and gene-specific risk stratification for defibrillator eligibility. AS is best understood as the end-stage of fibrotic atrial cardiomyopathy (EHRAS Class II-III); absence of trials, unvalidated risk tools, and incomplete genotype-phenotype correlation warrant a multicenter registry.